Journal articles on the topic 'Venous occlusion pressure'
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Maarek, J. M., T. S. Hakim, and H. K. Chang. "Analysis of pulmonary arterial pressure profile after occlusion of pulsatile blood flow." Journal of Applied Physiology 68, no. 2 (February 1, 1990): 761–69. http://dx.doi.org/10.1152/jappl.1990.68.2.761.
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In isolated canine lung lobes perfused with a pulsatile pump, arterial occlusions were performed and the postocclusion arterial pressure profiles were analyzed to estimate the pulmonary capillary pressure. A solenoid valve interposed between the pump and the lobar artery was used to perform arterial occlusions at several instants equally distributed within a pressure cycle. Double occlusions were also accomplished by simultaneously activating the solenoid valve and clamping the venous outflow of the lung lobe. To analyze an arterial occlusion pressure profile, we computed the best monoexponential fit of the pressure decay over a short period of time after the occlusion maneuvers. Two estimates of the capillary pressure were derived from this analysis: 1) the extrapolation of the exponential fit to the instant of occlusion, and 2) the point at which the recorded pressure decay curve merges with the exponential fit. The pressures thus determined were compared with the double occlusion pressure that provided an independent estimate of the pulmonary capillary pressure. Our results show that, under a wide range of conditions, the estimates of the capillary pressure obtained from the arterial occlusion data are nearly equal to the double occlusion pressures. Additionally, we estimated the capillary pressure variations within a pressure cycle by examining the occlusion pressures sampled at different instants of the cycle. The pulsatility of the pulmonary microvascular pressure varied with the pump frequency as well as the state of arterial and venous vasoaction. These variations are consistent with the representation of the lung vasculature as a low-pass filter.
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Baconnier, P. F., A. Eberhard, and F. A. Grimbert. "Theoretical analysis of occlusion techniques for measuring pulmonary capillary pressure." Journal of Applied Physiology 73, no. 4 (October 1, 1992): 1351–59. http://dx.doi.org/10.1152/jappl.1992.73.4.1351.
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We have developed a model including three serial compliant compartments (arterial, capillary, and venous) separated by two resistances (arterial and venous) for interpreting in vivo single pulmonary arterial or venous occlusion pressure profiles and double occlusion. We formalized and solved the corresponding system of equations. We showed that in this model 1) pulmonary capillary pressure (Pc) profile after arterial or venous occlusion has an S shape, 2) the estimation of Pc by zero time extrapolation of the slow component of the arterial occlusion profile (Pcao) always overestimates Pc, 3) symmetrically such an estimation on the venous occlusion profile (Pcvo) always underestimates Pc, 4) double occlusion pressure (Pcdo) differs from Pc. We evaluated the impact of varying parameter values in the model with parameter sets drawn either from the literature or from arbitrary arterial and venous pressures, being respectively 20 and 5 mmHg. Resulting Pcao-Pc differences ranged from 0.4 to 5.4 mmHg and resulting Pcvo-Pc differences ranged from -0.3 to -5.0 mmHg. Pcdo-Pc was positive or negative, its absolute value in general being negligible (< 1.1 mmHg).
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Calugaru, Dan. "Intraocular pressure modifications in patients with acute central/hemicentral retinal vein occlusions." International Journal of Ophthalmology 14, no. 6 (June 18, 2021): 931–35. http://dx.doi.org/10.18240/ijo.2021.06.20.
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Intraocular pressure (IOP) modifications in patients with acute central/hemicentral retinal vein occlusions (RVOs) consist in IOP reductions and increases. The IOP reduction is due to a transitional hyposecretory phase of the aqueous humor, that increases gradually until 3mo after the venous occlusion onset, and then finally disappears after month 4th. The IOP increases lead to the ocular hypertension and glaucoma. The possible pathogenetic correlations between ocular hypertension/glaucoma and acute central/hemicentral RVOs have been classified into three groups: 1) the venous occlusion precedes the ocular hypertension/glaucoma causing neovascular glaucoma and secondary angle-closure glaucoma without rubeosis; 2) the ocular hypertension and the glaucoma precede the venous occlusion and favor its appearance (ocular hypertension, primary angle-closure, primary angle-closure glaucoma, and open angle glaucomas); and 3) the venous occlusion and the ocular hypertension/glaucoma are mostly age dependent appearances due to common vascular and collagen alterations, lacking a causal connection between the 2 conditions.
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Perry, M. A., J. G. Colebatch, W. E. Glover, and I. C. Roddie. "Measurement of capillary pressure in humans using a venous occlusion method." Journal of Applied Physiology 60, no. 6 (June 1, 1986): 2114–17. http://dx.doi.org/10.1152/jappl.1986.60.6.2114.
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The venous occlusion technique was used to measure capillary pressure in the forearm and foot of man over a wide range of venous pressures. In six recumbent subjects venous pressure (Pv) in the forearm (mean +/- SE) was 9.3 +/- 1.4 mmHg and the venous occlusion estimate of capillary pressure (Pc) was 17.0 +/- 1.6 mmHg, whereas in another six subjects Pv in the foot was 17.1 +/- 1.2 mmHg and Pc was 23.4 +/- 2.5 mmHg. Venous pressure in the limbs was increased either by changes in posture or by venous congestion with a sphygmomanometer cuff. On standing Pv in the foot increased to 95.2 +/- 1.5 mmHg and Pc rose to 112.8 +/- 3.1 mmHg. The relationship established between venous pressure and capillary pressure in the forearm is Pc = 1.16 Pv + 8.1, whereas in the foot the relationship is Pc = 1.2 Pv + 1.6. The magnitude and duration of the changes in capillary pressure were also recorded during reactive hyperemia. The venous occlusion method of measuring capillary pressure is simple and easily applied to studies in humans.
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Savla, Jill J., Benjamin Kelly, Emil Krogh, Christopher L. Smith, Ganesh Krishnamurthy, Andrew C. Glatz, Aaron G. DeWitt, et al. "Occlusion Pressure of the Thoracic Duct in Fontan Patients With Lymphatic Failure: Does Dilatation Challenge Contractility?" World Journal for Pediatric and Congenital Heart Surgery 13, no. 6 (October 26, 2022): 737–44. http://dx.doi.org/10.1177/21501351221119394.
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Background The Fontan circulation challenges the lymphatic system. Increasing production of lymphatic fluid and impeding lymphatic return, increased venous pressure may cause lymphatic dilatation and decrease lymphatic contractility. In-vitro studies have reported a lymphatic diameter-tension curve, with increasing passive stretch affecting the intrinsic contractile properties of each thoracic duct segment. We aimed to describe thoracic duct occlusion pressure and asses if thoracic duct dilation impairs contractility in individuals with a Fontan circulation and lymphatic failure. Methods Central venous pressure and thoracic duct measurements were retrospectively collected from 31 individuals with a Fontan circulation. Thoracic duct occlusion pressure was assessed during a period of external manual compression and used as an indicator of lymphatic vessel contractility. Measurements of pressure were correlated with measurements of the thoracic duct diameter in images obtained by dynamic contrast-enhanced MR lymphangiography. Results The average central venous pressure and average pressure of the thoracic duct were 17 mm Hg. During manual occlusion, the thoracic duct pressure significantly increased to 32 mm Hg. The average thoracic duct diameter was 3.3 mm. Thoracic duct diameter correlated closely with the central venous pressure. The rise in pressure following manual occlusion showed an inverse correlation with the diameter of the thoracic duct. Conclusion Higher central venous pressures are associated with increasing diameters of the thoracic duct. When challenged by manual occlusion, dilated thoracic ducts display a decreased ability to increase pressure. Dilatation and a resulting decreased contractility may partly explain the challenged lymphatic system in individuals with a Fontan circulation.
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Fujita, Daisuke, Yusuke Kubo, and Tatsuya Tagawa. "Effect of Lower Limb Venous Dilation on the Autonomic Cardiac Response among Healthy Young Men." Healthcare 11, no. 4 (February 13, 2023): 548. http://dx.doi.org/10.3390/healthcare11040548.
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Venous occlusion of the lower limbs, which simulates edema, can alter heart rate variability (HRV) by increasing feedback information from group III/IV sensory fibers. Our aim was to quantify this effect among healthy young men. The study group included 13 men (mean age, 20.4 years). Venous occlusion of the lower limbs was induced using a pressure cuff around both thighs. The effect of occlusion on autonomic cardiac response was quantified under occlusion pressures of 20, 60, and 100 mmHg. Compression was applied for 5 min. HRV was evaluated from changes in the low-frequency (LF) and high-frequency (HF) power of the electrocardiogram and the resulting LF/HF balance. Near-infrared spectroscopy of the leg was used to quantify the effects of occlusion on deoxyhemoglobin, measured as the area under the curve (HHb-AUC). The occlusion pressure of 100 mmHg induced a significant increase in the LF/HF ratio, compared to the baseline (p < 0.05). HHb-AUC was highest for the 100 mmHg occlusion pressure compared with the 20 and 60 mmHg pressures (p < 0.01). These findings indicate that venous dilation may elicit a shift towards sympathetic dominance in the autonomic balance.
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Braam, B., H. A. Koomans, T. J. Rabelink, and R. Berckmans. "Pitfalls of venous occlusion method for determination of capillary pressure in humans." Journal of Applied Physiology 66, no. 2 (February 1, 1989): 997–1002. http://dx.doi.org/10.1152/jappl.1989.66.2.997.
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We tested the method of estimating capillary pressure from venous pressure transients obtained after sudden venous clamping in a hydrodynamic model. The basic principles were confirmed in the model, but it was found that when occlusion was caused over a relatively wide distance or in a predistended vessel, capillary pressure was overrated. This problem was due to volume backflow from the occlusion site, since it could be eliminated by placing a one-way valve upstream from the occlusion site. Upstream from the valve, the venous pressure transient accurately followed capillary pressure. Downstream, however, the reading of capillary pressure was impaired by the backflow volume squeezed between valve and occlusion clamp, which caused an immediate large pressure elevation. We also tested the method recently advanced to estimate capillary pressure in humans from venous pressure curves obtained after rapid venous occlusion with an air-filled compression cuff. With the cuff around the upper arm, venous pressure was recorded at different levels along the forearm. The tracings obtained from the dorsum of the hand and halfway along the forearm did not show the initial rapid upstrokes that might indicate the capillary pressure. Tracings obtained slightly below or above the cubital fossa were similar to those seen downstream from the one-way valve in the model. Extrapolation to zero-time, using the distally recorded curves as a template, yielded values equal to venous pressure. We conclude that although the problem of backflow can be circumvented by pressure recording distal from venous valves, the method of venous occlusion by a circular upper-arm cuff may not be appropriate to estimate capillary pressure in humans.
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Alomari, Mahmoud A., Angela Solomito, Rafael Reyes, Syed Muaz Khalil, Robert H. Wood, and Michael A. Welsch. "Measurements of vascular function using strain-gauge plethysmography: technical considerations, standardization, and physiological findings." American Journal of Physiology-Heart and Circulatory Physiology 286, no. 1 (January 2004): H99—H107. http://dx.doi.org/10.1152/ajpheart.00529.2003.
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The main purpose of the present study was to examine the relationships between measures of fitness [estimated peak oxygen consumption (V̇o2 peak) and handgrip strength] and forearm vascular function in 55 young (22.6 ± 3.5 yr) adults. In addition, the present study considered methodological and technical aspects regarding the examination of the venous system using mercury in-Silastic strain-gauge plethysmography (MSGP). Forearm venous capacitance and outflow were examined using five different [7, 14, 21, 28, and 35 mmHg < diastolic blood pressure (DBP)] venous occlusion pressures and after a 5- and 10-min period of venous occlusion. A pressure of 7 mmHg < DBP and a period of 10 min venous occlusion produced the greatest ( P < 0.05) venous capacitance and outflow, without altering arterial indexes. Reproducibility of forearm arterial and venous indexes were evaluated at rest and after 5 min of upper arm arterial occlusion at 240 mmHg on three different occasions within 10 days with the interclass correlation coefficient ranging from 0.70 and 0.94. Estimated V̇o2 peak correlated with postocclusion arterial inflow ( r = 0.54, P = 0.012) and resting venous outflow ( r = 0.56, P = 0.016). Finally, handgrip strength was associated with venous capacitance ( r = 0.57, P = 0.007) and outflow ( r = 0.67, P = 0.001). These results indicate that the examination of forearm vascular function using MSGP is reproducible. Moreover, the data show the importance of careful consideration of the selection of venous occlusion pressure and period when implementing these measures in longitudinal trials. Finally, the associations between fitness and venous measures suggest a link between venous function and exercise performance.
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Bishop, Frank S., Michael A. Finn, Mical Samuelson, and Richard H. Schmidt. "Endovascular balloon angioplasty for treatment of posttraumatic venous sinus thrombosis." Journal of Neurosurgery 111, no. 1 (July 2009): 17–21. http://dx.doi.org/10.3171/2009.2.jns08491.
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In severe cases, posttraumatic cerebral sinus thrombosis can result in venous congestion and persistent intracranial hypertension refractory to both conventional medical therapy and surgical decompression. The authors report a unique case of a patient successfully treated with endovascular mechanical thrombolysis using balloon angioplasty for clinically significant posttraumatic venous sinus thrombosis and review the reported treatments for cerebral venous sinus occlusive disease. This 18-year-old man suffered severe closed head injury from a fall while skateboarding. A head CT scan demonstrated basilar skull fractures involving the left jugular foramen. A CT angiogram revealed thrombosis of the left transverse sinus and occlusion of the sigmoid sinus and internal jugular vein. Despite treatment with anticoagulation therapy and decompressive hemi- and suboccipital craniectomies, intracranial hypertension remained refractory. Serial angiography demonstrated progressive sinus occlusion. Endovascular balloon thrombolysis of the left transverse and sigmoid sinuses resulted in immediate reduction of intracranial pressures and improved sinus patency. Intracranial pressure measurements remained low after the procedure. The patient eventually improved neurologically, was able to follow commands and walk, and was discharged to a rehabilitation facility for further recovery. Anticoagulation therapy, surgical decompression, and endovascular thrombolysis have been reported as treatment modalities for clinically significant posttraumatic venous sinus thrombosis. In this case, endovascular mechanical thrombolysis with balloon angioplasty resulted in resolution of thrombus and successful immediate reduction of intracranial pressure. This treatment may be considered in patients with critically elevated intracranial pressure from posttraumatic venous sinus occlusion refractory to other treatment measures.
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Moncrief, Karli, and Susan Kaufman. "Splenic baroreceptors control splenic afferent nerve activity." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 290, no. 2 (February 2006): R352—R356. http://dx.doi.org/10.1152/ajpregu.00489.2005.
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Stenosis of either the portal or splenic vein increases splenic afferent nerve activity (SANA), which, through the splenorenal reflex, reduces renal blood flow. Because these maneuvers not only raise splenic venous pressure but also reduce splenic venous outflow, the question remained as to whether it is increased intrasplenic postcapillary pressure and/or reduced intrasplenic blood flow, which stimulates SANA. In anesthetized rats, we measured the changes in SANA in response to partial occlusion of either the splenic artery or vein. Splenic venous and arterial pressures and flows were simultaneously monitored. Splenic vein occlusion increased splenic venous pressure (9.5 ± 0.5 to 22.9 ± 0.8 mmHg, n = 6), reduced splenic arterial blood flow (1.7 ± 0.1 to 0.9 ± 0.1 ml/min, n = 6) and splenic venous blood flow (1.3 ± 0.1 to 0.6 ± 0.1 ml/min, n = 6), and increased SANA (1.7 ± 0.4 to 2.2 ± 0.5 spikes/s, n = 6). During splenic artery occlusion, we matched the reduction in either splenic arterial blood flow (1.7 ± 0.1 to 0.7 ± 0.05, n = 6) or splenic venous blood flow (1.2 ± 0.1 to 0.5 ± 0.04, n = 5) with that seen during splenic vein occlusion. In neither case was there any change in either splenic venous pressure (−0.4 ± 0.9 mmHg, n = 6 and +0.1 ± 0.3 mmHg, n = 5) or SANA (−0.11 ± 0.15 spikes/s, n = 6 and −0.05 ± 0.08 spikes/s, n = 5), respectively. Furthermore, there was a linear relationship between SANA and splenic venous pressure ( r = 0.619, P = 0.008, n = 17). There was no such relationship with splenic venous ( r = 0.371, P = 0.236, n = 12) or arterial ( r = 0.275, P = 0.413, n = 11) blood flow. We conclude that it is splenic venous pressure, not flow, which stimulates splenic afferent nerve activity and activates the splenorenal reflex in portal and splenic venous hypertension.
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Hakim, T. S., and S. Kelly. "Occlusion pressures vs. micropipette pressures in the pulmonary circulation." Journal of Applied Physiology 67, no. 3 (September 1, 1989): 1277–85. http://dx.doi.org/10.1152/jappl.1989.67.3.1277.
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Because of the discrepancies between the arterial and venous occlusion technique and the micropuncture technique in estimating pulmonary capillary pressure gradient, we compared measurements made with the two techniques in the same preparations (isolated left lower lobe of dog lung). In addition, we also obtained direct and reliable measurements of pressures in 0.9-mm arteries and veins using a retrograde catheterization technique, as well as a microvascular pressure made with the double-occlusion technique. The following conclusions were made from dog lobes perfused with autologous blood at normal flow rate of 500–600 ml/min and pressure gradient of 12 mmHg. 1) The double-occlusion technique measures pressure in the capillaries, 2) a small pressure gradient (0.5 mmHg) exists between 30- to 50-micron arteries and veins, 3) a large pressure gradient occurs in arteries and veins greater than 0.9 mm, 4) the arterial and venous occlusion techniques measure pressures in vessels that are less than 900 microns diam but greater than 50 microns, very likely close to 100 microns, 5) serotonin constricts arteries (larger and smaller than 0.9 mm) whereas histamine constricts veins (larger and smaller than 0.9 mm). Thus three different techniques (small retrograde catheter, arterial and venous occlusion, and micropuncture) show consistent results, confirming the presence of significant resistance in large arteries and veins with minimal resistance in the microcirculation.
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Groothuis, Jan T., Linda van Vliet, Miriam Kooijman, and Maria T. E. Hopman. "Venous cuff pressures from 30 mmHg to diastolic pressure are recommended to measure arterial inflow by plethysmography." Journal of Applied Physiology 95, no. 1 (July 2003): 342–47. http://dx.doi.org/10.1152/japplphysiol.00022.2003.
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Venous occlusion strain gauge plethysmography (VOP) is based on the assumption that the veins are occluded and arterial inflow is undisturbed by the venous cuff pressure. Literature is not clear concerning the pressure that should be used. The purpose of this study was to determine the optimal venous occlusion pressure at which the highest arterial inflow is achieved in the forearm, calf, and leg by using VOP. We hypothesized that, for each limb segment, an optimal (range of) venous cuff pressure can be determined. Arterial inflow in each limb segment was measured in nine healthy individuals by VOP by using pressures ranging from 10 mmHg up to diastolic blood pressure. Arterial inflows were similar at cuff pressures between 30 and 60 mmHg for the forearm, leg, and calf. Arterial inflow in the forearm was significantly lower at 10 mmHg compared with the other cuff pressures. In addition, arterial inflows at 20 mmHg tended to be lower in each limb segment than flow at higher cuff pressures. In conclusion, no single optimum venous cuff pressure, at which a highest arterial inflow is achieved, exists, but rather a range of optimum cuff pressures leading to a similar arterial inflow. Venous cuff pressures ranging from 30 mmHg up to diastolic blood pressure are recommended to measure arterial inflow by VOP.
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Watenpaugh, Donald E., Jay C. Buckey, Lynda D. Lane, F. Andrew Gaffney, Benjamin D. Levine, Willie E. Moore, Sheryl J. Wright, and C. Gunnar Blomqvist. "Effects of spaceflight on human calf hemodynamics." Journal of Applied Physiology 90, no. 4 (April 1, 2001): 1552–58. http://dx.doi.org/10.1152/jappl.2001.90.4.1552.
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Chronic microgravity may modify adaptations of the leg circulation to gravitational pressures. We measured resting calf compliance and blood flow with venous occlusion plethysmography, and arterial blood pressure with sphygmomanometry, in seven subjects before, during, and after spaceflight. Calf vascular resistance equaled mean arterial pressure divided by calf flow. Compliance equaled the slope of the calf volume change and venous occlusion pressure relationship for thigh cuff pressures of 20, 40, 60, and 80 mmHg held for 1, 2, 3, and 4 min, respectively, with 1-min breaks between occlusions. Calf blood flow decreased 41% in microgravity (to 1.15 ± 0.16 ml · 100 ml−1 · min−1) relative to 1-G supine conditions (1.94 ± 0.19 ml · 100 ml−1 · min−1, P = 0.01), and arterial pressure tended to increase ( P = 0.05), such that calf vascular resistance doubled in microgravity (preflight: 43 ± 4 units; in-flight: 83 ± 13 units; P < 0.001) yet returned to preflight levels after flight. Calf compliance remained unchanged in microgravity but tended to increase during the first week postflight ( P > 0.2). Calf vasoconstriction in microgravity qualitatively agrees with the “upright set-point” hypothesis: the circulation seeks conditions approximating upright posture on Earth. No calf hemodynamic result exhibited obvious mechanistic implications for postflight orthostatic intolerance.
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Song, Myung Gyu, Tae-Seok Seo, Baek-hui Kim, and Jeong Ho Kim. "Mechanical recanalization for clot occlusion of venous access ports: experimental study using ports with clot occlusion." Journal of Vascular Access 18, no. 2 (March 2017): 158–62. http://dx.doi.org/10.5301/jva.5000677.
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Purpose To test the hypothesis that mechanical injection of saline is safe and effective in restoring patency of totally implantable venous access ports (TIVAPs) with clot occlusion. We devised an experimental port model for the evaluation of mechanical TIVAP recanalization prior to its clinical application. Materials and Methods The clot TIVAP occlusion model was constructed by filling the catheter with swine blood and incubating it at 37.5°C. The model was incubated for different lengths of time ranging from 1 day to 7 days. Each incubation time point included 20 ports. Total catheter occlusion of the TIVAPs was assessed with a 10-mL saline syringe equipped with a non-coring needle. Occlusion was defined as no passage of saline through the catheter when it was aspirated and infused gently with the 10-mL saline syringe. Pressure was evaluated during recanalization with an indeflator. Histological examination was performed on the clot obtained during recanalization. Results Among the 140 total experimental ports, 65 occlusions (46.4%) were detected. Of these 65 occlusions, 56 (86.1%) were recanalized by mechanical saline pressure via the indeflator. The indeflator pressure ranged from 29 pound per square-inch (psi) to 265 psi at mechanical catheter recanalization (mean: 110 psi). Histologically, all specimens from the model ports exhibited a similar appearance; specifically, erythrocytes, cells, and fibrin were evenly scattered throughout the clot. Conclusions Our data indicate that it is feasible to generate a TIVAP clot occlusion model with swine blood. Moreover, mechanical recanalization was suitable for resolving occluded catheters without thrombolytic agents.
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Hiatt, W. R., S. Y. Huang, J. G. Regensteiner, A. J. Micco, G. Ishimoto, M. Manco-Johnson, J. Drose, and J. T. Reeves. "Venous occlusion plethysmography reduces arterial diameter and flow velocity." Journal of Applied Physiology 66, no. 5 (May 1, 1989): 2239–44. http://dx.doi.org/10.1152/jappl.1989.66.5.2239.
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The measurement of peripheral blood flow by plethysmography assumes that the cuff pressure required for venous occlusion does not decrease arterial inflow. However, studies in five normal subjects suggested that calf blood flow measured with a plethysmograph was less than arterial inflow calculated from Doppler velocity measurements. We hypothesized that the pressure required for venous occlusion may have decreased arterial velocity. Further studies revealed that systolic diameter of the superficial femoral artery under a thigh cuff decreased from 7.7 +/- 0.4 to 5.6 +/- 0.7 mm (P less than 0.05) when the inflation pressure was increased from 0 to 40 mmHg. Cuff inflation to 40 mmHg also reduced mean velocity 38% in the common femoral artery and 47% in the popliteal artery. Inflation of a cuff on the arm reduced mean velocity in the radial artery 22% at 20 mmHg, 26% at 40 mmHg, and 33% at 60 mmHg. We conclude that inflation of a cuff on an extremity to low pressures for venous occlusion also caused a reduction in arterial diameter and flow velocity.
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Coffman, Stephanie A., Jasmeet Singh, Stacey Wolfe, and Kyle M. Fargen. "Unexpected occlusion of the contralateral transverse sinus after stenting for idiopathic intracranial hypertension." Interventional Neuroradiology 24, no. 6 (July 5, 2018): 718–21. http://dx.doi.org/10.1177/1591019918787161.
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A woman in her thirties with intracranial hypertension underwent stenting of the right transverse-sigmoid (TS) junction with resolution of the pressure gradient. Due to persisting symptoms at follow-up, she underwent a repeat study showing a patent right TS stent but the non-dominant left transverse sinus, patent on initial studies, was now completely occluded. According to the positive feedback loop hypothesis, stenting of the right transverse sinus should have resulted in a reduction in intracranial pressures (confirmed by post-stenting lumbar puncture), but also an increase in left transverse sinus diameter, opposed to the occlusion seen on venography. This unexpected finding can be explained by the positive feedback loop hypothesis if a revision is made accounting for intramural venous pressures as an opposing force of venous sinus stenosis, as venous outflow obstruction in the dominant venous sinus pathway provided an increased intramural venous pressure in the non-dominant sinus facilitating patency against extramural pressures.
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Legare, Dallas J., and W. Wayne Lautt. "Hepatic venous resistance site in the dog: localization and validation of intrahepatic pressure measurements." Canadian Journal of Physiology and Pharmacology 65, no. 3 (March 1, 1987): 352–59. http://dx.doi.org/10.1139/y87-061.
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Intrahepatic pressure (9.4 ± 0.3 mmHg; 1 mmHg = 133.32 Pa), measured proximal to a hepatic venous resistance site, was insignificantly different from portal venous pressure (9.6 ± 0.4 mmHg). This lobar venous pressure is not wedged hepatic venous pressure as it is measured from side holes in a catheter with a sealed tip. Validation of the lobar venous pressure measurement was done in a variety of ways and using different sizes and configurations of catheters. The site of hepatic venous resistance in the dog is localized to a narrow sphincterlike region about 0.5 cm in length and within 1–2 cm (usually within 1 cm) of the junction of the vena cava and hepatic veins. Sinusoidal and portal venous resistance appears insignificant in the basal state and large increases in liver blood volume (histamine infusion or passive vena caval occlusion) or large decreases in liver blood volume (passive vascular occlusion) do not alter the insignificant pressure gradient between portal and lobar venous pressures. Norepinephrine infusion (1.25 μg∙kg−1∙min−1 intraportal) and hepatic sympathetic nerve stimulation (10 Hz) led to a significantly greater rise in portal venous pressure than in lobar venous pressure, indicating some presinusoidal (and (or) sinusoidal) constriction and this indicates that lobar venous pressure cannot be assumed under all conditions to accurately reflect portal pressure. However, most of the rise in portal venous pressure induced by intraportal infusion of norepinephrine or nerve stimulation and virtually all of the pressure rise induced by histamine could be attributed to the postsinusoidal resistance site. This site was highly localized since 62% of the pressure drop from the portal vein to the inferior vena cava in the basal state occurred over a 0.5-cm length. However, the anatomical position of this site was different in the dog compared with the cat.
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Neumann, F., W. Mohl, and W. Schreiner. "Coronary sinus pressure and arterial flow during intermittent coronary sinus occlusion." American Journal of Physiology-Heart and Circulatory Physiology 256, no. 3 (March 1, 1989): H906—H915. http://dx.doi.org/10.1152/ajpheart.1989.256.3.h906.
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The relationship between coronary artery flow and coronary venous pressure during intermittent coronary sinus occlusion was studied in dogs at normal perfusion, left anterior descending artery occlusion, and reperfusion. Coronary sinus occlusion and release phases were varied systematically. The periodicity of the data and the assumption of a linear relationship between pressure and flow suggested Fourier analysis as a methodological approach. To show the systematic slow oscillations of coronary venous pressure and arterial flow induced by intermittent occlusion of the coronary sinus, the data were smoothed by superimposing consecutive cycles of identical occlusion-release timing and filtering the higher frequencies. A small number of Fourier components, corresponding to the time scale of the respective occlusion-release cycle, was sufficient to study the long wavelength behavior. The effect of arbitrarily varying the occlusion-to-release ratio at a given total cycle length was investigated in hypothetical pressure and flow curves based on interpolation of experimental Fourier coefficients. By means of a transfer function relating pressure and flow in the frequency domain, it was possible to predict the arterial flow curve using coronary venous pressure measurements only. Because at zero frequency the pressure-flow relationship cannot be assumed to be linear, the mean value of flow could not be obtained in this way. However, the deviation of flow from the mean, i.e., the shape of the flow curve, was reproduced satisfactorily.
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Kurstjens, RLM, MAF de Wolf, JHH van Laanen, MW de Haan, CHA Wittens, and R. de Graaf. "Hemodynamic significance of collateral blood flow in chronic venous obstruction." Phlebology: The Journal of Venous Disease 30, no. 1_suppl (February 28, 2015): 27–34. http://dx.doi.org/10.1177/0268355515569433.
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Introduction Complaints related to the post-thrombotic syndrome do not always correlate well with the extent of post-thrombotic changes on diagnostic imaging. One explanation might be a difference in development of collateral blood flow. The aim of this study is to investigate the hemodynamic effect of collateralisation in deep venous obstruction. Methodology Resting intravenous pressure of the common femoral vein was measured bilaterally in the supine position of patients with unilateral iliofemoral post-thrombotic obstruction. In addition, pressure in control limbs was also measured in the common femoral vein after sudden balloon occlusion in the external iliac vein. Results Fourteen patients (median age 42 years, 12 female) were tested. In eleven limbs post-thrombotic disease extended below the femoral confluence. Median common femoral vein pressure was 17.0 mmHg in diseased limbs compared to 12.8 mmHg in controls (p = 0.001) and 23.5 mmHg in controls after sudden balloon occlusion (p = 0.009). Results remained significant after correcting for non-occlusive post-thrombotic disease. Conclusion This study shows that common femoral vein pressure is increased in post-thrombotic iliofemoral deep venous obstruction, though not as much as after sudden balloon occlusion. The latter difference could explain the importance of collateralisation in deep venous obstructive disease and the discrepancy between complaints and anatomical changes; notwithstanding, the presence of collaterals does not eliminate the need for treatment.
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Hakim, T. S. "Criteria for analysis of arterial and venous occlusion." Journal of Applied Physiology 70, no. 2 (February 1, 1991): 665–75. http://dx.doi.org/10.1152/jappl.1991.70.2.665.
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To provide a better understanding of analysis of arterial (AO) and venous occlusion (VO) tracings, using a constant and nonpulsatile perfusion pressure system, we set up an isolated in situ dog lobe preparation perfused with autologous blood. Four signals were recorded: arterial pressure, arterial inflow rate, venous pressure, and venous outflow rate. The four signals were recorded into the memory of a computer. When flow into the lobe was abruptly stopped (AO), flow out of the lung continued unchanged for approximately 150 ms and then decreased slowly to zero. Likewise, when flow out of the lung was abruptly stopped (VO), the flow into the lung continued unchanged for approximately 130 ms and then decreased slowly to zero. A monoexponential curve was fitted to different stretches of data between 0.1 and 5 s postocclusion and extrapolated to the instant of occlusion (defined here as the instant when flow at the site of occlusion becomes zero). The results indicate that 1) the first 150 ms postocclusion should be avoided because of the oscillatory artifacts generated by the occlusion maneuver, 2) use of a long segment of postocclusion data (5 s) tends to underestimate the middle pressure gradient and overestimate the arterial and venous pressure gradients, and 3) the changes in segmental vascular resistance under different experimental conditions were found to be unaffected by the criteria of analysis. Analysis of the postocclusion (AO and VO) tracings was found to be most compatible with the double-occlusion capillary pressure by fitting a stretch of data between 0.2 and 2.5 s postocclusion and extrapolating back to the instant when flow becomes zero at the site of occlusion but no earlier.
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Isago, T., L. D. Traber, D. N. Herndon, S. Abdi, K. Fujioka, and D. L. Traber. "Determination of pulmonary microvascular reflection coefficient in sheep by venous occlusion." Journal of Applied Physiology 69, no. 6 (December 1, 1990): 2311–16. http://dx.doi.org/10.1152/jappl.1990.69.6.2311.
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We devised a technique that permitted elevation of pulmonary pressures in unanesthetized sheep by occluding their pulmonary veins. Using this technique, we raised pulmonary capillary pressure from a baseline of 13.2 +/- 2.2 to 35.3 +/- 5.1 mmHg. This increased lung lymph flow (from 8.8 +/- 2.7 to 53.1 +/- 13.9 ml/h). We estimated the pulmonary microvascular oncotic reflection coefficient and found it to be 0.82 +/- 0.05 (SD). The filtration coefficient was 0.019 +/- 0.005 ml.mmHg-1.min-1. During the period of increased pressure, the animals had stable arterial pressures and cardiac outputs. None of the animals developed blood coagulation problems. These data illustrate the usefulness of pulmonary venous occlusion to elevate pulmonary microvascular pressure to obtain plasma-to-lymph protein concentration ratios independent of flow, allowing for the calculation of the oncotic reflection coefficient.
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Vilela, P., R. Willinsky, and K. terBrugge. "Treatment of Intracranial Venous Occlusive Disease with Sigmoid Sinus Angioplasty and Stent Placement in a Case of Infantile Multifocal Dural Arteriovenous Shunts." Interventional Neuroradiology 7, no. 1 (March 2001): 51–60. http://dx.doi.org/10.1177/159101990100700108.
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The infantile dural arteriovenous shunts are multifocal involving different dural sinuses and progress to an occlusive venopathy with sigmoid sinus and/or jugular bulb stenosis and subsequent occlusion. We report a successful angioplasty and stent placement of a sigmoid sinus — jugular bulb stenosis due to venous occlusive disease in a patient with infantile dural arteriovenous shunts. A five-year-old patient presented with status epilepticus due to severe venous congestive encephalopathy. The angiogram revealed multifocal dural arteriovenous shunts, occlusion of the right sigmoid sinus, absence of cavernous sinuses and significant stenosis of the left sigmoid sinus — jugular bulb. By transvenous approach, percutaneous transluminal balloon angioplasty and stent placement of the stenosed left sigmoid sinus — jugular bulb segment was performed. This resulted in a significant decrease of the venous pressure gradient across the stenosis and allowed a dramatic clinical recovery. Dural sinus angioplasty and stent placement appears to be a safe and effective procedure and should be considered in the treatment of the venous occlusive disease associated with infantile dural arteriovenous shunts.
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Andrade, James N. B. M. de, Angelo J. Stopiglia, Denise T. Fantoni, Maria C. Abduch, and Marcia Kahvegian. "Outflow occlusion for circulatory arrest in dogs." Pesquisa Veterinária Brasileira 29, no. 2 (February 2009): 137–42. http://dx.doi.org/10.1590/s0100-736x2009000200009.
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The purpose of this study was to evaluate the possibility of producing circulatory arrest by occlusion of the pulmonary trunk as an alternative to the venous inflow occlusion through the left hemithorax. Eight healthy mongrel dogs were divided in two groups. Group I underwent 4 minutes of outflow occlusion and Group II was submitted to 8 minutes of circulatory arrest. Outflow occlusion was performed through left thoracotomy and pericardiotomy by passing a Rumel tourniquet around the pulmonary trunk. Physical examination, electrocardiography, echocardiography, blood gas analyses, hemodynamic, and oxygen transport variables were obtained before and after the procedure. The dogs from Group I did not have any clinical, electrocardiographic, echocardiographic, or hemo-dynamic abnormalities after anesthetic recover. In the Group II, only one dog survived, which had no clinical, electrocardiographic, or echocardiographic abnormalities. In this last dog, just after releasing the occlusion, it was detected increases in the following parameters: heart rate (HR), systolic, diastolic and mean arterial blood pressure (SAP; DAP; MAP), pulmonary artery pressure (PAP), pulmonary wedge pressure (PWP), central venous pressure (CVP), cardiac output (CO), systolic index (SI), cardiac index (CI), left and right ventricular stroke work (LVSW; RVSW), oxygen delivery index (DO2), oxygen consumption index (VO2), and oxygen extraction (O2 ext). Moreover, the oxygen content of arterial and mixed venous blood (CaO2; CvO2), and the arterial and mixed venous partial pressure of oxygen (PaO2; PvO2) were decreased 5 minutes after circulatory arrest. Outflow occlusion is a feasible surgical procedure for period of 4 minutes of circulatory arrest.
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Yoshimoto, Yuhei, Masaru Endo, Takashi Mori, and Susumu Wakai. "Correlation between venous stump pressure and brain damage after cortical vein occlusion: an experimental study." Journal of Neurosurgery 86, no. 4 (April 1997): 694–98. http://dx.doi.org/10.3171/jns.1997.86.4.0694.
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✓ A canine model of cortical vein occlusion was used to evaluate whether data obtained from monitoring venous stump pressure could help predict cerebral infarction after venous obstruction. Following bilateral parasagittal craniotomy, the cortical vein in each hemisphere was temporarily occluded and the increase in pressure was directly measured. Permanent venous obstruction was subsequently produced, and parenchymal brain damage 24 hours later was classified as: Stage 0, no parenchymal damage; Stage I, mild edema; Stage II, moderate parenchymal edema and/or ischemic changes in neurons; and Stage III, moderate-to-severe hemorrhage. The histological stages correlated closely with the rise in venous pressure: mean pressure increases (± standard deviation) were 5.5 ± 2.9 mm Hg in hemispheres graded as Stage 0 (12 hemispheres), 7.7 ± 3.2 mm Hg in those graded as Stage I (five), 11.2 ± 4.1 mm Hg in those classed as Stage II (five), and 16.4 ± 5 in those categorized as Stage III (seven). There were significant differences between Stages 0 and II (p < 0.01) and between Stages 0 and III (p < 0.001). Disruption of the blood-brain barrier as indicated by extravasation of Evans blue dye correlated well with the pressure increment. These results may indicate the threshold for injury after cortical venous occlusion. Venous stump pressure measurements obtained during a test occlusion may be a useful adjunct in predicting brain damage and may be helpful for intraoperative vessel selection for venous resection.
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Partsch, H. "Do we still need compression bandages? Haemodynamic effects of compression stockings and bandages." Phlebology: The Journal of Venous Disease 21, no. 3 (September 15, 2006): 132–38. http://dx.doi.org/10.1258/026835506778253283.
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Objective: To compare haemodynamic data obtained with elastic compression stockings and inelastic compression material applied with different pressure ranges on the lower extremities. Methods: Haemodynamic effects of compression therapy were demonstrated by measuring venous flow velocity, venous volume, venous reflux and venous pumping function using radioisotopes, phlebography, water displacement volumetry, duplex, air plethysmography, foot volumetry and phlebodynamometry. Results: Light-compression stockings are able to increase venous blood flow velocity in the supine position and to prevent leg swelling after prolonged sitting and standing. In the upright position an interface pressure of more than 50 mmHg is needed for an intermittent occlusion of incompetent veins and for a reduction of ambulatory venous hypertension during walking. Such high interface pressures may rather be achieved by short-stretch, multilayer bandages than by an elastic stocking. Conclusion: Elastic compression stockings exerting interface pressures up to 40 mmHg are effective in preventing or reducing oedema. Multilayer compression bandages with a pressure over 40 mmHg additionally improve severely disturbed venous pumping function.
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Audi, S. H., C. A. Dawson, D. A. Rickaby, and J. H. Linehan. "Localization of the sites of pulmonary vasomotion by use of arterial and venous occlusion." Journal of Applied Physiology 70, no. 5 (May 1, 1991): 2126–36. http://dx.doi.org/10.1152/jappl.1991.70.5.2126.
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In this study, we present a new approach for using the pressure vs. time data obtained after various vascular occlusion maneuvers in pump-perfused lungs to gain insight into the longitudinal distribution of vascular resistance with respect to vascular compliance. Occlusion data were obtained from isolated dog lung lobes under normal control conditions, during hypoxia, and during histamine or serotonin infusion. The data used in the analysis include the slope of the arterial pressure curve and the zero time intercept of the extrapolated venous pressure curve after venous occlusion, the equilibrium pressure after simultaneous occlusion of both the arterial inflow and venous outflow, and the area bounded by equilibrium pressure and the arterial pressure curve after arterial occlusion. We analyzed these data by use of a compartmental model in which the vascular bed is represented by three parallel compliances separated by two series resistances, and each of the three compliances and the two resistances can be identified. To interpret the model parameters, we view the large arteries and veins as mainly compliance vessels and the small arteries and veins as mainly resistance vessels. The capillary bed is viewed as having a high compliance, and any capillary resistance is included in the two series resistances. With this view in mind, the results are consistent with the major response to serotonin infusion being constriction of large and small arteries (a decrease in arterial compliance and an increase in arterial resistance), the major response to histamine infusion being constriction of small and large veins (an increase in venous resistance and a decrease in venous compliance), and the major response to hypoxia being constriction of the small arteries (an increase in arterial resistance). The results suggest that this approach may have utility for evaluation of the sites of action of pulmonary vasomotor stimuli.
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Little, John R., Robert L. Tomsak, Zeyd Y. Ebrahim, and Anthony J. Furlan. "Retinal Artery Pressure and Cerebral Artery Perfusion Pressure in Cerebrovascular Occlusive Disease." Neurosurgery 18, no. 6 (June 1, 1986): 716–20. http://dx.doi.org/10.1227/00006123-198606000-00006.
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Abstract The objectives of the investigation were to measure the retinal artery pressure (RAP) and cortical artery pressure (CAP) in patients undergoing superficial temporal artery to middle cerebral artery (STA-MCA) bypass, to study the relationship between these pressures, and to evaluate our ability to predict CAP on the basis of RAP. The 44 patients undergoing bypass surgery included 26 with ipsilateral internal carotid artery (ICA) occlusion (Group I), 5 with bilateral ICA occlusion (Group II), 4 with inaccessible ICA stenosis proximal to the ophthalmic artery (OA) (Group III), 2 with ICA stenosis distal to the OA (Group IV), 3 with ICA occlusion distal to the OA (Group V), 2 with MCA stenosis (Group VI), and 2 with MCA occlusion (Group VII). Five patients undergoing craniotomy for an asymptomatic saccular aneurysm were used as controls. Mean RAP (MRAP) was measured by ophthalmodynamometry (ODM) and was expressed as a ratio of the mean systemic arterial blood pressure (i.e., MRAP/MSAP). The mean MRAP/MSAP for combined Groups I, II, and III with ICA occlusion proximal to the OA was significantly lower than both the control group (P = 0.0001) and the combined Groups IV, V, VI, and VII with occlusive lesions distal to the OA (P = 0.0001). Six patients in Groups I and II with venous stasis retinopathy had a mean MRAP/MSAP of 0.18 + 0.11. Mean cortical artery pressure (MCAP) was measured by inserting a 26 gauge needle into a small cortical artery and was expressed as the MCAP/MSAP ratio. Mean MCAP/MSAP was less than 0.50 for all groups except Group III. The mean MCAP/MSAP for combined Groups IV, V, VI, and VII was significantly lower than in combined Groups I, II, and III (P = 0.02). RAP measured by ODM was moderately predictive of CAP in patients with an occlusive lesion of the ICA proximal to OA (r = 0.50). The degree of correlation was highest for those patients with a very low MCAP/MSAP (i.e., <0.25) ratio (r = 0.74). These findings indicate that ODM may be helpful in identifying patients with severe cerebral hypoperfusion secondary to ICA occlusive disease proximal to the OA.
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Skoog, Johan, Marcus Lindenberger, Mikael Ekman, Bengt Holmberg, Helene Zachrisson, and Toste Länne. "Reduced venous compliance: an important determinant for orthostatic intolerance in women with vasovagal syncope." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 310, no. 3 (February 1, 2016): R253—R261. http://dx.doi.org/10.1152/ajpregu.00362.2015.
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The influence of lower limb venous compliance on orthostatic vasovagal syncope (VVS) is uncertain. The most widespread technique to calculate venous compliance uses a nonphysiological quadratic regression equation. Our aim was therefore to construct a physiologically derived venous wall model (VWM) for calculation of calf venous compliance and to determine the effect of venous compliance on tolerance to maximal lower body negative pressure (LBNP). Venous occlusion plethysmography was used to study calf volume changes in 15 women with VVS (25.5 ± 1.3 yr of age) and 15 controls (22.8 ± 0.8 yr of age). The fit of the VWM and the regression equation to the experimentally induced pressure-volume curve was examined. Venous compliance was calculated as the derivative of the modeled pressure-volume relationship. Graded LBNP to presyncope was used to determine the LBNP tolerance index (LTI). The VWM displayed a better fit to the experimentally induced pressure-volume curve ( P < 0.0001). Calf blood pooling was similar in the groups and was not correlated to the LTI ( r = 0.204, P = 0.30). Venous compliance was significantly reduced at low venous pressures in women with VVS ( P = 0.042) and correlated to the LTI ( r = 0.459, P = 0.014) in the low pressure range. No correlation was found between venous compliance at high venous pressures and the LTI. In conclusion, the new VWM accurately adopted the curvilinear pressure-volume curve, providing a valid characterization of venous compliance. Reduced venous compliance at low venous pressures may adversely affect mobilization of peripheral venous blood to the central circulation during hypovolemic circulatory stress in women with VVS.
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Bunevičius, Kęstutis, Albinas Grunovas, and Jonas Poderys. "EFFECT OF DIFFERENT OCCLUSION PRESSURE ON PECULIARITIES OF MUSCLE BLOOD FLOW." Baltic Journal of Sport and Health Sciences 1, no. 108 (2018): 2–8. http://dx.doi.org/10.33607/bjshs.v1i108.3.
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Background. Occlusion pressure intensity influences the blood flow intensity. Immediately after the cuff pressure is released, reactive hyperaemia occurs. Increased blood flow and nutritive delivery are critical for an anabolic stimulus, such as insulin. The aim of study was to find which occlusion pressure was optimal to increase the highest level of post occlusion reactive hyperaemia. Methods. Participants were randomly assigned into one of the four conditions (n = 12 per group): control group without blood flow restriction, experimental groups with 120; 200 or 300 mmHg occlusion pressure. We used venous occlusion plethysmography and arterial blood pressure measurements. Results. After the onset of 120 and 200 mm Hg pressure occlusion, the blood flow intensity significantly decreased. Occlusion induced hyperaemia increased arterial blood flow intensity 134 ± 11.2% (p < .05) in the group with 120 mmHg, in the group with 200 mmHg it increased 267 ± 10.5% (p < .05), in the group with 300 mmHg it increased 233 ± 10.9% (p < .05). Applied 300 mmHg occlusion from the 12 minute diastolic and systolic arterial blood pressure decreased statistically significantly. Conclusions. Occlusion manoeuvre impacted the vascular vasodilatation, but the peak blood flow registered after occlusion did not relate to applied occlusion pressure. The pressure of 200 mmHg is optimal to impact the high level of vasodilatation. Longer than 12 min 300 mmHg could not be recommended due to the steep decrease of systolic and diastolic blood pressures.
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Roselli, R. J., and R. E. Parker. "Venous occlusion measurement of pulmonary capillary pressure: effects of embolization." Journal of Applied Physiology 63, no. 6 (December 1, 1987): 2340–42. http://dx.doi.org/10.1152/jappl.1987.63.6.2340.
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The effects of pulmonary arterial embolization on calculated pulmonary capillary pressure as determined by the venous occlusion technique are examined using a simple pressure-flow model for the lung. It is predicted that pulmonary, arterial embolization can induce significant underestimation of pulmonary capillary pressure in flowing vessels. This underestimation is related to the percent of vessels embolized and the caliber of pulmonary arteries that are embolized (i.e., the size of the emboli). Experimental verification of these theoretical findings is necessary before the conclusions can be extended to the interpretation of venous occlusion experiments in the lung.
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Takase, Shinya, Laurence Lerond, John J. Bergan, and Geert W. Schmid-Schönbein. "Enhancement of reperfusion injury by elevation of microvascular pressures." American Journal of Physiology-Heart and Circulatory Physiology 282, no. 4 (April 1, 2002): H1387—H1394. http://dx.doi.org/10.1152/ajpheart.01003.2000.
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Elevated venous pressure can be associated with severe tissue injury. Few links, however, between venous hypertension and tissue damage have been established. We examined here the effects of micropressure elevation on the outcome of venular occlusion/reperfusion in the mesenteric microvasculature of male Wistar rats. One hour of venular occlusion (diameter ∼50 μm) by micropipette occlusion followed by reperfusion were carried out with sham surgery without occlusion as control. Leukocyte rolling, adhesion, and migration, oxygen radicals detected by dichlorofluorescein (DCF), and parenchymal cell death detected by propidium iodide (PI) were recorded simultaneously in the same vessel at a location upstream of the occlusion site with elevated micropressure and at a downstream location with low micropressure. The number of rolling, adhering, and migrating leukocytes increased on the upstream side of the occlusion to a higher level than downstream of the occlusion site. During occlusion, DCF intensity on the venular endothelium was greater on the upstream side than in the downstream side, but there were no differences during reperfusion. The number of PI-positive cells adjacent to the venules increased significantly compared with controls, and it remained greater on the upstream higher-pressure side than the downstream side. Leukocyte adhesion and transvascular migration in postcapillary venules as well as parenchymal cell death could be significantly reduced by the hydroxyl radical scavenger dimethylthiourea. Microhemorrhages of blood cells into the mesentery interstitium were observed only on the upstream side of the occlusion. These results indicate that an elevation of the venular blood pressure during occlusion/reperfusion exacerbates the inflammatory cascade and tissue injury. Venous occlusion may constitute an important mechanism for tissue injury.
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Presson, Robert G., Said H. Audi, Christopher C. Hanger, Gerald M. Zenk, Richard A. Sidner, John H. Linehan, Wiltz W. Wagner, and Christopher A. Dawson. "Anatomic distribution of pulmonary vascular compliance." Journal of Applied Physiology 84, no. 1 (January 1, 1998): 303–10. http://dx.doi.org/10.1152/jappl.1998.84.1.303.
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Presson, Robert G., Jr., Said H. Audi, Christopher C. Hanger, Gerald M. Zenk, Richard A. Sidner, John H. Linehan, Wiltz W. Wagner, Jr., and Christopher A. Dawson. Anatomic distribution of pulmonary vascular compliance. J. Appl. Physiol. 84(1): 303–310, 1998.—Previously, the pressure changes after arterial and venous occlusion have been used to characterize the longitudinal distribution of pulmonary vascular resistance with respect to vascular compliance using compartmental models. However, the compartments have not been defined anatomically. Using video microscopy of the subpleural microcirculation, we have measured the flow changes in ∼40-μm arterioles and venules after venous, arterial, and double occlusion maneuvers. The quasi-steady flows through these vessels after venous occlusion permitted an estimation of the compliance in three anatomic segments: arteries >40 μm, veins >40 μm, and vessels <40 μm in diameter. We found that ∼65% of the total pulmonary vascular compliance was in vessels <40 μm, presumably mostly capillaries. The transient portions of the pressure and flow data after venous, arterial, and double occlusion were consistent with most of the arterial compliance being upstream from most of the arterial resistance and most of the venous compliance being downstream from most of the venous resistance.
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Gisolf, J., R. V. Immink, J. J. van Lieshout, W. J. Stok, and J. M. Karemaker. "Orthostatic blood pressure control before and after spaceflight, determined by time-domain baroreflex method." Journal of Applied Physiology 98, no. 5 (May 2005): 1682–90. http://dx.doi.org/10.1152/japplphysiol.01219.2004.
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Reduction in plasma volume is a major contributor to orthostatic tachycardia and hypotension after spaceflight. We set out to determine time- and frequency-domain baroreflex (BRS) function during preflight baseline and venous occlusion and postflight orthostatic stress, testing the hypothesis that a reduction in central blood volume could mimic the postflight orthostatic response. In five cosmonauts, we measured finger arterial pressure noninvasively in supine and upright positions. Preflight measurements were repeated using venous occlusion thigh cuffs to impede venous return and “trap” an increased blood volume in the lower extremities; postflight sessions were between 1 and 3 days after return from 10- to 11-day spaceflight. BRS was determined by spectral analysis and by PRVXBRS, a time-domain BRS computation method. Although all completed the stand tests, two of five cosmonauts had drastically reduced pulse pressures and an increase in heart rate of ∼30 beats/min or more during standing after spaceflight. Averaged for all five subjects in standing position, high-frequency interbeat interval spectral power or transfer gain did not decrease postflight. Low-frequency gain decreased from 8.1 (SD 4.0) preflight baseline to 6.8 (SD 3.4) postflight ( P = 0.033); preflight with thigh cuffs inflated, low-frequency gain was 9.4 (SD 4.3) ms/mmHg. There was a shift in time-domain-determined pulse interval-to-pressure lag, Tau, toward higher values ( P < 0.001). None of the postflight results were mimicked during preflight venous occlusion. In conclusion, two of five cosmonauts showed abnormal orthostatic response 1 and 2 days after spaceflight. Overall, there were indications of increased sympathetic response to standing, even though we can expect (partial) restoration of plasma volume to have taken place. Preflight venous occlusion did not mimic the postflight orthostatic response.
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Kamikado, Chiaki, Toshishige Shibamoto, Minoru Hongo, and Shozo Koyama. "Effects of Hct and norepinephrine on segmental vascular resistance distribution in isolated perfused rat livers." American Journal of Physiology-Heart and Circulatory Physiology 286, no. 1 (January 2004): H121—H130. http://dx.doi.org/10.1152/ajpheart.01136.2002.
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We studied the effects of blood hematocrit (Hct), blood flow, or norepinephrine on segmental vascular resistances in isolated portally perfused rat livers. Total portal hepatic venous resistance ( Rt) was assigned to the portal ( Rpv), sinusoidal ( Rsinus), and hepatic venous ( Rhv) resistances using the portal occlusion (Ppo) and the hepatic venous occlusion (Phvo) pressures that were obtained during occlusion of the respective line. Four levels of Hct (30%, 20%, 10%, and 0%) were studied. Rpv comprises 44% of Rt, 37% of Rsinus, and 19% of Rhv in livers perfused at 30% Hct and portal venous pressure of 9.1 cmH2O. As Hct increased at a given blood flow, all three segmental vascular resistances of Rpv, Rsinus, and Rhv increased at flow >15 ml/min. As blood flow increased at a given Hct, only Rsinus increased without changes in Rpv or Rhv. Norepinephrine increased predominantly Rpv, and, to a smaller extent, Rsinus, but it did not affect Rhv. Finally, we estimated Ppo and Phvo from the double occlusion maneuver, which occluded simultaneously both the portal and hepatic venous lines. The regression line analysis revealed that Ppo and Phvo were identical with those measured by double occlusion. In conclusion, changes in blood Hct affect all three segmental vascular resistances, whereas changes in blood flow affect Rsinus, but not Rpv or Rhv. Norepinephrine increases mainly presinusoidal resistance. Ppo and Phvo can be obtained by the double occlusion method in isolated perfused rat livers.
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Sencer, Altay, Serra Sencer, İnan Turantan, and Ömer Devecioğlu. "Cerebrospinal fluid dynamics of the cava septi pellucidi and vergae." Journal of Neurosurgery 94, no. 1 (January 2001): 127–29. http://dx.doi.org/10.3171/jns.2001.94.1.0127.
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✓ This case involved a 26-month-old boy who had recurrent hemorrhagic venous infarction caused by venous sinus occlusion. Distension and enlargement of the cavum septi pellucidi (CSP) and cavum vergae (CV), along with hydrocephalus, was detected during the course of the disease and was observed to regress together with resolution of the venous occlusion. Venous hypertension caused by sinus occlusion was thought to be responsible for the disturbed resorption of cerebrospinal fluid (CSF) in the CSP and CV in this patient. This case is unique because it is the first one to support the hypothesis of resorption of CSF in the cava by a pressure gradient involving the septal capillaries and veins.
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Mullan, Sean. "Reflections upon the nature and management of intracranial and intraspinal vascular malformations and fistulae." Journal of Neurosurgery 80, no. 4 (April 1994): 606–16. http://dx.doi.org/10.3171/jns.1994.80.4.0606.
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✓ Evidence is presented that dural fistulae are preceded by sinus thrombosis and that their danger lies in arterialized venous pressure within the cranium or the orbit. Arterial side occlusion leads to recurrence, while venous side occlusion leads to permanent cure. Vein of Galen aneurysms embrace some features of cerebral arteriovenous malformations (AVM's), namely a reticulum, and some features of dural fistulae, namely evidence of previous sinus anomaly and direct drainage into a sinus. These aneurysms are also permanently cured by venous side thrombosis, although the dangers inherent in their reticulum demand that this be done in stages or preceded by arterial side embolization. A very limited experience with venous end occlusion of cerebral (and spinal) AVM's suggests that they, too, can be permanently cured by venous side occlusion without excision. Their reticulum demands maximum, multistage, preliminary arterial side embolization together with intraoperative hypotension during the venous occlusion stage in order to minimize intracerebral hemorrhage or swelling. Schematic models of both fistulae and malformations are presented, together with reasons why particulate embolization is safer than glue embolization. The theory is advanced that dural fistulae, vein of Galen aneurysms, and AVM's are venous- rather than arterial-based lesions, which is consistent with the experience that permanent cure has been effected by venous side occlusion without excision in all three anomalies. It is speculated that there may be a developmental link between AVM and the venous malformation, the AVM being essentially a fistulized venous malformation.
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Townsley, M. I., R. J. Korthuis, B. Rippe, J. C. Parker, and A. E. Taylor. "Validation of double vascular occlusion method for Pc,i in lung and skeletal muscle." Journal of Applied Physiology 61, no. 1 (July 1, 1986): 127–32. http://dx.doi.org/10.1152/jappl.1986.61.1.127.
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Capillary pressures in isogravimetric lung and skeletal muscle measured with the double vascular occlusion technique (Pdo) were compared to those measured using the traditional gravimetric technique (Pc,i). Pressures were measured using both techniques in isolated blood-perfused canine lungs (n = 18), blood-perfused rat hindquarters before (n = 8) and after (n = 6) maximal dilatation with papaverine and in rat hindquarters perfused with an artificial plasma (n = 6). In both organs, regardless of vascular tone, the double vascular occlusion isogravimetric pressure was the same as the gravimetric Pc,i, and the two measurements were highly correlated. Lung: Pdo = -0.22 + 1.06 Pc,i (r = 0.85, P less than 0.01); hindquarter: Pdo = -1.03 + 0.99 Pc,i (r = 0.91, P less than 0.01). In addition, Pdo was the same at every combination of isogravimetric arterial and venous pressures tested. The results indicate that the more rapidly applied double vascular occlusion pressure yields an accurate measure of isogravimetric capillary pressure in isolated organs over a wide range of isogravimetric pressures.
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Anglade, Daniel, Michel Corboz, Ahmed Menaouar, James C. Parker, Sagazaga Sanou, Sam Bayat, Gila Benchetrit, and Francis A. Grimbert. "Blood flow vs. venous pressure effects on filtration coefficient in oleic acid-injured lung." Journal of Applied Physiology 84, no. 3 (March 1, 1998): 1011–23. http://dx.doi.org/10.1152/jappl.1998.84.3.1011.
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On the basis of changes in capillary filtration coefficient ( K fc) in 24 rabbit lungs, we determined whether elevations in pulmonary venous pressure (Ppv) or blood flow (BF) produced differences in filtration surface area in oleic acid-injured (OA) or control (Con) lungs. Lungs were cyclically ventilated and perfused under zone 3 conditions by using blood and 5% albumin with no pharmacological modulation of vascular tone. Pulmonary arterial, venous, and capillary pressures were measured by using arterial, venous, and double occlusion. Before and during each K fc-measurement maneuver, microvascular/total vascular compliance was measured by using venous occlusion. K fc was measured before and 30 min after injury, by using a Ppv elevation of 7 cmH2O or a BF elevation from 1 to 2 l ⋅ min−1 ⋅ 100 g−1 to obtain a similar double occlusion pressure. Pulmonary arterial pressure increased more with BF than with Ppv in both Con and OA lungs [29 ± 2 vs. 19 ± 0.7 (means ± SE) cmH2O; P < 0.001]. In OA lungs compared with Con lungs, values of K fc (200 ± 40 vs. 83 ± 14%, respectively; P < 0.01) and microvascular/total vascular compliance ratio (86 ± 4 vs. 68 ± 5%, respectively; P < 0.01) increased more with BF than with Ppv. In conclusion, for a given OA-induced increase in hydraulic conductivity, BF elevation increased filtration surface area more than did Ppv elevation. The steep pulmonary pressure profile induced by increased BF could result in the recruitment of injured capillaries and could also shift downstream the compression point of blind (zone 1) and open injured vessels (zone 2).
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Arthur Miller, Gregg, Alexander Friedman, Aleksandr Khariton, Manish C. Jotwani, and Yevgeny Savransky. "Long Thoracic Vein Embolization for the Treatment of Breast Edema Associated with Central Venous Occlusion and Venous Hypertension." Journal of Vascular Access 11, no. 2 (April 2010): 115–21. http://dx.doi.org/10.1177/112972981001100206.
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Purpose Breast edema is a rare complication in hemodialysis patients with central venous occlusions. The present study sought to determine whether coil embolization of the long thoracic vein is an effective long-term treatment for this pathology. Methods The study patients were 6 female hemodialysis patients whose primary clinical manifestation of central vein occlusion was breast edema. When conservative treatment (allowing collaterals to dilate over time), as well as recanalization of occlusions through angioplasty with or without stent placement, failed to alleviate symptoms, patients underwent coil embolization of the long (lateral) thoracic vein. Results In 4 of the 6 cases, the breast edema was completely resolved without recurrence, while the other 2 patients experienced durable symptomatic improvement with only mild residual swelling. Average follow-up was 22 months. There were no adverse sequelae and none of the patients experienced increased swelling elsewhere following the coil embolization procedure. Conclusions Coil embolization of the long thoracic vein effectively alleviates breast edema in hemodialysis patients with elevated venous hydrostatic pressure due to central venous occlusions.
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Kelly, S. M., A. E. Taylor, and R. P. Michel. "Bronchial collateral vessel micropuncture pressure in postobstructive pulmonary vasculopathy." Journal of Applied Physiology 73, no. 5 (November 1, 1992): 1914–24. http://dx.doi.org/10.1152/jappl.1992.73.5.1914.
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Postobstructive pulmonary vasculopathy, produced by chronic ligation of one pulmonary artery, markedly increases bronchial blood flow. Previously, using arterial and venous occlusion, we determined that bronchial collaterals enter the pulmonary circuit at the distal end of the arterial segment. In this study, we tested the hypothesis that pressure in bronchial collaterals (Pbr) closely approximates that at the downstream end of the arterial segment (Pao). We pump perfused [111 +/- 10 (SE) ml/min] left lower lobes of seven open-chest live dogs 3–15 mo after ligation of the left main pulmonary artery. Bronchial blood flow was 122 +/- 16 ml/min. We measured pulmonary arterial and venous pressures and, by arterial and venous occlusion, respectively, Pao and the pressure at the upstream end of the venous segment (Pvo). Pbr was obtained by micropuncture of 34 pleural surface bronchial vessels 201 +/- 16 microns in diameter. We found that Pbr (14.4 +/- 1.0 mmHg) was similar to Pao (15.0 +/- 0.8 mmHg) but differed significantly (P < 0.01) from Pvo (11.3 +/- 0.5 mmHg). In addition, Pbr was independent of systemic arterial pressure and bronchial vessel diameter. Light and electron microscopy revealed that, in the lobes with the ligated pulmonary artery, the new bronchial collaterals entered the thickened pleura from the parenchyma via either bronchovascular bundles or interlobular septa and had sparsely muscularized walls. We conclude that, in postobstructive pulmonary vasculopathy, bronchial collateral pressure measured by micropuncture is very close to the pressure in precapillary pulmonary arteries and that most of the pressure drop in the bronchial collaterals occurs in vessels > 350 microns in diameter.
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Bauer, Kenneth. "Conventional Fibrinolytic Assays for the Evaluation of Patients with Venous Thrombosis: Don’t Bother." Thrombosis and Haemostasis 85, no. 03 (2001): 377–78. http://dx.doi.org/10.1055/s-0037-1615592.
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SummaryHypofibrinolysis, as defined by an absent or deficient increase in blood or plasma fibrinolytic activity after an appropriate stimulus, has been known to be present in patients following an episode of deep venous thrombosis for over 30 years. The usual stimulus is 10 min of venous occlusion using a blood pressure cuff inflated to a pressure midway between systolic and diastolic pressures. The early screening fibrinolytic assays were relatively insensitive in detecting fibrinolytic system hypofunction and lacked standardization.Supported in part by the Medical Research Service of the Department of Veterans Affairs.
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Fischer, Charlotte, Anne Bruggemann, Annette Hager, Josep Callizo Planas, Johann Roider, and Hans Hoerauf. "Vascular Occlusions following Ocular Surgical Procedures: A Clinical Observation of Vascular Complications after Ocular Surgery." Journal of Ophthalmology 2017 (2017): 1–6. http://dx.doi.org/10.1155/2017/9120892.
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Background. Ocular vascular occlusions following intraocular procedures are a rare complication. We report a case series of patients with retinal vascular occlusions or anterior ischemic optic neuropathy (AION) after anterior and posterior segment surgery and demonstrate possible risk factors. Methods. Observational case series. Results. In ten patients, vascular occlusions were observed within ten weeks after intraocular surgery: branch retinal arterial occlusion (BRAO) (n=2), central retinal artery occlusion (CRAO) (n=2), central retinal vein occlusion (CRVO) (n=1), branch retinal vein occlusion (BRVO) (n=1), anterior ischemic optic neuropathy (AION) (n=3), and combined central artery and vein occlusion (n=1). AION occurred later (27–69 d) than arterial occlusions (14–60 d) or venous occlusions (1-2 d). In all cases, either specific surgical manipulations or general vascular disorders were identified as risk factors. In addition to general cardiovascular risk factors (arterial hypertension n=6, diabetes mellitus n=4), internal workup disclosed bilateral stenosis of the carotid arteries (n=1) and myeloproliferative syndrome (n=1). Conclusion. Vascular occlusions after surgical ocular procedures seem to be more frequent when cardiovascular diseases coexist. Surgical maneuvers and intra- or postoperative pressure changes may act as a triggering mechanism in patients with underlying systemic cardiovascular disorders. Affected patients should undergo thorough internal examination to identify possible underlying diseases.
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JORFELDT, Lennart, Torbjörn VEDUNG, Elisabeth FORSSTRÖM, and Jan HENRIKSSON. "Influence of leg position and environmental temperature on segmental volume expansion during venous occlusion plethysmography." Clinical Science 104, no. 6 (June 1, 2003): 599–605. http://dx.doi.org/10.1042/cs20020257.
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Blood flow determinations by venous occlusion plethysmography applying the strain-gauge technique are frequently used. A problem with the strain-gauge technique is that the relationship between venous volume and transmural pressure is not linear and, furthermore, changes with the sympathetic tone. The present study tests the hypothesis that these factors lead to a redistribution of venous blood, which may impair the accuracy of the technique. The relative volume expansion rates of four leg segments were studied with the leg in different positions and at disparate temperatures, thereby inducing varying venous pressures and sympathetic tone (n=6). With elevated leg and relaxed veins (at 50 °C), the distal thigh showed a relatively low expansion rate (25.8±4.5 ml·min-1·l-1), whereas values in the calf segments were higher (34.5–39.0 ml·min-1·l-1). With lower initial transmural pressure, calf segments can increase their volume much more during occlusion compared with the distal thigh. In a higher transmural pressure region (lowered leg), the difference in compliance between limb segments is less. In this case, compliance and volume expansion rate was higher in the distal thigh (14.2, 13.5 and 22.2 ml·min-1·l-1 at 10, 20 and 50 °C respectively) than in the calf segments (for the distal calf: 6.4, 7.7 and 16.2 ml·min-1·l-1 respectively). There was a significant interaction (P<0.001) between temperature and leg position, indicating a higher degree of sympathetic vasoactivity in the calf. It is concluded that blood flow determination by strain-gauge plethysmography is less accurate, due to a potential redistribution of the venous blood. Therefore possible influences of variations in sympathetic tone and venous pressure must be considered even in intra-individual comparisons, especially in interventional studies.
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Maarek, J. M., and H. K. Chang. "Pulsatile pulmonary microvascular pressure measured with vascular occlusion techniques." Journal of Applied Physiology 70, no. 3 (March 1, 1991): 998–1005. http://dx.doi.org/10.1152/jappl.1991.70.3.998.
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The periodic variations of the pulmonary microvascular pressure during pulsatile perfusion were studied in isolated left lower lobes of canine lungs by the arterial occlusion (AO) and double occlusion (DO) techniques. Sixteen AO and eight DO maneuvers evenly distributed within the pump cycle were performed for each of four frequencies: 36, 54, 72, and 90 beats/min. Nearly identical microvascular pressure contours were reconstructed from the AO and DO maneuvers by relocating the measured occlusion pressures in time. These contours lagged behind the pulmonary arterial pressure waveform. Their amplitude decreased from 25 to 14% of the arterial pulse pressure as the pump frequency was increased from 36 to 90 beats/min. The modulus of the pressure transfer function at the site of arterial occlusion decreased as the frequency increased. The phase was negative for all frequencies and it approached -90 degrees for the higher frequencies. Vasoconstriction induced by serotonin resulted in an increase of the magnitude of the AO pressure contour that was nearly proportional to the increase of the pulmonary arterial pulse pressure. In contrast, elevation of the lobar venous pressure to 10 mmHg increased the amplitude of the AO pressure contour, whereas it slightly decreased the pulmonary arterial pulse pressure. These experiments demonstrate that the AO and DO pressures fluctuate markedly during pulsatile perfusion. Their oscillations would be indicative of the pulsatility in the pulmonary microvascular bed.
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Terada, N., S. Koyama, J. Horiuchi, and T. Takeuchi. "Participation of adrenoceptors in liver blood flow regulation in anesthetized dogs." American Journal of Physiology-Heart and Circulatory Physiology 253, no. 5 (November 1, 1987): H1053—H1058. http://dx.doi.org/10.1152/ajpheart.1987.253.5.h1053.
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We evaluated involvement of adrenergic receptors in the responses of the hepatic vasculature to reduction either of portal venous flow or hepatic arterial inflow. Portal vein occlusion caused an increase in hepatic arterial blood flow (HAF) and decreases in hepatic arterial pressure (HAP) and hepatic arterial vascular resistance (HAR) in the intact group. After pretreatment with either yohimbine or prazosin, but not propranolol, occlusion of the portal vein produced a greater decrease in HAP as compared with that in the intact group. No significant changes in HAF, HAR, or hepatic tissue blood flow (HTF) occurred after the treatment. These results indicate that the compensatory response of the hepatic arterial vasculature to altered portal blood flow (PVF) is regulated independently of the intrahepatic adrenergic receptors. Hepatic arterial occlusion caused a significant decrease in portal venous pressure, PVF, and HTF. Portal venous vascular resistance (PVR) was reduced slightly, but not significantly. After pretreatment with either yohimbine or prazosin, but not propranolol, occlusion of the hepatic artery produced an opposite effect: to increase PVF and significantly decrease PVR. These results indicate that intrahepatic alpha-adrenoceptors participate in the regulation of portal vascular tone to maintain portal vein pressure at a steady level, when inflow from the hepatic artery is reduced.
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Moureau, Nancy, Lisa Mlodzik, and Susan Markel Pool. "The Use of Alteplase for Treatment of Occluded Central Venous Catheters in Home Care." Journal of the Association for Vascular Access 10, no. 3 (September 1, 2005): 123–29. http://dx.doi.org/10.2309/java.10-3-7.
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Abstract Purpose. The purpose of this trial was to confirm safety and efficacy with thrombolytic use on complete and partially occluded central catheters using alteplase for the home care population. This trial attempts to provide additional evidence for the safe and effective use of a thrombolytic agent for catheter clearance, specifically with home care patients. Method. Patients were eligible for inclusion if (1) blood could not be withdrawn for partial occlusion or (2) blood could not be withdrawn and inability to flush presented with complete occlusion. Through an established Protocol, using the negative-pressure technique, nurses administered alteplase, 1mg/1 cc concentration, to home care patients who met inclusion criteria. Instillations were repeated at 20-minute intervals for up to three repetitions, if needed, with the third instillation remaining overnight. Results. Instillation of alteplase was successful in clearing catheter thrombotic occlusions in 66. 7% of patients studied in this outpatient population without thrombolytic events or drug related adverse effects. Conclusions. The authors confirm that catheter occlusions can be safely resolved in the alternate care/home care setting using established negative-pressure protocols. Although overnight dwell was used successfully and unsuccessfully in this trial without adverse effects, the small sample size does not Provide adequate definitive conclusions.
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Dawson, C. A., D. A. Rickaby, and J. H. Linehan. "Location and mechanisms of pulmonary vascular volume changes." Journal of Applied Physiology 60, no. 2 (February 1, 1986): 402–9. http://dx.doi.org/10.1152/jappl.1986.60.2.402.
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We examined the influence of changing outflow pressure, P out, on the vascular and extravascular volumes (QV and QEV, respectively, as measured by indicator dilution) and on the outflow occlusion pressures in isolated dog lung lobes perfused with constant flow. Changing P out had a substantial effect on QV, but not on QEV, whether P out was less than or greater than alveolar pressure, PA. Since QEV did not change with QV, recruitment of previously unperfused vessels did not appear to contribute substantially to the increases in QV when P out was increased. The rapid jump in P out immediately following outflow occlusion was virtually independent of the difference between PA and P out suggesting that the alveolar vessels were an important volume storage site when P out was low relative to PA. We conclude that, over a certain range of pressures, alveolar vessel volume can be controlled by venous pressure even when the change in venous pressure has little effect on arterial pressure (zone 2). Further, we conclude that in zone 3 and within the transition from zone 2 to zone 3 increases in the intralobar blood volume occurring within the alveolar vessels may not require recruitment in the sense of opening of previously unperfused vessels.
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Hall, J. E., W. F. Hofman, and I. C. Ehrhart. "Venous occlusion pressure and vascular permeability in the dog lung after air embolization." Journal of Applied Physiology 65, no. 1 (July 1, 1988): 34–40. http://dx.doi.org/10.1152/jappl.1988.65.1.34.
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Pulmonary edema has frequently been associated with air embolization of the lung. In the present study the hemodynamic effects of air emboli (AE) were studied in the isolated mechanically ventilated canine right lower lung lobe (RLL), pump perfused at a constant blood flow. Air was infused via the pulmonary artery (n = 7) at 0.6 ml/min until pulmonary arterial pressure (Pa) rose 250%. While Pa rose from 12.4 +/- 0.6 to 44.6 +/- 2.0 (SE) cmH2O (P less than 0.05), venous occlusion pressure remained constant (7.0 +/- 0.5 to 6.8 +/- 0.6 cmH2O; P greater than 0.05). Lobar vascular resistance (RT) increased from 2.8 +/- 0.3 to 12.1 +/- 0.2 Torr.ml-1.min.10(-2) (P less than 0.05), whereas the venous occlusion technique used to determine the segmental distribution of vascular resistance indicated the increase in RT was confined to vessels upstream to the veins. Control lobes (n = 7) administered saline at a similar rate showed no significant hemodynamic changes. As an index of microvascular injury the pulmonary filtration coefficient (Kf) was obtained by sequential elevations of lobar vascular pressures. The Kf was 0.11 +/- 0.01 and 0.07 +/- 0.01 ml.min-1.Torr-1.100 g RLL-1 in AE and control lobes, respectively (P less than 0.05). Despite a higher Kf in AE lobes, total lobe weight gains did not differ and airway fluid was not seen in the AE group. Although air embolization caused an increase in upstream resistance and vascular permeability, venous occlusion pressure did not increase, and marked edema did not occur.
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Beverly, M., S. Mellon, J. A. Kennedy, and D. W. Murray. "Intraosseous pressure during loading and with vascular occlusion in an animal model." Bone & Joint Research 7, no. 8 (August 2018): 511–16. http://dx.doi.org/10.1302/2046-3758.78.bjr-2017-0343.r2.
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Objectives We studied subchondral intraosseous pressure (IOP) in an animal model during loading, and with vascular occlusion. We explored bone compartmentalization by saline injection. Materials and Methods Needles were placed in the femoral condyle and proximal tibia of five anaesthetized rabbits and connected to pressure recorders. The limb was loaded with and without proximal vascular occlusion. An additional subject had simultaneous triple recordings at the femoral head, femoral condyle and proximal tibia. In a further subject, saline injections at three sites were carried out in turn. Results Loading alone caused a rise in subchondral IOP from 11.7 mmHg (sd 7.1) to 17.9 mmHg (sd 8.1; p < 0.0002). During arterial occlusion, IOP fell to 5.3 mmHg (sd 4.1), then with loading there was a small rise to 7.6 mmHg (sd 4.5; p < 0.002). During venous occlusion, IOP rose to 20.2 mmHg (sd 5.8), and with loading there was a further rise to 26.3 mmHg (sd 6.3; p < 0.003). The effects were present at three different sites along the limb simultaneously. Saline injections showed pressure transmitted throughout the length of the femur but not across the knee joint. Conclusion This is the first study to report changes in IOP in vivo during loading and with combinations of vascular occlusion and loading. Intraosseous pressure is not a constant. It is reduced during proximal arterial occlusion and increased with proximal venous occlusion. Whatever the perfusion state, in vivo load is transferred partly by hydraulic pressure. We propose that joints act as hydraulic pressure barriers. An understanding of subchondral physiology may be important in understanding osteoarthritis and other bone diseases. Cite this article: M. Beverly, S. Mellon, J. A. Kennedy, D. W. Murray. Intraosseous pressure during loading and with vascular occlusion in an animal model. Bone Joint Res 2018;7:511–516. DOI: 10.1302/2046-3758.78.BJR-2017-0343.R2.
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Nakase, Hiroyuki, Kiyoshi Nagata, Hiroyuki Otsuka, Toshisuke Sakaki, and Oliver Kempski. "Local cerebral blood flow autoregulation following “asymptomatic” cerebral venous occlusion in the rat." Journal of Neurosurgery 89, no. 1 (July 1998): 118–24. http://dx.doi.org/10.3171/jns.1998.89.1.0118.
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Object. Maintenance of cerebral blood flow (CBF) autoregulation in the brain is of major importance for patient outcome in various clinical conditions. The authors assessed local autoregulation after “asymptomatic” cortical vein occlusion. Methods. In Wistar rats, a single cortical vein was occluded photochemically by using rose bengal and fiberoptic illumination. In rats with bilateral carotid artery occlusion, mean arterial blood pressure (MABP) was lowered in 5-mm Hg increments down to 40 mm Hg by using hypobaric hypotension. Local CBF at each pressure level was assessed by performing laser Doppler (LD) scanning at 25 (5 × 5) locations within bilateral cranial windows. In this manner, the lower limit of autoregulation (LLA) was detected. The LLA was 60 mm Hg in both right and left hemispheres in Group A (five rats), in which the animals received illumination without rose bengal and had no venous occlusion. Of the 11 rats that underwent vein occlusion, three developed severe reductions in local CBF and/or a growing venous thrombus and were distinguished as Group C (symptomatic; three rats); from previous work we know that those animals are bound to experience venous infarction. The remaining rats formed Group B (asymptomatic; eight rats). In this group the LLA remained at 60 mm Hg in the left hemisphere without occlusion, whereas, in the right cortex with the occluded vein, the LLA was found to be 65 mm Hg. Below a carotid stump pressure of 25 mm Hg regional CBF in the affected hemisphere dropped more abruptly to a possibly ischemic range than that in the opposite normal hemisphere. Conclusions. The results of the present study suggest that cerebral venous circulation disorders are manifested via additional pathways, that is, from a partially impaired local autoregulation in the vicinity of the occluded vein, even under conditions in which the vein occlusion itself does not cause brain damage. Care should be taken in the control of blood pressure in patients with this pathological condition.