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Artykuły w czasopismach na temat "Venous occlusion pressure"

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Maarek, J. M., T. S. Hakim i H. K. Chang. "Analysis of pulmonary arterial pressure profile after occlusion of pulsatile blood flow". Journal of Applied Physiology 68, nr 2 (1.02.1990): 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 i F. A. Grimbert. "Theoretical analysis of occlusion techniques for measuring pulmonary capillary pressure". Journal of Applied Physiology 73, nr 4 (1.10.1992): 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, nr 6 (18.06.2021): 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 i I. C. Roddie. "Measurement of capillary pressure in humans using a venous occlusion method". Journal of Applied Physiology 60, nr 6 (1.06.1986): 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 i in. "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, nr 6 (26.10.2022): 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 i Tatsuya Tagawa. "Effect of Lower Limb Venous Dilation on the Autonomic Cardiac Response among Healthy Young Men". Healthcare 11, nr 4 (13.02.2023): 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 i R. Berckmans. "Pitfalls of venous occlusion method for determination of capillary pressure in humans". Journal of Applied Physiology 66, nr 2 (1.02.1989): 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 i 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, nr 1 (styczeń 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 i Richard H. Schmidt. "Endovascular balloon angioplasty for treatment of posttraumatic venous sinus thrombosis". Journal of Neurosurgery 111, nr 1 (lipiec 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, i Susan Kaufman. "Splenic baroreceptors control splenic afferent nerve activity". American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 290, nr 2 (luty 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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Rozprawy doktorskie na temat "Venous occlusion pressure"

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Mungovan, Sean F., i n/a. "The Effect of Elevation and Venous Occlusion Pressure on Cardiovascular Function in Physically Active Men Who Are Paraplegic". Griffith University. School of Physiotherapy and Exercise Science, 2004. http://www4.gu.edu.au:8080/adt-root/public/adt-QGU20040917.084824.

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The purpose of the present investigation was to: 1) Determine the relationship between cardiac output (estimated using the acetylene rebreathing methodology) and oxygen consumption in a homogeneous group of men who are paraplegic. 2) Investigate whether lower limb elevation increases stroke volume and decreases heart rate at rest and during submaximal arm exercise. 3) Investigate whether the application of constant circumferential pneumatic pressure applied to dependent lower limbs increases stroke volume and decreases heart rate at rest and during submaximal arm exercise.
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Mungovan, Sean F. "The Effect of Elevation and Venous Occlusion Pressure on Cardiovascular Function in Physically Active Men Who Are Paraplegic". Thesis, Griffith University, 2004. http://hdl.handle.net/10072/365190.

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The purpose of the present investigation was to: 1) Determine the relationship between cardiac output (estimated using the acetylene rebreathing methodology) and oxygen consumption in a homogeneous group of men who are paraplegic. 2) Investigate whether lower limb elevation increases stroke volume and decreases heart rate at rest and during submaximal arm exercise. 3) Investigate whether the application of constant circumferential pneumatic pressure applied to dependent lower limbs increases stroke volume and decreases heart rate at rest and during submaximal arm exercise.
Thesis (Masters)
Master of Philosophy (MPhil)
School of Physiotherapy and Exercise Science
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Książki na temat "Venous occlusion pressure"

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Pluhar, Grace Elizabeth. The effect of acute, unilateral transverse venous sinus occlusion on intracranial pressure in normal dogs. 1995.

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Mathews, Letha, i John Barwise. Refractory Intracranial Hypertension. Redaktorzy Matthew D. McEvoy i Cory M. Furse. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190226459.003.0067.

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Intracranial pressure remains constant in adults at 10–15 mmHg under normal conditions with some fluctuations associated with respirations, coughing, sneezing, and so forth. Refractory intracranial hypertension (ICH) is defined by recurrent episodes of intracranial pressure elevation above 20 mmHg for sustained periods (10–15 min) despite medical therapy. The common causes of ICH are traumatic brain injury, brain tumors, subarachnoid hemorrhage, and brain infarction from arterial occlusion, cerebral venous thrombosis, and anoxic encephalopathy. Intracranial infections, abscesses, acute liver encephalopathy, and idiopathic ICH are also recognized causes of ICH. For the purposes of this chapter, the discussion is limited to ICH related to traumatic brain injury.
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Części książek na temat "Venous occlusion pressure"

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Mohl, W., i F. Neumann. "Pressure-controlled intermittent coronary sinus occlusion (PICSO)". W Myocardial Perfusion, Reperfusion, Coronary Venous Retroperfusion, 145–59. Heidelberg: Steinkopff, 1990. http://dx.doi.org/10.1007/978-3-662-12556-4_8.

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Nishino, S., M. Gotoh, T. Shirakawa, T. Saijo, H. Niimi, T. Murota, H. Kuyama, T. Ohmoto i A. Nishimoto. "Effect of External Decompression on Cerebral Venous System Occlusion". W Intracranial Pressure VIII, 186–90. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-77789-9_41.

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Cenzato, Marco, Davide Boeris, Maurizio Piparo, Alessia Fratianni, Maria Angela Piano, Flavia Dones, Francesco M. Crisà i Giuseppe D’Aliberti. "Complications in AVM Surgery". W Acta Neurochirurgica Supplement, 77–81. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-63453-7_11.

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AbstractIn AVM surgery perioperative complications can arise and can have serious perioperative consequences. Surgically related complications in AVM treatment, in many cases, can be avoided by paying attention to details:1. Careful selection of the patient: - addressing a patient with eloquent AVM to Gamma Knife treatment - preoperative treatment with selective embolization of the accessible deep feeders - preoperative gamma knife or embolize those patient with an over-expressed venous pattern2. Meticulous coagulation of deep medullary feeders: - Using dirty coagulation - Using dry non-stick coagulation - Using micro clips - Using laser - Reaching the choroidal vessel in the ventricle when possible - Avoiding occlusive coagulation with hemostatic agents3. Check and avoiding any residual of the AVM4. Keep the patient under pressure control during postoperative periodFulfilling these steps contributes to reduce complications in this difficult surgery, leading to a safer treatment that compares favorably with natural history of brain arteriovenous malformations.
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Magee, Patrick, i Mark Tooley. "Intravenous Pumps and Syringe Drivers". W The Physics, Clinical Measurement and Equipment of Anaesthetic Practice for the FRCA. Oxford University Press, 2011. http://dx.doi.org/10.1093/oso/9780199595150.003.0031.

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Many infusions are given by gravity assisted, drip sets that give a flowrate dependent on the height of the reservoir above the patient, the length of the tubing, the bore of the IV cannula, the density and viscosity of the fluid being delivered, and the patient’s venous pressure. However there is an increasing tendency to use programmable volumetric intravenous pumps and syringe drivers to deliver intravenous anaesthesia, fluids, patient controlled analgesia, epidural infusions and other drugs. Not only are they programmable, but they can also be adjusted to give desired flowrates or volumes. Some infusion devices are powered only by gravity, but the flowrate is controlled by a photoelectric drip rate detector in conjunction with a microprocessor controlled drip occlusion device. Other infusion devices use a stepper motor to control the rate of infusion. A stepper motor is designed so that the rotation is by a fixed amount per supplied electrical pulse, independent of the mechanical load it is carrying. The pulses are controlled by a microprocessor in the pump and the rate of infusion is dependent on the stepper motor’s output. Syringe drivers are designed to use a range of syringe sizes and some require special delivery tubing. The flow is a continuous, pulsatile flow and accuracy is 2–5%. Some syringe drivers are driven by clockwork motors, others by a battery powered motor that is intermittently on and off, depending on required flowrate. The driving mechanism is usually by a screw threaded rod connected to the syringe plunger. Other syringe drivers use a stepper motor connected to the screw threaded rod. Care should be taken not to position the syringe driver above the patient’s venous cannula or the syringe may siphon a drug additional to that programmed on the driver, by virtue of the weight of the column of fluid in the tubing above the patient. Care should also be taken to avoid any bubbles in the syringe reaching the patient. Modern syringe drivers are usually sufficiently accurate over the desired range of infusion [Stokes et al. 1990]. However, there may be a delay before the drug is delivered to the patient as the parts attached to the syringe take up slack [O’Kelly et al. 1992].
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Becker, Richard C., i Frederick A. Spencer. "Fibrinolytic Agents". W Fibrinolytic and Antithrombotic Therapy. Oxford University Press, 2006. http://dx.doi.org/10.1093/oso/9780195155648.003.0011.

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The fibrinolytic system plays a vital role in maintaining vital organ homeostasis. Fibrinolysis, defined as the dissolution of fibrin (the major scaffold for intravascular thrombus), is the process that regulates thrombus growth after hemostasis has been achieved, thus preserving tissue perfusion. An understanding of fibrinolysis has led to the development of pharmacologic agents that can be used in the treatment of arterial and venous thrombotic disorders, including acute myocardial infarction, acute ischemic stroke, and pulmonary embolism. Fibrinolytic therapy makes use of the vascular system’s intrinsic defense mechanism by accelerating and amplifying the conversion of an inactive enzyme precursor (zymogen), plasminogen, to the active enzyme plasmin. In turn, plasmin hydrolyzes several key bonds in the fibrin (clot) matrix, causing dissolution (lysis). A single-chain glycoprotein consisting of 790 amino acids, plasminogen is converted to plasmin by cleavage of the Arg560–Val561 peptide bond. The plasminogen molecule also contains specific lysine binding sites, which mediate its interaction with fibrin and α2-plasmin inhibitor. A serine protease with trypsinlike activity, plasmin attacks lysyl and arginyl bonds of fibrin at two principal sites: (1) the carboxyterminal portion α-chain (polar region) and (2) the coiled coil connectors containing α-, β-, and γ-chains. The ability of a fibrinolytic agent to dissolve an occlusive thrombus is determined by several factors. After administration the agent must be delivered to, perfuse, and ultimately infiltrate the thrombus while concomitantly being provided with an adequate amount of substrate (plasminogen) and the appropriate metabolic environment for an enzymatic reaction (conversion of plasminogen to plasmin) to take place. The intrinsic composition or ultrastructure of a thrombus also affects its lysability. Changes in the total amount and distribution of blood flow determine oxygen delivery to metabolically active tissues. They also determine the delivery of enzymatic substrate and plasminogen activators to the occlusive thrombus. In the heart, coronary blood flow correlates directly with mean arterial pressure. The flow-pressure curve is relatively flat above 65 to 70 mmHg, but becomes steeper as the mean arterial pressure decreases below this point. The relationship within the brain is more complex.
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Streszczenia konferencji na temat "Venous occlusion pressure"

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Haaland, K. A., H. O. SkjØnsberg, E. Thaulow, G. GjØnnes i C. H. Godal. "INTRAVENOUS PRESSURE AND t-PA ANTIGEN RELEASE DURING VENOUS OCCLUSION OF UPPER AND LOWER LIMBS". W XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644431.

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Venous occlusion by means of a sphygmomanometer cuff is a well-established part of the procedure for assessment of fibrinolytic capacity. It has been suggested that the resultant intravenous pressure is responsible for plasminogen activator release.In this present study we wanted to compare i .v. pressure in the upper and lower limbs, during venous occlusion, and measure t-PA ag release. 8 male volunteers participated. A VenfIon(O.D. 1.2 mm) was inserted in a distal, superficial vein. Blood samples, discarding the first 2-3 ml. were drawn at 4 min. intervals and pressure recordings (Hewlett-Packard)made every min. during the first 8 min. of venous occlusion and thereafter at 4 min. intervals. The cuff was inflated to a pressure midway between systolic and diastolic values after separate measurements of blood pressures of the upper and lower extremities. The occlusion lasted for 20 min.Blood pressure measurements in the lower limbs gave consistently higher values than for the upper limbs. Hence, the resultant cuff pressure was on the average 20 mmHg higher in the legs.There was no significant difference in i.v. pressure, evaluated as total area beneath a pressure/time graph, between the upper and lower extremities. In the arms the i.v. pressure reached a plateau phase after 2-4 min. The pressure buildup was slower in the legs.t-PA values for the upper limbs after 20 min. of venous occlusion: median 15 ng/ml (range 9.4-26.0) and for the lower limbs: 8.15 ng/ml (range 4.8-13.3). This difference is significant, p = 0.035. There was no sifnificant difference between resting t-PA ag' levels prior to occlusion.We conclude that the fibrinolytic response, measured as t-PA ag, after venous occlusion, is twice as high in the upper as in the lower limbs and not 4-times as high as previously claimed. A possible explanation for the lower fibrinolytic response, could be the slower buildup of i.v. pressure during venous occlusion in the lower extremities.
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Kozak, M., i D. Keber. "FIBRINOLYTIC RESPONSE AFTER VENOUS OCCLUSION AND DDAVP IN PATIENTS WITH DEEP VENOUS THROMBOSIS". W XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644430.

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After prolonged stimulation venous endothelium becomes refractory to otherwise efficacious stimuli for tissue plasminogen activator (t-PA) release. When the stimulus is removed, the restitution of the response is observed. The distention of the veins distally from the occlusion site in deep venous thrombosis (DVT) could represent such a chronic stimulus. We studied t-PA release in patients with DVT during 20-min venous occlusion (VO) and DDAVP infusion (0,4 ug/kg b.w. in 10 min). t-PA release was estimated as the difference in euglobulin clot lysis time (ECLT in U) and fibrin plates (FP in mm2) before and after VO (fibrinolytic potential). Two groups of patients were studied: 15 recumbent patients with oneside iliofemoral DVT, and 15 patients with oneside postthrombotic syndrome.In both groups the response of legs was lower than that of arms. The comparison of the healthy and the affected leg in postthrombotic group showed no difference in t-PA release after VO. A higher release of t-PA was seen in the acute DVT group in all three tested limbs, explainable by a restitution of fibrinolytic potential due to the reduction of hydrostatic stimulus. However, the response was slightly lower in the diseased leg. In 5 patients from the acute DVT group DDAVP infusion induced higher t-PA release after VO in both legs compared to VO before DDAVP. We can conclude that hydrostatic pressure in upright position is such a strong stimulus that an additional decrease of t-PA release due to chronic venous stasis cannot be expressed. In recumbent patients DVT hinders the restitution of the response to V0 in the diseased leg. DDAVP seems to act independently of hydrostatic pressure and venous stasis.
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Carriero, M. R., F. Annoni, L. Mussoni, C. Cerletti i G. de Gaetano. "FIBRINOLYTIC ACTIVITY OF ARMS AND LE6S IN PERIPHERAL VENOUS HYPERTENSION IN MAN". W XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644428.

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Spontaneous fibrinolytic activity of venous specimens Is greater In the arms than in the legs of normal subjects. This difference might be caused by the different hydrostatic pressure In arms and legs. We tested, on standard fibrin plates, the fibrinolytic activity of euglobulins prepared from venous blood obtained from arms and legs of normal subjects and patients with chronic peripheral hypertension. Normal subjects (26-38 yrs old, n=5) were tested both before and after 10 min venous occlusion (V0) of an arm and after 10 min occlusion of a leg. V0 was obtained by applying the cuff of a sphlgmomanometer at a pressure value Intermediate between systolic and diastolic pressure. Patients (39-64 yrs old, n=7) were tested both before and after V0 of the arm and after 10 min orthostatic posture (mean 100 mmHg). For each Individual the fibrinolytic activity In the arm before V0 was considered as basal value of both the arm and the leg. In normal subjects fibrinolytic activity Induced by V0 was greater In the arm than In the leg (262.9°74.9 versus 165.5°52.9 mm2). The average Increase of fibrinolytic activity after V0 was 3.4 (arms) and 2.1 (legs). In patients with peripheral venous hypertension fibrinolytic activity was 298.3°46.7 mm2 In the arm and 131.1 °19.2 mm2 In the leg. The average Increase Induced by VO In the arm was 3.5 while the activity of the legs after orthostatic pressure was 1.6. In conclusion patients with peripheral venous hypertension did not show any reduced fibrinolytic response after VO of the arms. Fibrinolytic activity in patients" legs after orthostatic pressure was also similar to that In the legs of volunteers after venous occlusion.
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Boisseau, M. R., J. Bonnet, G. Freyburger, P. Desbordes, L. Brottier, J. M. Orgogozo i H. Bricaud. "HEMOSTASIS AND HEMORHEOLOGY AFTER ISCHEMIC STROKE IN PATIENTS WITHOUT CARDIOPATHY AND OTHER LOCALISATION OF ATHEROSCLEROSIS". W XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644210.

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Hemorheological parameters (whole blood filtration, whole blood viscosity, plasma viscosity and erythrocyte deformability by ektacytometry) and fibrinolysis parameters (Euglobulin Lysis Time ELT, t-PA activity, and Plasminogen ActivatorInhibitor -PAI- before and after Venous Occlusion Test -VOT-) were measured in 20 stroke patients. All these patients had a crerebrovascular accident (CVA) localised to the carotid arterial tree. They has no signs of heart disease and were without risk factors for atherosclerosis (high blood pressure, diabetes) ; they were investigated in the week following the CVA. They were divided into 4 groups : 1/ transcient ischemic accident, 2,3,4/ size of infarct classified from results of C. T. Scan carried out 2 or 3 days after the stroke (2/small +, 3/moderate ++, 4/large +++).For the hemorheological parameters we noted only a slight increase in whole blood filtration (27±8“ vs 21±2”, p<0,05).The ELT was however significantly increased in these patients (258 ±57 min. vs 133 ±33,p<0,001)suggesting impairement of fibrinolysis. The following points were noteworthy : the ELT return to normal after to VOT,there was a relationship between stroke severity and the PAI levels and the viscosity at low shear stress. These two parameters were dramatically impaired in the most severely affected patients. Transcient ischemic accidents had comparable features to the CVA of moderate size.The extend of the disorders of the hemorheological disorders and the abnormalities in fibrinolysis seemed to be related to the severity of the involvement in patients with ischemic stroke with no evidence of heart disease or atherosclerosis in other systems.
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Hossmann, V., H. J. Schäfer, H. Auel i H. Etti. "TREATMENT OF ADVANCED STAGES OF PERIPHERAL OBLITERATIVE DISEASE WITH THE THROMBOXANE RECEPTOR ANTAGONIST BM 13.177: A PLACEBOCONTROLLED DOUBLE BLIND STUDY". W XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643471.

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Twenty patients (67.2 ± 12.3 yrs; aged 39-86 yrs, 10 males, 10 females) with stage IV of peripheral obliterative arterial disease received at random either a) BM 13.177, a thromboxane receptor antagonist, at a dose of 6 g/24 hrs for 7 days i.v., followed by oral treatment of 6.4 g/day in four doses for 2 weeks and a subsequent placebo week, or b) placebo alone with the same protocol. The clinical course was followed by measurement of blood pressure (by Riva-Rocci on the left brachial artery and by Doppler of the ankle artries), blood flow at restand after 3 min of tourniquet ischemia (by venous occlusion plethysmography), TcpCf2 at the wrist of the affected limb, and by subjective estimation of pain with visual analog scale before, at the end of the infusion period, as well as on day 7 and 14 of oral treatment, and 7 days after treatment while patients of both groups were on placebo. In addition spontaneous platelet aggregation by PAT III, induced platelet aggregation in whole blood by collagen and in PRP by ADP at different doses on the same days were measured on the same days as described above.Results: BM 13.177 completely inhibited aggregation in whole blood induced by collagen 0.3 (ig/ml, however one week after treatment a rebound phenomenon was observed with 16.0 ± 3.8 OHM compared to pretreatment value of 11.0 ± 3.8 OHM (p < 0.01). At a higher dose of 1.2 |ig/ml the same inhibiting effect on platelet aggregation was observed. Spontaneous platelet aggregation as measured by PAT III was evident in only 2/10 pat. pre-treatment, was abolished in all patients on i.v. BM 13.177, returned in 1/10 pat. during oral treatment, but in 4/10 pat. on day 7 after treatment, while being on placebo, again indicating a rebound phenomenon (p < 0.03) ADP induced platelet aggregation was not significantly affected by BM 13.177. In the placebo group, too, no significant differences were observable between the different treatment regimens. Clinical data did not show any significant alteration in either verum or placebo group during the six week period, indicating no benificial effect of thromboxane receptor antagonists in advanced stages of peripheral obliterative arterial disease, although platelet inhibiting effects were clearly demonstable.
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