Journal articles: 'Vascular resistance Measurement'

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O'DWYER, J. P., J. E. KING, C. E. WOOD, B. L. TAYLOR, and G. B. SMITH. "Continuous measurement of systemic vascular resistance." Anaesthesia 49, no. 7 (February 22, 2007): 587–90. http://dx.doi.org/10.1111/j.1365-2044.1994.tb14225.x.

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Abbas, Amr E., F. David Fortuin, Bhavesh Patel, Carlos A. Moreno, Nelson B. Schiller, and Steven J. Lester. "Noninvasive measurement of systemic vascular resistance using Doppler echocardiography." Journal of the American Society of Echocardiography 17, no. 8 (August 2004): 834–38. http://dx.doi.org/10.1016/j.echo.2004.04.008.

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Schrijen, F., C. Saunier, and F. Chabot. "Peripheral pulmonary vascular resistance." Journal of Applied Physiology 74, no. 2 (February 1, 1993): 613–16. http://dx.doi.org/10.1152/jappl.1993.74.2.613.

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The pressure-flow relationship has been studied in a peripheral portion of the lung vasculature in anesthetized dogs with use of a double-lumen catheter wedged in a distal pulmonary artery. One lumen was used to infuse mixed venous blood in the wedged area and the other to measure the corresponding perfusion pressure. Flow ranged from 0 to 9.2 ml/min, and the mean volume of the wedged area (n = 59) was 0.75 +/- 0.05 (SE) ml. In the areas where the distal pulmonary artery was in the same direction as the catheter ("coaxial"), the mean pressure-flow curve showed a negligible gamma-intercept and no significant difference between ascending and descending flow. The slope of the initial part of the ascending limb (peripheral pulmonary vascular resistance) varied from site to site and did not show a significant correlation with the overall pulmonary vascular resistance; it was inversely correlated with the volume of the wedged area (r = -0.35, P < 0.05) and directly, as expected, correlated with the y-intercept (r = 0.78, P < 0.001) and hysteresis (r = 0.48, P < 0.001). The results of two consecutive pressure-flow runs in the same site showed similar results, with no difference exceeding the error of measurement. In contrast, the slope increased by 71% during hypoxia (fraction of inspired O2 was 0.10, n = 5). This procedure seems suitable to determine the effects of physiological or pharmacological interventions on the pulmonary vessels, without interference of the systemic circulation.

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Moriyasu, Fuminori, Osamu Nishida, Nobuyuki Ban, Takefumi Nakamura, Kensuke Miura, Masahiko Sakai, Takeo Miyake, and Haruto Uchino. "Measurement of Portal Vascular Resistance in Patients With Portal Hypertension." Gastroenterology 90, no. 3 (March 1986): 710–17. http://dx.doi.org/10.1016/0016-5085(86)91127-3.

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Lautt, W. W., C. V. Greenway, D. J. Legare, and H. Weisman. "Localization of intrahepatic portal vascular resistance." American Journal of Physiology-Gastrointestinal and Liver Physiology 251, no. 3 (September 1, 1986): G375—G381. http://dx.doi.org/10.1152/ajpgi.1986.251.3.g375.

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The pressure drop from the portal vein to the vena cava occurs primarily across a postsinusoidal site localized to a narrow segment (less than 0.5 cm) of hepatic veins (roughly 1.5 mm diam) in the anesthetized cat. Portal venous pressure (PVP = 8.9 +/- 0.3 mmHg) and lobar hepatic venous pressure (LVP = 8.7 +/- 0.4 mmHg) are insignificantly different, and pressure changes imposed from the presinusoidal or postsinusoidal side are equally transmitted to both pressure sites. Several types of experiments were done to validate the LVP measurement. The portal vein, hepatic sinusoids, and hepatic veins proximal to the resistance site are all under a similar pressure. Previously reported calculations of hepatic vascular resistance are in error because of incorrect assumptions of sinusoidal pressure and localization of the portal resistance site as presinusoidal. Stimulation of hepatic sympathetic nerves for 3 min caused LVP and PVP to increase equally, showing that the increased "portal" resistance is postsinusoidal across the same region of the hepatic veins that was previously localized as the site of resistance in the basal state.

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Allison, R. C., B. Rippe, V. R. Prasad, J. C. Parker, and A. E. Taylor. "Pulmonary vascular permeability and resistance measurements in control and ANTU-injured dog lungs." American Journal of Physiology-Heart and Circulatory Physiology 256, no. 6 (June 1, 1989): H1711—H1718. http://dx.doi.org/10.1152/ajpheart.1989.256.6.h1711.

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Because questions have arisen regarding pulmonary vascular permeability and resistance measurements in isolated, perfused lungs, we sought to determine the 1) stability of repeated measurements of permeability and resistance in control lungs; and 2) magnitude of change in these measurements when permeability was greatly increased. Using blood-perfused dog lungs, we measured filtration coefficient (Kf) and isogravimetric capillary pressure (Pci) as indexes of vascular permeability, and we also determined total vascular resistance (Rt) as well as the segmental resistances using the double-occlusion pressure (Pdo). In a control group (n = 8), the base-line measurement of Kf (0.21 +/- 0.02 ml.min-1.cmH2O-1.100 g-1) and Pci (10.2 +/- 0.9 cmH2O) did not change over 4 h, indicating no changes in endothelial barrier function. Base-line Rt (13.9 +/- 2.6 cmH2O.l-1.min.100 g) also did not significantly increase. In a second group (n = 5), alpha-naphthylthiourea (ANTU) increased the initial Kf more than eight times (from 0.17 +/- 0.03 to 1.40 +/- 0.32 ml.min-1.cmH2O-1.100 g-1) and decreased Pci by 56% (from 9.4 +/- 0.6 to 4.1 +/- 0.4 cmH2O) at 1 h, indicating severely damaged endothelium. In addition, the Pdo determined during isogravimetric conditions correlated very well with Pci not only in control lungs (observed previously) but also in very permeable lungs (not previously reported). We conclude that this experimental model provides an excellent means of assessing changes in pulmonary microvascular permeability, with a spectrum ranging from no changes in hourly measurements for 4 h to obvious changes in permeability by 1 h.

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Parker, James C., Mark N. Gillespie, Aubrey E. Taylor, and Sherri L. Martin. "Capillary filtration coefficient, vascular resistance, and compliance in isolated mouse lungs." Journal of Applied Physiology 87, no. 4 (October 1, 1999): 1421–27. http://dx.doi.org/10.1152/jappl.1999.87.4.1421.

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Although many recently produced transgenic mice possess gene alterations affecting pulmonary vascular function, there are few baseline measurements of vascular resistance and permeability. Therefore, we excised the lungs of C57/BL6 mice and perfused them with 5% bovine serum albumin in RPMI-1640 culture medium at a nominal flow of 0.5 ml/min and ventilated them with 20% O2-5% CO2-75% N2. The capillary filtration coefficient, a sensitive measurement of hydraulic conductivity, was unchanged over 2 h (0.33 ± 0.03 ml ⋅ min−1 ⋅ cmH2O−1 ⋅ 100 g−1) in a control group ventilated with low peak inflation pressures (PIP) but increased 4.3-fold after high PIP injury. Baseline pulmonary vascular resistance was 6.1 ± 0.4 cmH2O ⋅ ml−1 ⋅ min ⋅ 100 g−1 and was distributed 34% in large arteries, 18% in small arteries, 14% in small veins, and 34% in large veins on the basis of vascular occlusion pressures. Baseline vascular compliance was 5.4 ± 0.3 ml ⋅ cmH2O−1 ⋅ 100 g−1 and decreased significantly with increased vascular pressures. Baseline pulmonary vascular resistance was inversely related to both perfusate flow and microvascular pressure and increased to 202% of baseline after infusion of 10−4 M phenylephrine due to constriction of large arterial and venous segments. Thus isolated mouse lung vascular permeability, vascular resistance, and the longitudinal distribution of vascular resistance are similar to those in other species and respond in a predictable manner to microvascular injury and a vasoconstrictor agent.

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Giesen, Leonie A., Michelle White, and Robert M. R. Tulloh. "Comparison of the effect of inhaled anaesthetic with intravenous anaesthetic on pulmonary vascular resistance measurement during cardiac catheterisation." Cardiology in the Young 25, no. 2 (February 19, 2014): 368–72. http://dx.doi.org/10.1017/s1047951114000195.

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AbstractBackground: Children with pulmonary hypertension routinely undergo pulmonary vascular resistance studies to assess the disease severity and vasodilator responsiveness. It is vital that results are accurate and reliable and are not influenced by the choice of anaesthetic agent. However, there are anecdotal data to suggest that propofol and inhalational agents have different effects on pulmonary vascular resistance. Methods: A total of 10 children with pulmonary hypertension were selected sequentially to be included in the study. To avoid confounding because of baseline anatomic or demographic details, a crossover protocol was implemented, using propofol or isoflurane, with time for washout in between each agent and blinding of the interventionalist. Results: Pulmonary and systemic vascular resistance were not significantly different when using propofol or isoflurane. However, the calculated resistance fraction – ratio of pulmonary resistance to systemic resistance – was significantly lower when using propofol than when using isoflurane. Conclusions: Although no difference in pulmonary vascular resistance was demonstrated, this pilot study suggests that the choice of anaesthetic agent may affect the calculation of relative pulmonary and systemic vascular resistance, and provides some preliminary evidence to favour propofol over isoflurane. These findings require replication in a larger study, and thus they should be considered in future calculations to make informed decisions about the management of children with pulmonary hypertension.

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Parvin, S. D., D. H. Evans, and P. R. F. Bell. "Peripheral resistance measurement in the assessment of severe peripheral vascular disease." British Journal of Surgery 72, no. 9 (September 1985): 751–53. http://dx.doi.org/10.1002/bjs.1800720928.

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Rothe, C. F., and R. Maass-Moreno. "Gastrointestinal hemodynamics during compensation for hemorrhage and measurement of Pmcf." American Journal of Physiology-Heart and Circulatory Physiology 266, no. 3 (March 1, 1994): H1242—H1250. http://dx.doi.org/10.1152/ajpheart.1994.266.3.h1242.

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To quantify the degree of autonomic reflex control of the gastrointestinal vasculature, we studied the responses to a 10-ml/kg hemorrhage or transfusion and autonomic blockade in fentanyl- and pentobarbital-anesthetized dogs. The active total blood volume was estimated by indocyanine green dilution. Transfusion and hemorrhage did not significantly change gastrointestinal vascular compliance [1.82 +/- 0.68 (SD) ml/mmHg], but autonomic blockade with hexamethonium and atropine increased it by 0.57 +/- 0.37 ml/mmHg. Neither hemorrhage nor autonomic blockade significantly changed gastrointestinal vascular resistance from its control value of 10.8 +/- 4 mmHg.ml-1.min.kg body wt, but transfusion reduced it by 3.0 +/- 1.2 mmHg.ml-1.min.kg body wt. The ratio of gastrointestinal vascular resistance to total peripheral resistance was not significantly changed, however. We conclude that vascular compliance and resistance of the gastrointestinal bed are minimally influenced by the autonomic nervous system under the conditions studied. Portal pressure and flow measurements (transit-time ultrasound) during the above maneuvers were also combined with estimations of mean circulatory filling pressure (Pmcf) to test the hypothesis that, when the heart is stopped to measure Pmcf, portal pressure equals central venous pressure (Pcv) and hence that portal flow is zero. Seven seconds after the heart was stopped, portal venous pressure (Ppv) remained 0.83 +/- 0.78 mmHg higher than Pcv and portal flow decreased to only 25% of its control value. However, gastrointestinal compliance times (Ppv-Pcv), an estimate of the extra distending volume, was only 0.07 +/- 0.07 ml/kg body wt. Thus we conclude that the error in estimating Pmcf, given this (Ppv-Pcv) difference, is physiologically insignificant.

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Bishop, R., D. McLeod, S. McIlveen, R. Blake, R. Gunther, J. Davis, L. Talken, et al. "Long-Term Measurement of Bronchial Vascular Resistance in Awake Sheep and Dogs." Archives of Physiology and Biochemistry 111, no. 4 (January 2003): 315–16. http://dx.doi.org/10.3109/13813450312331337478.

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R., Bishop, McLeod D., McIlveen S., Blake R., Gunther R., Davis J., Talken L., et al. "Long-Term Measurement of Bronchial Vascular Resistance in Awake Sheep and Dogs." Archives of Physiology and Biochemistry 111, no. 4 (April 1, 2003): 315–16. http://dx.doi.org/10.1080/13813450312331337478.

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Tinkanen, Helena, and Erkki Kujansuu. "The Reproducibility of the Doppler Ultrasound Measurement of Uterine Artery Vascular Resistance." Gynecologic and Obstetric Investigation 39, no. 3 (1995): 188–91. http://dx.doi.org/10.1159/000292406.

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Aleksic, M., J. Heckenkamp, M. Gawenda, and J. Brunkwall. "Pulsatility Index Determination by Flowmeter Measurement: A New Indicator for Vascular Resistance?" European Surgical Research 36, no. 6 (2004): 345–49. http://dx.doi.org/10.1159/000081642.

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Davies, A. H., T. R. Magee, R. N. Baird, and M. Horrocks. "Intraoperative measurement of vascular graft resistance as a predictor of early outcome." British Journal of Surgery 80, no. 7 (July 1993): 854–57. http://dx.doi.org/10.1002/bjs.1800800712.

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Krohova, J., L. Faes, B. Czippelova, R. Pernice, Z. Turianikova, R. Wiszt, N. Mazgutova, A. Busacca, and M. Javorka. "Vascular resistance arm of the baroreflex: methodology and comparison with the cardiac chronotropic arm." Journal of Applied Physiology 128, no. 5 (May 1, 2020): 1310–20. http://dx.doi.org/10.1152/japplphysiol.00512.2019.

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Baroreflex response consists of several arms, but the cardiac chronotropic arm (blood pressure changes evoking heart rate response) is usually analyzed. This study introduces a method to assess the vascular baroreflex arm with the continuous noninvasive measurement of peripheral vascular resistance as an output considering causality in the interaction between oscillations and slower dynamics of vascular tone changes. We conclude that although vascular baroreflex arm involvement becomes dominant during orthostasis, gain of this interaction is relatively stable.

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Raj, J. U., P. Kaapa, and J. Anderson. "Effect of pulsatile flow on microvascular resistance in adult rabbit lungs." Journal of Applied Physiology 72, no. 1 (January 1, 1992): 73–81. http://dx.doi.org/10.1152/jappl.1992.72.1.73.

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We have determined the effect of pulsatile flow on segmental vascular resistance in lungs from 29 adult rabbits. In group I (n = 4), II (n = 8), and III (n = 8) lungs were isolated. In group IV (n = 9) rabbits were anesthetized, their chests were opened, and lungs were studied in vivo. Group I and II lungs had steady-flow perfusion: group I with intact vasotonus and group II with papaverine treatment. Group III lungs (papaverine treated) were perfused for two consecutive 45-min periods with steady and pulsatile flow. In all isolated lungs and in lungs of five anesthetized rabbits, we measured pressures in subpleural 20- to 50-microns-diam arterioles and venules by use of the micropipette servo-nulling method. Measurement of distribution of blood flow in lungs of four anesthetized rabbits by use of radiolabeled microspheres revealed no abnormality of blood flow to the micropunctured lobe. We found that total and segmental vascular resistances were similar in group I and II lungs, with microvessels representing 55% of total resistance. In group III lungs, total resistance was 30% lower during pulsatile flow than during steady flow because of a lower microvascular resistance. Lungs in vivo (group IV) had a significantly lower total vascular resistance than isolated lungs and had a low fractional resistance in microvessels (approximately 28%). We conclude that, in isolated perfused adult rabbit lungs, vascular resistance is very high, particularly in the microvascular segment, and that pulsatile flow decreases microvascular resistance.

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Parkinson, S., C. Belleau, J. Homan, and B. Richardson. "Flow and velocity waveform indices in the ovine fetal abdominal aorta with changes in behavioural state." Reproduction, Fertility and Development 7, no. 5 (1995): 1299. http://dx.doi.org/10.1071/rd9951299.

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The purpose of this study was to determine the extent to which flow and velocity waveform indices are comparable as measured from the ovine fetal abdominal aorta and reflect downstream vascular resistance with changes in electrocortical activity. Nine chronically catheterized fetal sheep were studied near term with continuous measurement of electrocortical activity, perfusion pressure, and fetal heart rate. A cuffed Doppler crystal and a Transonic flow probe on the descending abdominal aorta were used for the simultaneous measurement of velocity waveforms and flow waveforms, with the Resistance Index (RI), calculated for each. Mean blood flow was also obtained from the Transonic flow probe. Whereas the change in cardiovascular parameters between the low- and high-voltage electrocortical activity (ECOG) states was small, with little relationship to the change in RI measurements, across all animals there was an inverse correlation between the RI measurements and fetal heart rate, perfusion pressure and aortic blood flow during both low- and high-voltage ECOG states. The RI as measured from the velocity waveforms showed only a modest correlation to those measured from the flow waveforms. It is concluded that over the range of circulatory change generated with spontaneous change in behavioural state, the RI as measured in the abdominal aorta of the ovine fetus is primarily determined by pulsatile cardiovascular variables rather than lower body vascular resistance.

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Bush, A., C. M. Busst, W. B. Knight, J. S. Carvalho, M. L. Rigby, and E. A. Shinebourne. "Preoperative measurement of pulmonary vascular resistance in complete transposition of the great arteries." Heart 63, no. 5 (May 1, 1990): 300–303. http://dx.doi.org/10.1136/hrt.63.5.300.

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Spokes, Rachel A., and Vicki C. Middlefell. "Simultaneous measurement of plasma protein extravasation and carotid vascular resistance in the rat." European Journal of Pharmacology 281, no. 1 (July 1995): 75–79. http://dx.doi.org/10.1016/0014-2999(95)00231-9.

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Bates, D. O., and F. E. Curry. "Vascular endothelial growth factor increases hydraulic conductivity of isolated perfused microvessels." American Journal of Physiology-Heart and Circulatory Physiology 271, no. 6 (December 1, 1996): H2520—H2528. http://dx.doi.org/10.1152/ajpheart.1996.271.6.h2520.

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These experiments report the first direct measurement of microvessel permeability coefficients after exposure to vascular endothelial growth factor (VEGF). The Landis technique was extended to enable measurement of the resistance of the microvessel wall to water flow, hydraulic conductivity (Lp), on the same microvessel in the frog mesentery during the initial exposure to VEGF (acute) and 24 and 72 h after initial exposure (chronic). Control measurements of Lp showed no change either acutely or chronically. Exposure to 1 nM VEGF rapidly and transiently increased microvessel Lp within 30 s (to 7.8-fold greater than baseline values) and returned to control within 2 min. The baseline Lp was fivefold greater after 24 h than the initial baseline as a result of VEGF perfusion and returned to its original value after 72 h. These experiments confirm the hypothesis that VEGF acts both acutely (over a period of a few minutes) and chronically (over a few hours) to increase microvascular permeability.

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Ghorbani-Shirkouhi, Samaneh, Fatemeh Ashouri, Saeideh Aghayari Sheikh Neshin, Alia Saberi, Bahador Hasanzadeh, and Parisa Shahshahani. "The prevalence and associated factors of aspirin resistance among prophylactic aspirin users." Romanian Journal of Neurology 20, no. 1 (March 31, 2021): 50–56. http://dx.doi.org/10.37897/rjn.2021.1.7.

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Background. Aspirin is an antiplatelet used for the secondary prevention after vascular events. It is also suggested for the primary prevention of vascular events in high risk people, however, despite using standard prophylactic doses, aspirin resistance may result in therapeutic failure and arterial thrombosis. Since the prevalence of aspirin resistance and its associated factors were heterogeneous in different studies, this study was conducted to determine the prevalence and associated factors of aspirin resistance in an Iranian population under aspirin for primary prevention of vascular events. Methods. 264 patients without documented vascular disease with 80 mg daily aspirin consumption for at least one month enrolled in this cross-sectional study. Aspirin resistance was assessed by the measurement of thromboxane B2 in the urine samples using the enzyme-linked immunosorbent assay method. Aspirin resistance was defined as a urine level of thromboxane B2 ≥ 1700 ng/dl. Results. The prevalence of aspirin resistance in this study was 9.8%. Age (OR = 0.935, 95% CI: 0.880-0.993, P = 0.028) and geographical regions (OR = 0.117, 95% CI: 0.014-0.958, P = 0.045) showed independent correlation with aspirin resistance. No significant association observed between aspirin resistance and gender, diabetes mellitus, hypertension, hyperlipidemia, smoking, duration of aspirin use, body mass index, and drug history. Conclusions. Despite the standard daily dose of aspirin for primary prevention of vascular events, some of our patients exhibited aspirin resistance that was directly related to a higher age and geographical region. More studies are required to clarify the beneficial role of aspirin resistance test before planning a preventive strategy in high risk individuals.

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Polska, Elzbieta, Karl Kircher, Paulina Ehrlich, Pia V. Vecsei, and Leopold Schmetterer. "RI in central retinal artery as assessed by CDI does not correspond to retinal vascular resistance." American Journal of Physiology-Heart and Circulatory Physiology 280, no. 4 (April 1, 2001): H1442—H1447. http://dx.doi.org/10.1152/ajpheart.2001.280.4.h1442.

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The aim of the present study was to investigate the association between ultrasound Doppler measurements of resistive index (RI) in the central retinal artery and retinal vascular resistance ( R) assessed with laser Doppler velocimetry, vessel size measurement, and calculation of ocular perfusion pressure (PP) in healthy subjects. An increase in vascular resistance was induced by inhalation of 100% O2. During hyperoxia no significant changes in PP were observed. Mean flow velocity in main retinal veins was reduced by −27.5 ± 2.0%. The average decrease in diameter was −11.5 ± 1.0%. R, which was calculated as the ratio of PP to flow rate, increased by 97.6 ± 7.7%. RI increased as well, but the effect was much smaller (6.6 ± 2.2%). In addition, a negative correlation was found between baseline values of R and RI ( r = −0.83). During hyperoxia R and RI were not associated. In conclusion, our data indicate that RI as assessed with color Doppler imaging in the central retinal artery is not an adequate measure of R.

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Zanaboni, P. B., J. D. Bradley, R. O. Webster, and T. E. Dahms. "Cyclooxygenase inhibition prevents PMA-induced increase in pulmonary vascular permeability to albumin." Journal of Applied Physiology 73, no. 5 (November 1, 1992): 2011–15. http://dx.doi.org/10.1152/jappl.1992.73.5.2011.

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In a previous study, we demonstrated that phorbol myristate acetate-(PMA) induced injury in isolated blood-perfused rabbit lungs was characterized by increased pulmonary vascular resistance (PVR) and permeability to water as measured by fluid filtration coefficient (Kf). The Kf increase was prevented by pretreatment with three cyclooxygenase inhibitors, indomethacin, ibuprofen, and meclofenamate. Other studies have shown that PMA causes a decrease in pulmonary vascular surface area, probably due to the increase in arterial resistance. Measurement of Kf requires increased microvascular pressure, and therefore Kf estimates the permeability of the entire vascular bed. Thus the permeability of the flowing vessels may be overestimated by Kf. In this study, we chose to investigate the effect of PMA on vascular permeability to protein by measuring albumin leak. Because this measurement does not require a hydraulic stress, it is more likely to reflect the permeability of flowing vessels. PMA administration (5 x 10(-8) M) caused significant increases in both PVR and 125I-labeled bovine serum albumin leak. Cyclooxygenase inhibition with indomethacin, ibuprofen, or meclofenamate prevented the PMA-induced increase in albumin leak without affecting the PVR increase. These results suggest that cyclooxygenase-mediated products of arachidonic acid mediate the PMA-induced increase in vascular permeability to both water and protein.

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Evlakhov, Vadim I., Ilya Z. Poyassov, and Tatiana P. Berezina. "The peculiarities of pulmonary macro- and microhemodynamics changes after treatment with agonists and blockers of cholinoceptors." Medical academic journal 20, no. 4 (March 18, 2021): 35–44. http://dx.doi.org/10.17816/maj55326.

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Background. The pulmonary arterial and venous vessels are innervated by parasympathetic cholinergic nerves. However, the studies, performed on the isolated rings of pulmonary vessels, can not give answer to the question about the role of cholinergic mechanisms in the changes of pulmonary circulation in full measure. Aim. The comparative analysis of the changes of the pulmonary macro- and microhemodynamics after acetylcholine, atropine, pentamine and nitroglycerine treatment. Materials and methods. The study was carried out on the anesthetized rabbits in the condition of intact circulation with the measurement of the pulmonary artery pressure and flow, venae cavae flows, cardiac output, and also on isolated perfused lungs in situ with stabilized pulmonary flow with measurement of the perfused pulmonary artery pressure, capillary hydrostatic pressure, capillary filtration coefficient and calculation of the pulmonary vascular resistance, pre- and postcapillary resistances. Results. In the conditions of intact circulation after acetylcholine, pentamine and nitroglycerine treatment the pulmonary artery pressure and flow decreased, the pulmonary vascular resistance did not change as a result of decreasing of pulmonary artery flow and left atrial pressure due to diminution of venous return and venae cavaе flows. On perfused isolated lungs acetylcholine caused the increasing of pulmonary artery pressure, capillary hydrostatic pressure, pulmonary vascular resistance, pre- and postcapillary resistance and capillary filtration coefficient. After M-blocker atropine treatment the indicated above parameters of pulmonary microcirculation increased, on the contrary, after N-blocker pentamine treatment they decreased. Nitroglycerine infusion caused less decreasing of the parameters of pulmonary microcirculation in comparison with effects of pentamine, but capillary filtration coefficient decreased to a greater extent. These data indicate that nitroglycerine decreases endothelial permeability of pulmonary microvessels. Conclusion. After activation or blockade of cholinergic mechanisms in the condition of intact circulation the calculated parameter of pulmonary vascular resistance is depended from the ratio of the pulmonary artery pressure and flow and left atrial pressure, which are determined by the venous return. The different character of the changes of pulmonary microcirculatory parameters after M-blocker atropine and N-blocker pentamine treatment is evidence of reciprocal relations of M- and N-cholinoceptors in the nervous regulation of the pulmonary microcirculatory bed.

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Constable, Peter D., Geoffrey W. Smith, George E. Rottinghaus, Mike E. Tumbleson, and Wanda M. Haschek. "Fumonisin-induced blockade of ceramide synthase in sphingolipid biosynthetic pathway alters aortic input impedance spectrum of pigs." American Journal of Physiology-Heart and Circulatory Physiology 284, no. 6 (June 1, 2003): H2034—H2044. http://dx.doi.org/10.1152/ajpheart.00155.2002.

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The sphingolipid signaling pathway appears to play an important role in regulating vascular tone. We examined the effect of fumonisin B1, a fungal toxin in corn that blocks ceramide synthase in the sphingolipid signaling pathway, on the ascending aortic impedance spectrum of pigs. Sixteen pigs were fed culture material containing fumonisin B1 (20 mg/kg body wt) ( n = 7) or a control diet ( n = 9) daily for 3 days and then instrumented under α-chloralose anesthesia for measurement of ascending aortic pressure and flow. Fumonisin ingestion increased serum sphinganine and sphingosine concentrations. Fumonisin ingestion also decreased cardiac output and characteristic impedance and increased the frequency of the first minimum impedance modulus, systemic vascular resistance, and the terminal, first, and second harmonic reflection coefficients, without changing mean arterial pressure. Thus blockade of ceramide synthase is accompanied by decreased vascular tone in systemic conduit arteries and increased vascular tone in systemic resistance vessels. The results indicate that the sphingolipid signaling pathway influences vascular tone in α-chloralose-anesthetized pigs.

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Parker, R. E., and K. L. Brigham. "Effects of endotoxemia on pulmonary vascular resistances in unanesthetized sheep." Journal of Applied Physiology 63, no. 3 (September 1, 1987): 1058–62. http://dx.doi.org/10.1152/jappl.1987.63.3.1058.

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Ten experiments were conducted on nine sheep to determine the effects of endotoxemia (1.0 microgram/kg iv over 15 min) on the vascular resistances of two segments of the pulmonary circulation. The first segment (S1) was from the main pulmonary artery to the site in the pulmonary veins corresponding to the pressure measured with a deflated and wedged 7-Fr Swan-Ganz catheter. The second segment (S2) was from the wedge pressure measurement site to the left atrium. Endotoxemia caused both pulmonary arterial pressure and pulmonary arterial wedge pressure to increase significantly during early (phase 1) and late (phase 2) periods of response; left atrial pressure was significantly decreased during both phases. Normalized cardiac output decreased significantly at 35 and 180 min but not at 240 min after starting endotoxin infusion. The calculated resistance of S1 significantly increased from a base-line value of 3.03 +/- 0.31 (cmH2O.1–1.min) to 7.60 +/- 0.71, 6.34 +/- 1.22, and 6.66 +/- 1.35 at 35, 180, and 240 min, respectively. Calculated resistance of S2 was 1.32 +/- 0.14 at base line and increased significantly to 11.43 +/- 1.66 at 35 min, 4.45 +/- 0.47 at 180 min, and 3.32 +/- 0.61 at 240 min. The calculated percent of total pulmonary resistance in S2 increased significantly from approximately 31 to 59% during phase 1 and remained significantly increased at 41% from 90 to 180 min after endotoxin. Hematocrit increased by 40% at 35 min, whereas plasma total protein concentration increased by only 8% at 35 min.(ABSTRACT TRUNCATED AT 250 WORDS)

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Fisher, Lyle E., Attila Cziraki, Curt M. Steinhart, and John D. Catravas. "Unaltered pulmonary capillary surface area in the presence of changing arterial resistance." American Journal of Physiology-Lung Cellular and Molecular Physiology 274, no. 2 (February 1, 1998): L264—L269. http://dx.doi.org/10.1152/ajplung.1998.274.2.l264.

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We hypothesized that capillary recruitment may not be solely dependent on extracapillary factors. To test this hypothesis, rabbits were anesthetized and placed on total cardiac bypass at a constant, physiological pulmonary blood flow. Vascular occlusion techniques were combined with measurement of the transpulmonary metabolism of an angiotensin-converting enzyme substrate, allowing the concomitant assessment of changes in segmental resistances and dynamically perfused capillary surface area. Intra-arterial serotonin infusion increased upstream pulmonary vascular resistances without affecting dynamically perfused capillary surface area. Intra-arterial isoproterenol infusion diminished serotonin-induced increased upstream resistances, also without affecting capillary surface area. These findings support the hypothesis that pulmonary capillary recruitment may not be solely dependent on extracapillary factors.

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Cochrane, E., and I. D. McCarthy. "Rapid effects of parathyroid hormone(1–34) and prostaglandin E2 on bone blood flow and strontium clearance in the rat in vivo." Journal of Endocrinology 131, no. 3 (December 1991): 359–65. http://dx.doi.org/10.1677/joe.0.1310359.

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ABSTRACT The vascular effects of noradrenaline, ATP, parathyroid hormone (PTH) and prostaglandin E2 (PGE2) were investigated in the rat. Additionally, the exchange of mineral ions between bone and blood was assessed by measuring strontium clearance, with the aim of investigating whether the vascular effects of these agents altered uptake of mineral ions or if this exchange could be changed independently of blood flow. Radioactive microspheres and 85Sr were used to establish bone blood flow and mineral clearance. Measurements of bone blood flow and arterial pressure were made in each animal and used to calculate vascular resistance. A measurement of 85Sr clearance was also obtained. Arterial blood pressure was significantly affected by noradrenaline (P ≤ 0·003) and ATP (P ≤ 0·015). Additionally, noradrenaline significantly (P ≤ 0·03) reduced bone blood flow. This decrease was related to a significant increase in vascular resistance. Arterial blood pressure and bone blood flow were significantly reduced by both bovine PTH(1–34) (P ≤ 0·001, P ≤ 0·02) and PGE2 (P ≤ 0·005, P ≤ 0·001). Vascular resistance to bone was increased by both agents but this was only statistically significant in the case of PGE2 (P ≤ 0·01). A significant (P ≤ 0·001) reduction in strontium was also produced by PGE2. In each group the relationship between bone blood flow and strontium clearance was then analysed. Only the PGE2-treated group had a slope of the regression which was statistically different from both the control animals and the other drug-treated groups. Treatment with PGE2 therefore resulted in a dose-related decrease in 85Sr clearance which was not related to the reduction in bone blood flow. Journal of Endocrinology (1991) 131, 359–365

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Ulett, Kimberly B., and Thomas H. Marwick. "Incorporation of Pulmonary Vascular Resistance Measurement into Standard Echocardiography: Implications for Assessment of Pulmonary Hypertension." Echocardiography 24, no. 10 (November 2007): 1020–22. http://dx.doi.org/10.1111/j.1540-8175.2007.00539.x.

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Siegel, Lawrence G., and Ronald G. Pearl. "Measurement of the Longitudinal Distribution of Pulmonary Vascular Resistance from Pulmonary Artery Occlusion Pressure Profiles." Anesthesiology 68, no. 2 (February 1, 1988): 305–6. http://dx.doi.org/10.1097/00000542-198802000-00036.

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Collee, George. "Measurement of the Longitudinal Distribution of Pulmonary Vascular Resistance from Pulmonary Artery Occlusion Pressure Profiles." Anesthesiology 68, no. 2 (February 1, 1988): 307. http://dx.doi.org/10.1097/00000542-198802000-00037.

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Godden, D. J., E. M. Wagner, P. D. Pare, W. Mitzner, and E. M. Baile. "Measurement of airway wall blood flow in sheep by laser-Doppler flowmetry: interpretation and problems." Journal of Applied Physiology 70, no. 2 (February 1, 1991): 641–49. http://dx.doi.org/10.1152/jappl.1991.70.2.641.

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This study investigated the pulmonary vascular response to endothelin (ET) in rats. In conscious rats, an incremental intravenous bolus of ET-1 (100-1,000 pM) caused, after an initial drop in systemic arterial pressure (Psa), a secondary dose-dependent increase of Psa concomitant with a decrease of cardiac output (CO) and heart rate (HR). Pulmonary arterial pressure (Ppa) remained unchanged, and pulmonary vascular resistance (PVR) increased significantly only after 1,000 pM (+ 40.0 +/- 10.4 at 15 min). Meclofenamate (6 mg/kg iv) did not alter hemodynamic response to ET (300 pM). After autonomic blockade with hexamethonium (6 mg/kg iv) plus atropine (0.75 mg/kg iv), bradycardia response to ET (300 pM) was blocked, but CO decreased, systemic vascular resistance increased, and PVR remained unchanged as in controls. In anesthetized ventilated rats, bolus injections of ET (10-1,000 pM) induced a transient dose-related decrease in compliance (-10.9 +/- 1.8% after 1,000 pM) but no change of conductance. In isolated lungs, Ppa increased at doses greater than 100 pM, and edema developed in response to 1,000 pM ET. The rise of Ppa in response to 300 pM was not altered by meclofenamate (3.2 x 10(-6) M) but was potentiated by inhibitors of endothelium-derived relaxing factor(s) (EDRF), methylene blue (10(-4) M), pyrogallol (3 x 10(-5) M), and NG-monomethyl-L-arginine (6 x 10(-4) M) (3.9 +/- 0.3, 4.6 +/- 0.5, and 5.9 +/- 0.3 mmHg, respectively, compared with 1.5 +/- 0.5 mmHg in control lungs). These results suggest that circulating ET is a more potent constrictor of the systemic circulation than of the pulmonary vascular bed.(ABSTRACT TRUNCATED AT 250 WORDS)

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Bell, L. B., E. J. Zuperku, and J. P. Kampine. "Technique for continuous measurement of compliance in isolated vascular segments." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 250, no. 1 (January 1, 1986): R142—R149. http://dx.doi.org/10.1152/ajpregu.1986.250.1.r142.

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A method has been developed that provides an on-line (1/s) measurement of elastance [E = 1/compliance (C)] in a perfused isolated vessel segment in situ. Values of E can be obtained as a function of perfusion pressure (P) or in response to drug interventions. Noncompliant stainless steel tubes are used as inflow and outflow cannulas. Segment P is obtained from a short small-bore stainless steel catheter and miniature pressure transducer. During constant flow through the inflow cannula, an adjustable outflow resistance is used to set the segment P. Simultaneous activation of solenoid pinch valves, for 200 ms, compresses in-line Silastic tubing next to each cannula and serves to simultaneously 1) isolate the segment and 2) inject a small volume into the segment (delta V). This delta V results in a step increase in segment P (delta P). delta V is not significantly altered by changing the volume of air in the in-line windkessel reservoir (when air volume is greater than or equal to 100 ml), mean perfusion pressure (over a range of 50-150 mmHg) or compliance of the test cell. Therefore, delta P alpha E, and 1/delta P alpha C. Since this recorded variable is linearly related to C, actual C can be continuously recorded on a recorder after a simple two-point calibration process. C as determined by this method was found to be linearly related (r = 0.997) to calculated C of a test cell air bubble (range: 0.1 less than C less than 0.7 microliter/mmHg; resolution: 0.001 microliter/mmHg).(ABSTRACT TRUNCATED AT 250 WORDS)

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Geierlehner, Alexander, Raymund E. Horch, Ingo Ludolph, and Andreas Arkudas. "Intraoperative Blood Flow Analysis of DIEP vs. ms-TRAM Flap Breast Reconstruction Combining Transit-Time Flowmetry and Microvascular Indocyanine Green Angiography." Journal of Personalized Medicine 12, no. 3 (March 16, 2022): 482. http://dx.doi.org/10.3390/jpm12030482.

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Background: Vascular patency is the key element for high flap survival rates. The purpose of this study was to assess and compare the blood flow characteristics of deep inferior epigastric perforator (DIEP) and muscle-sparing transverse rectus abdominis musculocutaneous (ms-TRAM) flaps for autologous breast reconstruction. Methods: This prospective clinical study combined Transit-Time Flowmetry and microvascular Indocyanine Green Angiography for the measurement of blood flow volume, vascular resistance, and intrinsic transit time. Results: Twenty female patients (mean age, 52 years) received 24 free flaps (14 DIEP and 10 ms-TRAM flaps). The mean arterial blood flow of the flap in situ was 7.2 ± 1.9 mL/min in DIEP flaps and 11.5 ± 4.8 mL/min in ms-TRAM flaps (p < 0.05). After anastomosis, the mean arterial blood flow was 9.7 ± 5.6 mL/min in DIEP flaps and 13.5 ± 4.2 mL/min in ms-TRAM flaps (p = 0.07). The arterial vascular resistance of DIEP flaps was significantly higher than that of ms-TRAM flaps. The intrinsic transit time of DIEP flaps was 52 ± 18 s, and that of ms-TRAM flaps was 33 ± 11 s (p < 0.05). The flap survival rate was 100%. One DIEP flap with the highest intrinsic transit time (77 s) required surgical revision due to arterial thrombosis. Conclusion: In this study, we established the blood flow characteristics of free DIEP and ms-TRAM flaps showing different blood flow rates, vascular resistances, and intrinsic transit times. These standard values will help to determine the predictive values for vascular compromise, hence improving the safety of autologous breast reconstruction procedures.

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Huonker, M., Y. O. Schumacher, A. Ochs, S. Sorichter, J. Keul, and M. Rössle. "Cardiac function and haemodynamics in alcoholic cirrhosis and effects of the transjugular intrahepatic portosystemic stent shunt." Gut 44, no. 5 (May 1, 1999): 743–48. http://dx.doi.org/10.1136/gut.44.5.743.

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BACKGROUNDA portosystemic stent shunt may impair cardiac function and haemodynamics.AIMSTo investigate the effects of a transjugular intrahepatic portosystemic shunt (TIPS) on cardiac function and pulmonary and systemic circulation in patients with alcoholic cirrhosis.PATIENTS/METHODS17 patients with alcoholic cirrhosis and recent variceal bleeding were evaluated by echocardiography and catheterisation of the splanchnic and pulmonary circulation before and after TIPS. The period of catheter measurement was extended to nine hours in nine of the patients. The portal vein was investigated by Doppler ultrasound before and nine hours after TIPS.RESULTSBaseline echocardiography showed the left atrial diameter to be slightly increased and the left ventricular volume to be in the upper normal range. Nine hours after TIPS, the left atrial diameter and left ventricular end diastolic volume were increased (by 6% (p<0.01) and 7% (p<0.01) respectively); end systolic volume had not changed significantly. Invasive measurements showed a sharp increase in right atrial pressure (by 101%; p<0.01), mean pulmonary artery pressure (by 92%; p<0.01), pulmonary capillary wedge pressure (by 111%; p<0.01), and cardiac output (8.1 (1.6) to 11.9 (2.4) l/min; p<0.01). Systemic vascular resistance decreased (824 (242) to 600 (265) dyn·s·cm−5 p<0.01), and total pulmonary resistance increased (140 (58.5) to 188 (69.5) dyn·s·cm−5; p<0.05). Total pulmonary resistance (12%; NS), cardiac output (1.4 l/min; p<0.05), and portal vein blood flow (1.4 l/min; p<0.05) remained elevated for nine hours after TIPS in the subgroup. Portoatrial pressure gradient (43%; p<0.05), portohepatic vascular resistance (72%; p<0.05), and systemic vascular resistance (27%; p<0.01) were consistently reduced.CONCLUSIONSThe increase in the left atrial diameter, the pulmonary capillary wedge pressure, and total pulmonary resistance observed after the TIPS procedure reflected diastolic dysfunction of the hyperdynamic left ventricle in patients with alcoholic cirrhosis. The haemodynamic effects of the portosystemic stent shunt itself on the splanchnic circulation seem to be mainly responsible for the further decrease in systemic vascular resistance. TIPS may unmask a coexisting preclinical cardiomyopathy in patients with alcoholic cirrhosis and portal hypertension.

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Charan, N. B., G. M. Turk, and R. Ripley. "Measurement of bronchial arterial blood flow and bronchovascular resistance in sheep." Journal of Applied Physiology 59, no. 2 (August 1, 1985): 305–8. http://dx.doi.org/10.1152/jappl.1985.59.2.305.

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We studied the bronchial arterial blood flow (Qbr) and bronchial vascular resistance (BVR) in sheep prepared with carotid-bronchial artery shunt. Nine adult sheep were anesthetized, and through a left thoracotomy a heparinized Teflon-tipped Silastic catheter was introduced into the bronchial artery. The other end of the catheter was brought out through the chest wall and through a neck incision was introduced into the carotid artery. A reservoir filled with warm heparinized blood was connected to this shunt. The height of blood column in the reservoir was kept constant at 150 cm by adding more blood. Qbr was measured, after interrupting the carotid-bronchial artery flow, by the changes in the reservoir volume. The bronchial arterial back pressure (Pbr) was measured through the shunt when both carotid-bronchial artery and reservoir Qbr had been temporarily interrupted. The mean Qbr was 34.1 +/- 2.9 (SE) ml/min, Pbr = 17.5 +/- 3.3 cmH2O, BVR = 3.9 +/- 0.5 cmH2O X ml-1 X min, mean pulmonary arterial pressure = 21.5 +/- 3.6 cmH2O, and pulmonary capillary wedge pressure (Ppcw) = 14.3 +/- 3.7 cmH2O. We further studied the effect of increased left atrial pressure on these parameters by inflating a balloon in the left atrium. The left atrial balloon inflation increased Ppcw to 25.3 +/- 3.1 cmH2O, Qbr decreased to 21.8 +/- 2.4 ml/min (P less than 0.05), and BVR increased to 5.5 +/- 1.0 cmH2O.ml-1.min (P less than 0.05).

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Ichinose, Masashi, Shunsaku Koga, Naoto Fujii, Narihiko Kondo, and Takeshi Nishiyasu. "Modulation of the spontaneous beat-to-beat fluctuations in peripheral vascular resistance during activation of muscle metaboreflex." American Journal of Physiology-Heart and Circulatory Physiology 293, no. 1 (July 2007): H416—H424. http://dx.doi.org/10.1152/ajpheart.01196.2006.

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Continuous measurement of leg blood flow (LBF) using Doppler ultrasound with simultaneous noninvasive mean arterial blood pressure (MAP) measurement permits beat-to-beat estimates of leg vascular resistance (LVR) in humans. We tested the hypothesis that the beat-to-beat fluctuations in LVR and the dynamic relationship between MAP and LVR are modulated by the activation of muscle metaboreflex. Twelve healthy subjects performed a 1-min isometric handgrip exercise at 50% maximal voluntary contraction, which was followed by a period of imposed postexercise muscle ischemia (PEMI). We then employed transfer function analysis to examine the dynamic relationships between MAP and LBF and between MAP and LVR, both at rest (control) and during PEMI. We found the following. 1) The spectral power for LBF and LVR in low-frequency (∼0.03–0.15 Hz) range significantly increased from control during PEMI without a significant change in the high-frequency (∼0.15–0.35 Hz) power. 2) During PEMI, the transfer function gains for MAP-LBF and MAP-LVR relationships in the low-frequency (∼0.05–0.15 Hz) range were significantly increased during PEMI (vs. control) but were unchanged in the high-frequency (∼0.2–0.3 Hz) range. 3) The phases for MAP-LBF and MAP-LVR relationships were not different during control and PEMI. The phase for MAP-LVR relationship revealed that changes in MAP were followed by directionally similar changes in LVR, which is consistent with the characteristics of intrinsic vascular regulatory mechanisms such as the myogenic response of the resistance arteries. We suggest that, in humans, modulation of the dynamic MAP-LVR relationship during activation of the muscle metaboreflex reflects complex interactions between intrinsic vascular regulatory mechanisms and sympathetic vascular regulation.

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Abe, Michiaki, Tae Yamamoto, Ryusuke Inoue, Hideyasu Kiyomoto, Hiroshi Sato, and Sadayoshi Ito. "728 ULTRASOUND DOPPLER MEASUREMENT OF AORTIC BLOOD FLOW AND INTRARENAL VASCULAR RESISTANCE IN CHRONIC KIDNEY DISEASE." Journal of Hypertension 30 (September 2012): e211. http://dx.doi.org/10.1097/01.hjh.0000420404.67000.81.

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Durkin, Robert J., Timothy W. Evans, and Stephen M. Winter. "Noninvasive Estimation of Pulmonary Vascular Resistance by Stroke Index Measurement With an Inert Gas Rebreathing Technique." Chest 106, no. 1 (July 1994): 59–66. http://dx.doi.org/10.1378/chest.106.1.59.

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Kanda, Takashi, Masashi Fujita, Osamu Iida, Masaharu Masuda, Shin Okamoto, Takayuki Ishihara, Kiyonori Nanto, Tatsuya Shiraki, and Masaaki Uematsu. "The Accurate Measurement of Pulmonary Vascular Resistance Using Echocardiography in Patients with Mild Left Heart Failure." Journal of Cardiac Failure 21, no. 10 (October 2015): S196. http://dx.doi.org/10.1016/j.cardfail.2015.08.288.

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Crissinger, K. D., P. R. Kvietys, and D. N. Granger. "Developmental intestinal vascular responses to venous pressure elevation." American Journal of Physiology-Gastrointestinal and Liver Physiology 254, no. 5 (May 1, 1988): G658—G663. http://dx.doi.org/10.1152/ajpgi.1988.254.5.g658.

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The response to venous pressure elevation is an important criterion for determining whether metabolic or myogenic mechanisms are involved in local vasoregulation. We studied the effects of venous pressure elevation on intestinal hemodynamics and oxygenation in 20 mixed-breed piglets, divided equally among 1-day-, 3-day-, 2-wk-, and 1-mo-old animals. A venous circuit was established between the superior mesenteric and jugular veins, which allowed measurement of superior mesenteric blood flow, venous pressure, capillary pressure, and arteriovenous oxygen difference at venous pressures between 0 and 20 mmHg. The resting intestinal oxygen uptake in 1-day-old piglets was significantly higher than in 2-wk-old and 1-mo-old piglets. The vascular response to venous pressure elevation in 1-day-old piglets was characterized by reductions in total and precapillary resistance and increased oxygen uptake, while older animals responded to venous pressure elevation with increases in total and precapillary vascular resistance and reductions in oxygen uptake. These results indicate that metabolic factors exert a dominant influence on the intestinal vasculature of the newborn, while myogenic factors predominate in older animals in response to venous pressure elevation.

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Axelsson, M., and S. Nilsson. "Blood pressure control during exercise in the Atlantic cod, Gadus morhua." Journal of Experimental Biology 126, no. 1 (November 1, 1986): 225–36. http://dx.doi.org/10.1242/jeb.126.1.225.

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Atlantic cod were subjected to 12–15 min swimming exercise at 2/3 body lengths s-1 in a Blazka-type swim tunnel. Pre- and postbranchial blood pressures, cardiac output (ventral aortic blood flow) and heart rate were continuously recorded, and blood samples for measurement of arterial and mixed venous oxygen tension were taken before and at the end of the exercise period. In a second group of fish, subjected to similar exercise regimes, blood samples were taken for analysis of the plasma concentrations of catecholamines. Pre- and postbranchial blood pressures and cardiac output increase during exercise, while the mixed venous oxygen tension decreases. The effect on cardiac output is due to an increase of both heart rate and stroke volume. There are no significant changes in either systemic or branchial vascular resistances, or in the plasma concentrations of catecholamines. Injection of the adrenergic neurone-blocking drug bretylium produces a decrease in postbranchial blood pressure in resting cod, due to a decrease in the systemic vascular resistance. Exercising cod treated with bretylium have a significantly lower pre- and postbranchial blood pressure than exercising control cod. This is due mainly to a dramatic reduction in the systemic vascular resistance. The alpha-adrenoceptor antagonist phentolamine does not further affect the blood pressure in cod treated with bretylium. It is concluded that the exercise hypertension observed in cod depends on the effect of adrenergic vasomotor fibres maintaining the systemic vascular resistance, and also on the increase in cardiac output. An adrenergic innervation of the heart may play some role in the control of cardiac performance both at rest and during exercise, but the main cardioregulatory mechanism is likely to be non-adrenergic, most probably including cardiac control via variation of the cholinergic vagal cardioinhibitory tonus.

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Yin, Tan Ying, Farhanahani Mahmud, and Nur Ilyani Ramli. "Near-Infrared Spectroscopy (NIRS)-based Digit Skin Tissue Blood Flow Measurement System." International Journal of Engineering & Technology 7, no. 4.30 (November 30, 2018): 131. http://dx.doi.org/10.14419/ijet.v7i4.30.22076.

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The tissue blood flow (BF) and vascular resistance are the important information for consult peripheral vascular system which related to cardiovascular disease. Unfortunately, most of the current BF monitors are costly, built in huge size and preferable use in hospital and clinic. In the present study, a portable digit skin tissue BF measurement system had been developed using Near-infrared spectroscopy (NIRS) method with simple circuitry and low cost that can be afforded by patients to monitor their cardiovascular information. This system consists of a self-developed NIRS probe; LED and a photodiode, and an Arduino Uno board with MATLAB software as the processing unit. The NIR LED transmits 810 nm light source through biological tissue then detected by the photodiode. The output signal from the NIRS probe is based on resistance changes in the photodiode and by applying the voltage divider law, the signal is further processed by the Arduino with the MATLAB software. Then, according to the modified Lambert-Beer Law in scattering medium, the change in total concentration of haemoglobin ( ) is plotted in order to get a quantitative BF reading which based on its maximum change during venous occlusion. To evaluate the proposed BF measurement system, BF measurement tests had been conducted on four healthy subjects during resting and after exercise. The study had shown that the results of BF after the exercise were in average of 1.5 time higher than the resting BF and this finding agrees with previous research works.

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HIRATA, Kumiko, Kadirvelu AMUDHA, Raja ELINA, Takeshi HOZUMI, Junichi YOSHIKAWA, Shunichi HOMMA, and Chim C. LANG. "Measurement of coronary vasomotor function: getting to the heart of the matter in cardiovascular research." Clinical Science 107, no. 5 (October 26, 2004): 449–60. http://dx.doi.org/10.1042/cs20040226.

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Measurement of endothelial function in patients has emerged as a useful tool for cardiovascular research. Although no gold standard for the measurement of endothelial function exists, the measurement of flow-mediated dilation in the brachial artery, assessed with Doppler ultrasonography, is the most studied method. However, the assumption that endothelial dysfunction detected in brachial arteries is a manifestation of systemic endothelial dysfunction including the coronary circulation may not be entirely valid. Brachial and myocardial circulations differ in terms of the microvascular architecture, the pattern of blood flow and vascular resistance (e.g. shunt vessels occur in the hand but not in the myocardium), their metabolic regulation, type of receptors that contribute to humoral regulation and the pathways that are activated to induce hyperaemia. In this context, measuring coronary vasomotor function may be more useful than brachial artery measures to predict and assess potential myocardial damage related to limited vascular responsiveness. This review aims to provide an overview of the basic concept of coronary flow reserve and its different modalities of measurement, as well as its utility in cardiovascular research.

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Balasubramanian, Lavanya, Kay-Pong Yip, Tai-Hsin Hsu, and Chun-Min Lo. "Impedance analysis of renal vascular smooth muscle cells." American Journal of Physiology-Cell Physiology 295, no. 4 (October 2008): C954—C965. http://dx.doi.org/10.1152/ajpcell.00009.2008.

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Impedance of renal vascular smooth muscle cells (VSMCs) cultured on microelectrodes was measured by electric cell-substrate impedance sensing. Changes in measured impedance as a function of frequency were compared with the calculated values obtained from an extended cell-electrode model to estimate the junctional resistance, distance between the ventral cell surface and the substratum, and apical and basolateral membrane capacitances of renal VSMCs. This cell-electrode model was derived to accommodate the slender and rectangular shape of VSMCs. The calculated changes in impedance ( Zcal) based on the model agreed well with the experimental measurement ( Zexp), and the percentage error defined as |( Zcal − Zexp)/ Zexp| was 1.0%. To test the sensitivity of the new model for capturing changes in cell-cell and cell-substrate interactions induced by changes in cellular environment, we then applied this model to analyze timpedance changes induced by an integrin binding peptide in renal VSMCs. Our result demonstrates that integrin binding peptide decreases junctional resistance between cells, increases the distance between the basolateral cell surface and substratum, and increases the apical membrane capacitance, whereas the basolateral membrane capacitance stays relatively stable. This model provides a generic approach for impedance analysis of cell layers composed of slender, rectangular cells.

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MORIYASU, Fuminori, Osamu NISHIDA, Nobuyuki BAN, Takefumi NAKAMURA, Yasunari SOH, Jiroh OCHI, Kensuke MIURA, et al. "Measurement of portal vascular resistance in patients with chronic liver diseases by simultaneous measurement of portal blood flow and portal venous pressure." Kanzo 26, no. 4 (1985): 485–92. http://dx.doi.org/10.2957/kanzo.26.485.

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Ju, Bin, Yun Tao Qian, and Huo Jie Ye. "Wavelet Based Measurement on Photoplethysmography by Smartphone Imaging." Applied Mechanics and Materials 380-384 (August 2013): 773–77. http://dx.doi.org/10.4028/www.scientific.net/amm.380-384.773.

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[Purpose] Smartphones video cameras can be used to detect the photoplethysmograph (PPG) signal.The pulse wave signal detected by smartphone always mixed mass noise because of finger moving, unevenness of pressure and outer light interference. Previous studies limit to the filtering algorithm that denoising signals, without considering characteristics information of pulse wave itself. [Method] In this paper, we propose an algorithm based on wavelet to detect qualified PPG, which captures three critical characteristic quantities through wavelet high frequency coefficient. [Results] Experiment illustrates that the detected PPG signal contain dicrotic wave, and whats more, further experiment on artery elasticity indexes indicates good robust of the algorithm. [Conclusions] Wavelet Based Measurement on Photoplethysmography by Smartphone Imaging can be used for the calculation of cardiovascular parameter such as angiosclerosis, arrhythmia, and vascular resistance.

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Baines, A. D. "Is there a role for renal α2-adrenoceptors in the pathogenesis of hypertension?" Canadian Journal of Physiology and Pharmacology 65, no. 8 (August 1, 1987): 1638–43. http://dx.doi.org/10.1139/y87-257.

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Current information suggests that α2-adrenoceptors do not directly influence vascular resistance or Na reabsorption in the rat kidney. To reexamine the effects of α2-agonists we used isolated rat kidneys perfused at 37.5 °C with precise measurement of renal artery pressure and flow. The recirculating perfusate contained pyruvate as the sole metabolic substrate which enabled us to use gluconeogenesis as an index of proximal tubular α1-responses. Clonidine and guanfacine in 100 nM concentrations decreased phosphate excretion without altering Na, Cl, or K reabsorption or gluconeogenesis; 500 nM concentrations increased vascular resistance and decreased glomerular filtration rate and Na, Cl, and K excretion with no significant effect on gluconeogenesis. Prior thyroparathyroidectomy prevented the antiphosphaturic but not the antinatriuretic or vascular responses. Clonidine, an α2-agonist with some α1-activity, was a more potent vasoconstrictor than methoxamine or guanfacine. In the presence of prazosin (1 μM), norepinephrine (60 nM) stimulated phosphate reabsorption; norepinephrine alone did not stimulate phosphate reabsorption which indicates α1-antagonism of this α2-response to NE. These results and a literature review suggest that increased renal α2-adrenoceptors could raise renal vascular resistance, reduce renin secretion, and antagonize parathyroid hormone effects on Pi Ca, HCO3, and Na reabsorption to produce a low renin type of hypertension with increased proximal Na reabsorption and abnormal Ca and Pi excretion.

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Cassano, Velia, Daniele Crescibene, Marta Letizia Hribal, Corrado Pelaia, Giuseppe Armentaro, Marcello Magurno, Alfredo Toscani, et al. "Uric Acid and Vascular Damage in Essential Hypertension: Role of Insulin Resistance." Nutrients 12, no. 9 (August 19, 2020): 2509. http://dx.doi.org/10.3390/nu12092509.

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Increased levels of uric acid (UA) have been shown to be correlated with many clinical conditions. Uric acid may adversely affect the insulin signalling pathway inducing insulin resistance (IR). Several studies report the association between arterial stiffness (AS), an early indicator of atherosclerosis, and UA. The purpose of the present study was to evaluate the association between UA and AS, considering the potential role of IR. We enrolled 1114 newly diagnosed, never-treated hypertensive patients. Insulin resistance was assessed by the homeostatic model assessment (HOMA) index. Arterial stiffness was evaluated as the measurement of the carotid–femoral pulse wave velocity (PWV). The study cohort was divided into subgroups, according to increasing tertiles of UA. The mean values of UA were 5.2 ± 1.6 mg/dL in the overall population. Pulse wave velocity was linearly correlated with UA (p < 0.0001), HOMA (p < 0.0001), high sensitivity C-reactive protein (p < 0.0001), systolic blood pressure (p < 0.0001) and LDL cholesterol (p = 0.005). Uric acid was the strongest predictor of PWV and was associated with the highest risk for increased AS. The interaction analysis showed that the joint effect of increased UA and HOMA was significantly higher than that expected in the absence of interaction under the additive model, indicating that the two biomarkers synergically interacted for promoting vascular damage. Our data showed that UA interacted with IR to increase AS in a large cohort of newly diagnosed, never-treated hypertensive patients.

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Journal articles on the topic 'Vascular resistance Measurement'

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