Vascular capacitance and reversal of 2-kidney, 1-clip hypertension in rats

1989 ◽  
Vol 256 (2) ◽  
pp. H502-H507 ◽  
Author(s):  
M. E. Edmunds ◽  
G. I. Russell ◽  
J. D. Swales

Vascular capacitance was studied in conscious early-phase (less than 6 wk) 2-kidney, 1-clip (2K, 1C) hypertension and compared with sham-clipped control rats. Two other groups of 2K, 1C rats were studied before and 6 h after unclipping or a sham operation. Mean circulatory filling pressure (MCFP) was measured during a brief circulatory arrest caused by inflation of a right atrial balloon. Blood volume (BV) was determined from plasma volume (125I-labeled albumin) and hematocrit. MCFP was measured at resting BV and after rapid BV changes. Vascular compliance was derived from the MCFP-BV curve. Hypertensive 2K, 1C rats had an increase in hematocrit (46 +/- 1.3 vs. 42 +/- 0.4%, P less than 0.01) and no difference in BV compared with controls. MCFP was increased (8.6 +/- 1.0 vs. 7.2 +/- 0.2 mmHg, P less than 0.01) with no difference in compliance, indicating decreased unstressed vascular volume in the 2K, 1C group. After unclipping, there was a significant fall in mean arterial pressure to normal, with a fall in MCFP (8.14 +/- 0.32 to 6.78 +/- 0.11 mmHg, P less than 0.01), but there was no difference in BV or compliance compared with the 2K, 1C group, indicating an increase in unstressed vascular volume after unclipping. These studies for the first time show an important role for vascular capacitance in modulating the circulatory changes accompanying the fall in blood pressure in surgical reversal of 2K, 1C hypertension.

2020 ◽  
Vol 319 (1) ◽  
pp. F76-F83
Author(s):  
Shereen M. Hamza ◽  
Xiaohua Huang ◽  
Tayyaba Zehra ◽  
Wenqing Zhuang ◽  
William A. Cupples ◽  
...  

Acutely increased renal venous pressure (RVP) impairs renal function, but the long-term impact is unknown. We investigated whether chronic RVP elevation impairs baseline renal function and prevents exacerbation of renal dysfunction and cardiovascular instability upon further RVP increase. RVP elevation (20–25 mmHg) or sham operation (sham) was performed in rats. After 1 wk ( n = 17) or 3 wk ( n = 22), blood pressure, RVP, renal blood flow (RBF), renal vascular conductance (RVC), and glomerular filtration rate (GFR) were measured at baseline and during superimposed RVP increase. Chronic RVP elevation induced extensive renal venous collateral formation. RVP fell to 6 ± 1 mmHg at 1 wk and 3 ± 1 mmHg at 3 wk. Baseline blood pressure and heart rate were unaltered compared with sham. RBF, RVC, and GFR were reduced at 1 wk but normalized by 3 wk. Upon further RVP increase, the drop in mean arterial pressure was attenuated at 3 wk compared with 1 wk ( P < 0.05), whereas heart rate fell comparably across all groups; the mean arterial pressure-heart rate relationship was disrupted at 1 and 3 wk. RBF fell to a similar degree as sham at 1 wk (−2.3 ± 0.7 vs. −3.9 ± 1.2 mL/min, P = 0.066); however, at 3 wk, this was attenuated compared with sham (−1.5 ± 0.5 vs. −4.2 ± 0.7 mL/min, P < 0.05). The drop in RVC and GFR was attenuated at 1 and 3 wk ( P < 0.05). Thus, chronic RVP elevation induced by partial renal vein ligation elicits extensive renal venous collateral formation, and although baseline renal function is impaired, chronic RVP elevation in this manner induces protective adaptations in kidneys of healthy rats, which attenuates the hemodynamic response to further RVP increase.


1990 ◽  
Vol 68 (3) ◽  
pp. 431-438 ◽  
Author(s):  
Richard I. Ogilvie ◽  
Danuta Zborowska-Sluis

The hemodynamic effects of nifedipine and captopril at doses producing similar reductions in arterial pressure were studied in pentobarbital- anesthetized ventilated dogs after splenectomy during ganglion blockade with hexamethonium. Mean circulatory filling pressure (Pmcf) was determined during transient circulatory arrest induced by acetylcholine at baseline circulating blood volumes and after increases of 5 and 10 mL/kg. Central blood volumes (pulmonary artery to aortic root) were determined from transit times, and separately determined cardiac outputs (right atrium to pulmonary artery) were estimated by thermodilution. Nifedipine (n = 5) increased Pmcf at all circulating blood volumes and reduced total vascular capacitance without a change in total vascular compliance. Central blood volume, right atrial pressure, and cardiac output were increased with induced increases in circulating blood volume. In contrast, captopril (n = 5) did not alter total vascular capacitance, central blood volume, right atrial pressure, or cardiac output at baseline or with increased circulating volume. Thus, at doses producing similar reductions in arterial pressure, nifedipine but not captopril increased venous return and cardiac output in ganglion-blocked dogs.Key words: mean circulatory filling pressure, vascular compliance, vascular capacitance, nifedipine, captopril.


Author(s):  
M.A. Bubnova ◽  
O.N. Kryuchkova

Patients with hypertension (HT) and chronic obstructive pulmonary disease (COPD) have a high risk of cardiovascular complications. Up to now, there is no optimal strategy for combined antihypertensive therapy. Still, the data of 24-hour blood pressure monitoring (BPM) are important while choosing treatment tactics. The aim of the paper is to study the features of indicators in patients with arterial hypertension (AH) and COPD. Materials and methods. 130 patients with HT were included in the study. The main group (n=90) included comorbid patients with HT and COPD, their average age was 61.30±1.01; the comparison group (n=40) consisted of patients with HT, their average age was 59.10±1.53. All patients underwent 24-hour BPM. Results. Comorbid patients revealed an increase in the mean 24-hour and night systolic and mean arterial pressure values as well as a significant increase in the load index of systolic, diastolic and mean arterial pressure. Also, comorbid patients demonstrated higher blood pressure in contrast to the patients of the comparison group. They had increased systolic, diastolic and mean blood pressure variability and a quicker rate of morning blood pressure rise. According to 24-hour blood pressure dynamics, pathological types of the 24-hour blood pressure curve, a higher frequency of the night-peaker profile dominated in patients with COPD if compared to patients with HT. Conclusion. The obtained data indicated a high risk of cardiovascular complications in comorbid patients, early target organ damage and an unfavorable disease prognosis. It means that both further study of hypertension clinical course in such patients and personalization of antihypertensive therapy are relevant. Keywords: hypertension, chronic obstructive pulmonary disease, 24-hour monitoring, blood pressure. Пациенты с артериальной гипертензией (АГ) и хронической обструктивной болезнью легких (ХОБЛ) имеют высокий риск возникновения кардиоваскулярных осложнений. В настоящее время в лечении не определена наиболее оптимальная стратегия комбинированной антигипертензивной терапии. Для выбора тактики терапии важную роль играют показатели суточного мониторирования артериального давления (СМАД). Цель. Изучить особенности показателей СМАД у пациентов с АГ на фоне ХОБЛ. Материалы и методы. В исследование включено 130 пациентов с АГ. В основную группу (n=90) вошли пациенты с АГ и ХОБЛ (средний возраст – 61,30±1,01 года), в группу сравнения (n=40) – больные только АГ (средний возраст – 59,10±1,53 года). Всем пациентам проведено СМАД. Результаты. У пациентов с коморбидностью выявлены следующие особенности суточных показателей артериального давления: увеличение значений среднесуточных и средненочных показателей систолического и среднего артериального давления; существенное повышение индекса нагрузки систолическим, диастолическим и средним артериальным давлением. Также эти больные отличались от пациентов группы сравнения более высокими значениями пульсового давления, имели повышенную вариабельность систолического, диастолического и среднего артериального давления, у них наблюдалось увеличение скорости утреннего подъема артериального давления. Суточная динамика артериального давления у пациентов с ХОБЛ характеризовалась преобладанием патологических типов суточной кривой АД, более высокой частотой профиля night-peaker по сравнению с больными только АГ. Выводы. Выявленные особенности свидетельствуют о высоком риске сердечно-сосудистых осложнений у пациентов с коморбидностью, раннем поражении органов-мишеней и неблагоприятном прогнозе заболевания, что требует дальнейшего изучения особенностей клинического течения АГ у таких больных и индивидуализации антигипертензивной терапии. Ключевые слова: артериальная гипертензия, хроническая обструктивная болезнь легких, суточное мониторирование, артериальное давление.


1982 ◽  
Vol 243 (1) ◽  
pp. R152-R158 ◽  
Author(s):  
J. K. Stene ◽  
B. Burns ◽  
S. Permutt ◽  
P. Caldini ◽  
M. Shanoff

Occlusion of the thoracic aorta (AO) in dogs with a constant volume right ventricular extracorporeal bypass increased cardiac output (Q) by 43% and mean arterial pressure by 46%, while mean systemic pressure (MSP) was unchanged. We compared AO with occlusion of the brachiocephalic and left subclavian arteries (BSO) which decreased cardiac output by 5%, increased mean arterial pressure by 32%, and increased MSP by 11%. We feel these results confirm that AO elevates preload by transferring blood volume from the splanchnic veins to the vascular system drained by the superior vena cava. If the heart is competent to keep right arterial pressure at or near zero, this increase in preload will elevate Q above control levels. Comparing our data with results of other authors who have not controlled right atrial pressure, emphasizes the importance of a competent right ventricle in allowing venous return to determine Q.


2015 ◽  
Vol 309 (10) ◽  
pp. R1273-R1284 ◽  
Author(s):  
Jennifer Magnusson ◽  
Kevin J. Cummings

The role of serotonin (5-HT) neurons in cardiovascular responses to acute intermittent hypoxia (AIH) has not been studied in the neonatal period. We hypothesized that a partial loss of 5-HT neurons would reduce arterial blood pressure (BP) at rest, increase the fall in BP during hypoxia, and reduce the long-term facilitation of breathing (vLTF) and BP following AIH. We exposed 2-wk-old, 5,7-dihydroxytryptamine-treated and controls to AIH (10% O2; n = 13 control, 14 treated), acute intermittent hypercapnia (5% CO2; n = 12 and 11), or acute intermittent hypercapnic hypoxia (AIHH; 10% O2, 5% CO2; n = 15 and 17). We gave five 5-min challenges of AIH and acute intermittent hypercapnia, and twenty ∼20-s challenges of AIHH to mimic sleep apnea. Systolic BP (sBP), diastolic BP, mean arterial pressure, heart rate (HR), ventilation (V̇e), and metabolic rate (V̇o2) were continuously monitored. 5,7-Dihydroxytryptamine induced an ∼35% loss of 5-HT neurons from the medullary raphe. Compared with controls, pups deficient in 5-HT neurons had reduced resting sBP (∼6 mmHg), mean arterial pressure (∼5 mmHg), and HR (56 beats/min), and experienced a reduced drop in BP during hypoxia. AIHH induced vLTF in both groups, reflected in increased V̇e and V̇e/V̇o2, and decreased arterial Pco2. The sBP of pups deficient in 5-HT neurons, but not controls, was increased 1 h following AIHH. Our data suggest that a relatively small loss of 5-HT neurons compromises resting BP and HR, but has no influence on ventilatory plasticity induced by AIHH. AIHH may be useful for reversing cardiorespiratory defects related to partial 5-HT system dysfunction.


1998 ◽  
Vol 94 (1) ◽  
pp. 49-55 ◽  
Author(s):  
Sharmini Puvi-Rajasingham ◽  
Gareth D. P. Smith ◽  
Adeola Akinola ◽  
Christopher J. Mathias

1. In human sympathetic denervation due to primary autonomic failure, food and exercise in combination may produce a cumulative blood pressure lowering effect due to simultaneous splanchnic and skeletal muscle dilatation unopposed by corrective cardiovascular reflexes. We studied 12 patients with autonomic failure during and after 9 min of supine exercise, when fasted and after a liquid meal. Standing blood pressure was also measured before and after exercise. 2. When fasted, blood pressure fell during exercise from 162 ± 7/92 ± 4 to 129 ± 9/70 ± 5 mmHg (mean arterial pressure by 22 ± 5%), P < 0.0005. After the meal, blood pressure fell from 159 ± 8/88 ± 6 to 129 ± 6/70 ± 4 mmHg (mean arterial pressure by 22 ± 3%), P < 0.0001, and further during exercise to 123 ± 6/61 ± 3 mmHg (mean arterial pressure by 9 ± 3%), P < 0.01. The stroke distance—heart rate product, an index of cardiac output, did not change after the meal. During exercise, changes in the stroke distance—heart rate product were greater when fasted. 3. Resting forearm and calf vascular resistance were higher when fasted. Calf vascular resistance fell further after exercise when fasted. Resting superior mesenteric artery vascular resistance was lower when fed; 0.19 ± 0.02 compared with 032 ± 0.06, P < 0.05. After exercise, superior mesenteric artery vascular resistance had risen by 82%, to 0.53 ± 0.12, P < 0.05 (fasted) and by 47%, to 0.29 ± 0.05, P < 0.05 (fed). 4. On standing, absolute levels of blood pressure were higher when fasted [83 ± 7/52 ± 7 compared with 71 ± 2/41 ± 3 (fed), each P < 0.05]. Subjects were more symptomatic on standing post-exercise when fed. 5. In human sympathetic denervation, exercise in the fed state lowered blood pressure further than when fasted and worsened symptoms of postural hypotension.


2002 ◽  
Vol 93 (6) ◽  
pp. 1966-1972 ◽  
Author(s):  
Maria T. E. Hopman ◽  
Jan T. Groothuis ◽  
Marcel Flendrie ◽  
Karin H. L. Gerrits ◽  
Sibrand Houtman

The purpose of the present study was to determine the effect of a spinal cord injury (SCI) on resting vascular resistance in paralyzed legs in humans. To accomplish this goal, we measured blood pressure and resting flow above and below the lesion (by using venous occlusion plethysmography) in 11 patients with SCI and in 10 healthy controls (C). Relative vascular resistance was calculated as mean arterial pressure in millimeters of mercury divided by the arterial blood flow in milliliters per minute per 100 milliliters of tissue. Arterial blood flow in the sympathetically deprived and paralyzed legs of SCI was significantly lower than leg blood flow in C. Because mean arterial pressure showed no differences between both groups, leg vascular resistance in SCI was significantly higher than in C. Within the SCI group, arterial blood flow was significantly higher and vascular resistance significantly lower in the arms than in the legs. To distinguish between the effect of loss of central neural control vs. deconditioning, a group of nine SCI patients was trained for 6 wk and showed a 30% increase in leg blood flow with unchanged blood pressure levels, indicating a marked reduction in vascular resistance. In conclusion, vascular resistance is increased in the paralyzed legs of individuals with SCI and is reversible by training.


Author(s):  
Sidharth Sraban Routray ◽  
Ramakanta Mohanty

ABSTRACTObjective: During laparoscopic surgeries, pneumoperitoneum can lead to various pathophysiologic changes in the cardiovascular system resulting inhypertension and tachycardia. Search for ideal drug to prevent this hemodynamic response goes on. The aim of our study was to evaluate the effect oforally administered moxonidine in attenuating the hemodynamic responses that occur during the laparoscopic surgeries.Methods: A total of 50 adult acetylsalicylic acid I and II patients scheduled for elective laparoscopic surgeries were selected for this prospectiverandomized double-blinded study. They were randomly allocated into two groups: moxonidine group (M) and placebo group (P). M group receivedoral moxonidine 0.3 mg at 8 pm on the day before surgery and at 8 am on the day of surgery. P group received a placebo at the same timing as that ofthe M group.Results: Following pneumoperitoneum rise in systolic blood pressure (SBP), diastolic BP (DBP), mean arterial pressure (MAP), and heart rate (HR)was higher in P group in comparison to M group which was statistically significant.Conclusion: Significant rise in HR, SBP, DBP, and mean BP was noted in the P group in comparison to moxonidine group. Moxonidine provided betterperioperative hemodynamic stability in patients undergoing laparoscopic surgeries.Keywords: Moxonidine, Stress response, Laparoscopic.


1999 ◽  
Vol 91 (3) ◽  
pp. 677-677 ◽  
Author(s):  
Basil F. Matta ◽  
Karen J. Heath ◽  
Kate Tipping ◽  
Andrew C. Summors

Background The effect of volatile anesthetics on cerebral blood flow depends on the balance between the indirect vasoconstrictive action secondary to flow-metabolism coupling and the agent's intrinsic vasodilatory action. This study compared the direct cerebral vasodilatory actions of 0.5 and 1.5 minimum alveolar concentration (MAC) sevoflurane and isoflurane during an propofol-induced isoelectric electroencephalogram. Methods Twenty patients aged 20-62 yr with American Society of Anesthesiologists physical status I or II requiring general anesthesia for routine spinal surgery were recruited. In addition to routine monitoring, a transcranial Doppler ultrasound was used to measure blood flow velocity in the middle cerebral artery, and an electroencephalograph to measure brain electrical activity. Anesthesia was induced with propofol 2.5 mg/kg, fentanyl 2 micro/g/kg, and atracurium 0.5 mg/kg, and a propofol infusion was used to achieve electroencephalographic isoelectricity. End-tidal carbon dioxide, blood pressure, and temperature were maintained constant throughout the study period. Cerebral blood flow velocity, mean blood pressure, and heart rate were recorded after 20 min of isoelectric encephalogram. Patients were then assigned to receive either age-adjusted 0.5 MAC (0.8-1%) or 1.5 MAC (2.4-3%) end-tidal sevoflurane; or age-adjusted 0.5 MAC (0.5-0.7%) or 1.5 MAC (1.5-2%) end-tidal isoflurane. After 15 min of unchanged end-tidal concentration, the variables were measured again. The concentration of the inhalational agent was increased or decreased as appropriate, and all measurements were repeated again. All measurements were performed before the start of surgery. An infusion of 0.01% phenylephrine was used as necessary to maintain mean arterial pressure at baseline levels. Results Although both agents increased blood flow velocity in the middle cerebral artery at 0.5 and 1.5 MAC, this increase was significantly less during sevoflurane anesthesia (4+/-3 and 17+/-3% at 0.5 and 1.5 MAC sevoflurane; 19+/-3 and 72+/-9% at 0.5 and 1.5 MAC isoflurane [mean +/- SD]; P&lt;0.05). All patients required phenylephrine (100-300 microg) to maintain mean arterial pressure within 20% of baseline during 1.5 MAC anesthesia. Conclusions In common with other volatile anesthetic agents, sevoflurane has an intrinsic dose-dependent cerebral vasodilatory effect. However, this effect is less than that of isoflurane.


1990 ◽  
Vol 258 (6) ◽  
pp. H1925-H1932 ◽  
Author(s):  
R. I. Ogilvie ◽  
D. Zborowska-Sluis ◽  
B. Tenaschuk

To measure mean circulatory filling pressure (Pmcf), a balloon was placed in the right atrium of seven pentobarbital sodium-anesthetized open-chest pigs for transient occlusion of flow combined with mechanical transfer of blood from the arterial to the venous circulation. Equilibration occurred within 6-8 s at a pressure at 12.3 +/- 0.3 (SE) mmHg after a 2.9 +/- 0.2 ml/kg transfer of blood. In another group of pentobarbital sodium-anesthetized closed-chest pigs, acetylcholine (ACh) was used to induce cardiac arrest. The Pmcf was 11.6 +/- 1.0 mmHg in the 7:17 pigs that arrested for 6-8 s. In four isoflurane-anesthetized closed-chest pigs, the Pmcf was 12.0 +/- 1.0 mmHg after terminal cardiac arrest induced by KCl. The pressure gradient for venous return [Pmcf--right atrial pressure (Pra)] averaged 5.9 +/- 0.2 mmHg. Total vascular compliance estimated from plots of Pmcf at base line, 5, and 10 ml/kg increases in circulating volume was 2.1 +/- 0.3 and 3.5 +/- 0.9 ml.kg-1.mmHg-1 in the balloon and ACh groups, respectively compared with 2.8 +/- 0.4 ml.kg-1.mmHg-1 using a volume infusion-withdrawal method without circulatory arrest. The use of ACh for the estimate of Pmcf in the pig is not recommended because of failure to consistently induce circulatory arrest and probable failure to achieve sufficient equilibrium of vascular pressures 6-8 s postarrest when it occurs.


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