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PubMed1994

Amrinone: its effect on vascular resistance and capacitance in human subjects.

Reports evaluating amrinone's effects in normal (intact) human subjects are complex and difficult to interpret because of the drug's diverse effects on myocardial function, resistance vessels, and vascular capacitance. In this study, 1.5 mg/kg of amrinone was administered as an intravenous bolus to cardiac surgical patients during constant flow cardiopulmonary bypass to determine its isolated effects on venous capacitance and vascular resistance. We noted a significant decrease in vascular resistance up to 8 min after injection and a 460 +/- 160 ml (mean +/- SD) decrease in venous reservoir volume 10 min after injection. Amrinone has potent venous and arterial vasodilating properties that make it a unique drug for treating congestive heart failure in addition to its reported positive inotropic effects.

Amrinone↗
PubMed2006

Relationship of pulmonary arterial capacitance and mortality in idiopathic pulmonary arterial hypertension.

OBJECTIVES: The purpose of this study was to determine if pulmonary vascular capacitance predicts survival in patients with idiopathic pulmonary arterial hypertension (IPAH). BACKGROUND: The prognosis of patients with IPAH is difficult to predict, despite knowledge of clinical and hemodynamic parameters previously identified as predictors. METHODS: We proposed a capacitance index of stroke volume divided by pulmonary pulse pressure (SV/PP) and prospectively gathered data on IPAH patients who underwent a right heart catheterization. SV/PP was analyzed as a predictor of mortality after adjusting for other modifiers of risk. RESULTS: During 4-year follow-up of 104 patients, 21 patients died. When compared with conventional markers, SV/PP was the strongest univariate predictor of mortality (hazard ratio 17.0 per ml.mm Hg(-1) decrease, 95% confidence interval 13.0 to 22.0; p < 0.0001). In successive bivariate analysis, SV/PP was the only predictor of mortality. In quartile analysis, the lowest SV/PP quartile had a 4-year mortality of 61%; the highest SV/PP had no deaths. CONCLUSIONS: The capacitance index (SV/PP) is a strong independent predictor of mortality in patients with IPAH.

Adult↗
PubMed1994

Mathematical model of cardiovascular mechanics for diagnostic analysis and treatment of heart failure: Part 1. Model description and theoretical analysis.

The planning of drug therapy for heart failure should involve both the diagnostic analysis of the patient's defective state and a prediction of the drug effects on the identified state. We have devised a mathematical model of cardiovascular system mechanics, on which both quantitative diagnosis and evaluation of drug effects can be made. The model was composed of systemic and pulmonary circulatory networks including the dynamics of the left and right ventricles. The model of the ventricles can represent both systolic and diastolic problems in heart failure through the parameters of ventricular contractility and diastolic stiffness. Each vascular network was composed of arterial and venous resistances and total vascular capacitance. Patient's ventricular and vascular parameters were estimated simultaneously from the clinically measurable haemodynamic variables based on the model. Despite the simplicity of the model, the results showed good agreement with clinical and experimental data. The clinically significant haemodynamic classification of heart failure by Forrester et al. (Forrester et al., 1977) was simulated well by the model. This model provides a useful basis for analysing pathophysiological states in heart failure and evaluating drug effects on the disease.

Heart↗
PubMed1980

[Peripheral effects of nitrate compounds (author's transl)].

Nitroglycerin primarily acts on smooth muscle fibers, and this effect is dose-dependent. High doses seem to affect mainly coronary blood flow; moderate doses act on both systemic arterial blood flow (resistance vascular bed) and return venous blood flow (capacitance vascular bed), while low doses influence only the latter. These various modes of action account for the discrepancies observed between the results of experimental studies, the final effect being the algebraical resultant of combined individual actions. In coronary insufficiency, where treatment aims at reducing myocardial oxygen consumption without lowering coronary perfusion pressure, nitroglycerin should be given in low doses. In congestive heart failure, where the primary target is reduction in preload and, consequently, heart work without excessive reduction in afterload that would result in decreased stroke index through Frank-Starling's mechanism, a detailed knowledge of the physiological mechanisms involved is required to guide nitroglycerin treatment.

Angina Pectoris↗
PubMed2006

Adrenergic control of venous capacitance during moderate hypoxia in the rainbow trout (Oncorhynchus mykiss): role of neural and circulating catecholamines.

Central venous blood pressure (P(ven)) increases in response to hypoxia in rainbow trout (Oncorhynchus mykiss), but details on the control mechanisms of the venous vasculature during hypoxia have not been studied in fish. Basic cardiovascular variables including P(ven), dorsal aortic blood pressure, cardiac output, and heart rate were monitored in vivo during normoxia and moderate hypoxia (P(W)O(2) = approximately 9 kPa), where P(W)O(2) is water oxygen partial pressure. Venous capacitance curves for normoxia and hypoxia were constructed at 80-100, 90-110, and 100-120% of total blood volume by transiently (8 s) occluding the ventral aorta and measure P(ven) during circulatory arrest to estimate the mean circulatory filling pressure (MCFP). This allowed for estimates of hypoxia-induced changes in unstressed blood volume (USBV) and venous compliance. MCFP increased due to a decreased USBV at all blood volumes during hypoxia. These venous responses were blocked by alpha-adrenoceptor blockade with prazosin (1 mg/kg body mass). MCFP still increased during hypoxia after pretreatment with the adrenergic nerve-blocking agent bretylium (10 mg/kg body mass), but the decrease in USBV only persisted at 80-100% blood volume, whereas vascular capacitance decreased significantly at 90-110% blood volume. In all treatments, hypoxia typically reduced heart rate while cardiac output was maintained through a compensatory increase in stroke volume. Despite the markedly reduced response in venous capacitance after adrenergic blockade, P(ven) always increased in response to hypoxia. This study reveals that venous capacitance in rainbow trout is actively modulated in response to hypoxia by an alpha-adrenergic mechanism with both humoral and neural components.

Adrenergic alpha-Antagonists↗
PubMed1994

Renal hemodynamics and volume homeostasis in pregnancy.

Maternal hemodynamic adaptation to pregnancy consists of profound changes in various interdependent systems. Of crucial importance in the early adaptation of the volume homeostatic mechanisms to pregnancy is the resetting of the volume and osmoreceptors. This resetting may be induced by a reduction in vascular tone and leads to early changes in plasma osmolality and glomerular filtration rate. After this initial adaptation other volume-regulating mechanisms such as the renin-angiotensin-aldosterone system, pregnancy hormones, and alpha-ANP adapt to the rising blood volume. The initial adaptation results in a state of relative vascular underfill, inducing secondary compensations in the volume homeostasis. The initially increased vascular capacitance in pregnancy is compatible with the signals of vascular overfill. Contrarily, the protracted filling of this enlarged vascular bed triggers signals compatible with vascular underfill.

Adaptation, Physiological↗
PubMed1983

Responses of abdominal vascular resistance and capacitance to stimulation of carotid chemoreceptors in anaesthetized dogs.

1. In anaesthetized dogs the regions of the carotid bifurcations were isolated vascularly and perfused at constant non-pulsatile pressures. The abdominal circulation was isolated vascularly, perfused at constant flow and drained through the inferior vena cava at constant pressure. Vascular resistance and capacitance responses were determined from the changes in perfusion pressure and changes in venous outflow. 2. Stimulation of carotid chemoreceptors with venous blood resulted in an increase in arterial perfusion pressure of 38% (S.E. +/- 4.6) and a decrease in vascular capacitance of 24.4 +/- 2.5 ml. (1.05 +/- 0.24 ml. kg-1). 3. When carotid perfusion pressure was higher than 17 kPa, stimulation of chemoreceptors resulted in significantly (P less than 0.05) smaller resistance responses but significantly (P less than 0.05) greater capacitance responses than those obtained at lower carotid pressures. 4. These results show that abdominal resistance and capacitance vessels constrict in response to stimulation of carotid chemoreceptors. We suggest that the larger responses of capacitance and the smaller responses of resistance obtained at higher carotid sinus pressures may be due to different sensitivities of resistance and capacitance vessels to efferent sympathetic nerve activity.

Abdomen↗
PubMed2006

Cerebrovascular dynamics and vascular endothelial growth factor in acute mountain sickness.

OBJECTIVE: To determine if serum vascular endothelial growth factor (VEGF) and ultrasonic monitoring of vascular dynamics with dynamic vascular analysis at sea level and high altitude correlate with acute mountain sickness symptoms. METHODS: Nine volunteers participated in a staged ascent from sea level to 4300 m undergoing complete transcranial Doppler studies with dynamic vascular analysis. Serum VEGF levels, Lake Louise scores, Spielberger-1 scores, Subjective Exercise Experiences Scale positive scores, and Symptom Checklist-90 surveys were collected after 24 hours at each altitude. RESULTS: Symptom scores, index of pulsatility, and dynamic flow index differentiated the subjects into 2 distinct groups. Symptomatic subjects had increased VEGF levels at sea level but decreased levels at 4300 m. The dynamic flow index increased in symptomatic subjects at 4300 m compared with the asymptomatic subjects. The mean flow velocity increased in both groups and could not be used to differentiate the subjects. CONCLUSIONS: Altered vascular physiology is associated with acute mountain sickness. Increased vascular permeability increases vascular capacitance, with an increase in dynamic flow index to meet these demands. Altered vascular dynamics were associated with high-altitude cerebral edema in 1 subject. Dynamic vascular analysis demonstrated altered vascular pathophysiology associated with acute mountain sickness. Changes in VEGF were meaningful when interpreted with the dynamic vascular analysis findings. These physiological findings may help explain the vascular changes associated with hypocarbic hypoxemia at altitude.

Acute Disease↗
PubMed1985

Alpha-1 adrenergic control of the venous circulation in intact dogs.

To study alpha adrenergic control of the venous circulation, 17 dogs were lightly sedated and instrumented with thermodilution pulmonary flow and aortic catheters. Hemodynamics, cardiac output and central blood volume were measured at rest. Mean circulatory filling pressure, pressure gradient for venous return and resistance to venous return were calculated from pressures obtained during transient acetylcholine-induced circulatory arrest. Phenylephrine was then infused at two steady-state levels to increase mean aortic pressure by 50 and 100% above control values. Heart rate was controlled with atropine. Phenylephrine increased (P less than .025) mean aortic pressure from 80.7 +/- 2.9 to 121.3 +/- 7.6 to 164.7 +/- 6.1 mm Hg and systemic vascular resistance from 23.3 +/- 2.0 to 32.2 +/- 3.5 to 43.5 +/- 4.1 mm Hg/min/ml and did not change cardiac output (161.9 +/- 12.6-175.6 +/- 13.8-169.6 +/- 11.9 ml/min/kg). Mean circulatory filling pressure increased from 7.1 +/- 0.5 to 9.7 +/- 0.6 to 13.2 +/- 1.3 mm Hg (P less than .025). Pressure gradient for venous return increased from 6.4 +/- 0.4 to 7.7 +/- 0.4 to 8.9 +/- 0.4 mm Hg (P less than .025). Central blood volume increased from 16.2 +/- 0.9 to 19.4 +/- 1.4 to 22.0 +/- 1.9 ml/kg (P less than .025). To eliminate reflex changes in vascular tone, eight dogs received ganglionic blockade with trimethaphan. After ganglionic blockade phenylephrine increased cardiac output, systemic vascular resistance, mean circulatory filling pressure, pressure gradient for venous return and central blood volume (P less than .025). Thus, in conscious dogs, phenylephrine reduces peripheral vascular capacitance and shifts blood from the venous circulation to the central and arterial vascular compartments.

Animals↗
PubMed1997

Autoregulation of human optic nerve head blood flow in response to acute changes in ocular perfusion pressure.

BACKGROUND: Studies in animals have demonstrated that optic nerve head (ONH) blood flow (F(onh)) is autoregulated, but there is a lack of evidence for such a process in humans. Therefore, we investigated the relationship between F(onh) and mean ocular perfusion pressure (PPm) in normal volunteers when PPm is decreased through elevation of the intraocular pressure (IOP). METHODS: Laser Doppler flowmetry (LDF) was used to measure relative mean velocity (Velohn), volume (Volonh) and F(onh) of blood at sites of the ONH away from visible vessels, while PPm was decreased in two ways: (1) rapidly, by IOP increments of 15 s duration, and (2) slowly, by IOP increments of 2 min duration, both by scleral suction cup in one eye of each of nine subjects. RESULTS: A rapid and large decrease of PPm of more than 100% induced a decrease of more than 80% in F(onh). With the slower decrease in PPm, F(onh) remained constant down to a PPm of approximately 22 mm Hg (IOP = 40 mm Hg) and then decreased, predominantly due to a decrease in Velohn. Immediately after removal of the suction cup, F(onh) increased transiently by 44% above baseline. CONCLUSIONS: This study demonstrates efficient blood flow autoregulation in the OHN, which is probably brought about by an increase in vascular capacitance. The magnitude of the reactive hyperaemia agrees with the compensatory decrease in ONH vascular resistance during IOP elevation. The time scale of the autoregulatory process and the dependence of the hyperaemia upon duration of IOP elevation suggest a metabolic mechanism of autoregulation.

Adult↗
PubMed1984

Preload and afterload reduction in treating congestive heart failure.

The importance of changes in the resistance and capacitance vessels in the development of congestive heart failure was demonstrated over 30 years ago. The beneficial effects of reducing total peripheral resistance and increasing vascular capacitance were also demonstrated. These studies illustrate the old adage "there is nothing new under the sun."

Autonomic Nerve Block↗
PubMed1992

Regional venous outflow, blood volume, and sympathetic nerve activity during hypercapnia and hypoxic hypercapnia.

We examined the changes in systemic blood volume and regional venous outflow from the splanchnic, coronary, and other remaining vascular beds in response to acute hypercapnia or hypoxic hypercapnia in dogs, using cardiopulmonary bypass and a reservoir. Hypercapnia (PCO2 = 105 mmHg) (1 mmHg = 133 Pa) and hypoxic hypercapnia (PO2 = 23 mmHg, PCO2 = 99 mmHg) caused marked decreases in systemic blood volume of 14 +/- 3 and 16 +/- 3 mL/kg in spleen-intact dogs, and 3 +/- 2 and 10 +/- 2 mL/kg in splenectomized dogs, respectively. Splanchnic venous outflow increased by 12% at 3.5 min hypercapnia, whereas it decreased by 60% at 3.5 min hypoxic hypercapnia. Coronary venous outflow increased by 85 and 400% at 3.5 min hypercapnia and hypoxic hypercapnia, respectively. Sympathetic efferent nerve activity revealed a significant augmentation during hypoxic hypercapnia and a relatively smaller increase (30% of the response to hypoxic hypercapnia) during hypercapnia. Carotid and aortic chemoreceptor and baroreceptor denervation attenuated significantly the response of systemic blood volume to hypercapnia and hypoxic hypercapnia. The regional venous outflow responses to hypercapnia were not altered after chemodenervation, but those to hypoxic hypercapnia were significantly attenuated after chemodenervation. These results suggest that acute hypercapnia and hypoxic hypercapnia caused a marked decrease in vascular capacitance owing primarily to an increase in sympathetic efferent nerve activity via chemoreceptor stimulation. They also indicate that blood flow to the splanchnic vascular bed during hypercapnia increased (even though the cardiac output was constant), whereas it increased to the extrasplanchnic and coronary vascular beds during hypoxic hypercapnia.

Animals↗
PubMed1985

Early increases in coronary vascular reserve in exercised rats are independent of cardiac hypertrophy.

To evaluate the relationship between the physiological cardiac hypertrophy associated with physical training and the increases in vascular capacitance associated with this stimuli, male and female rats trained by a swimming program were studied. Both sexes were used so that the coronary vascular response to exercise could be studied in the presence (females) and absence (males) of cardiac hypertrophy. Coronary vascular reserve was assessed in isolated retrograde buffer-perfused hearts under conditions of minimal coronary resistance (15 microM adenosine or anoxia). Both groups demonstrated an increase in coronary vascular reserve after 8 wk of exercise swim training, male animals increasing flow (per g of myocardium) by 15% and females by 18%. When the time course of this response was compared in female animals with the time course of the development of myocardial hypertrophy, it was evident that the vascular changes occurred early, greater than 80% of the response was seen within the first 10 days of exercise, compared with an approximately 35% increase in cardiac mass. These data suggest that the vascular response to exercise swim training is independent of the hypertrophic response and further that the increase in coronary vascularity is an early event in the cardiac adaptation to a physiological load.

Animals↗
PubMed1976

The actions of natural secretin on the small intestinal vasculature of the anaesthetized cat.

1 A plethysmographic preparation of cat jejunum was used to measure changes in tissue volume and capillary filtration coefficient (CFC), simultaneously with measurements of arterial and venous pressures, and total blood flow. 2 Secretin was infused and injected intravenously and also infused intra-arterially in relatively small doses. Probable resulting blood concentrations were compared with those determined under physiological conditions in other investigations. 3 By intravenous or intra-arterial infusion, secretin caused increases in CFC, indicating an increased functional exchange vessel area, and increases in jejunal volume, indicating increased vascular capacitance. The jejunal blood flow increased whilst the blood pressure remained essentially unchanged. 4 By intravenous injection, secretin caused rises in jejunal volume and reductions in calculated jejunal vascular resistance over the same dose range. Effects were statistically significant at 500 mu/kg and higher doses caused reductions in systemic arterial pressure. 5 The calculated peak blood concentrations of secretin resulting from the lower doses used in this investigation were of the same order of magnitude as those determined under physiological conditions in man. 6 It is possible that at physiological concentrations secretin causes an increased functional exchange vessel area in the small intestine, and may also increase the total blood flow through this tissue.

Animals↗
PubMed1997

Regulation of hepatic vascular volume: contributions from active and passive mechanisms during catecholamine and sodium nitroprusside infusion.

BACKGROUND: It is unclear how the liver contributes to regulation of cardiac filling. The aims of this study were to establish an animal model to quantify hepatic vascular capacitance and to determine the mechanisms whereby catecholamines and sodium nitroprusside modify hepatic blood volume. METHODS AND RESULTS: In 8 anesthetized pigs we measured hepatic and systemic pressures and flows. Liver vascular volume was measured by sonomicrometry calibrated against integrated hepatic inflow during outflow occlusion. Pressure-volume (P-V) curves were constructed during outflow occlusion. Sonomicrometry accurately reflected hepatic blood volume (r=.99+/-.001), and hepatic P-V curves were highly reproducible. Norepinephrine (0.3 and 0.7 microg x kg body weight (bwt)(-1) min(-1) intraportally) significantly reduced hepatic blood volume by 3.3+/-1 and 4.3+/-1 mL x kg bwt(-1), respectively. Nitroprusside (8 and 18 microg x kg bwt(-1) x min(-1) intraportally) increased hepatic blood volume by 1.1+/-0.2 and 1.9+/-0.3 mL x kg bwt(-1), respectively. Norepinephrine and nitroprusside parallel shifted the hepatic P-V curves, indicating reduced and increased unstressed blood volume, respectively. These curve shifts accounted for more than 90% of the respective blood volume changes. Compliance was unchanged. Phenylephrine but not isoprenaline yielded similar results as norepinephrine. CONCLUSIONS: The pig model used in this study, accurately quantified hepatic capacitance. Alpha-adrenergic stimulation decreased and nitroprusside increased capacitance by changing unstressed blood volume. These changes in capacitance correspond to expulsion of 300 mL and pooling of 130 mL of blood, respectively, in a 70-kg individual, reflecting that the liver is not only a passive blood reservoir but can respond actively and vigorously to pharmacological interventions.

Animals↗
PubMed1992

Baroreflex control of regional capacitance and blood flow distribution with or without alpha-adrenergic blockade.

Regional blood volumes (Vb), unstressed volumes (V0), blood flow distribution, venous compliances (Cv), venous resistances (Rv), and time constants of drainage (tau v) were determined in dogs anesthetized with alpha-chloralose at carotid sinus pressures (Pcs) of 50 and 200 mmHg and dosed with alpha-adrenergic or ganglionic blockade at a Pcs of 50 mmHg. Vb was measured in each region from indicator dilution curves and mean transit times. V0 was extrapolated from the pressure-volume curves. Pcs of 50 and 200 mmHg were maintained in random order. With a decrease in Pcs, arterial pressure increased from 58.7 +/- 4.1 to 104.6 +/- 6.4 mmHg (P < 0.01), peripheral fractional blood flow decreased from 69.8 +/- 3.8 to 55.8 +/- 3.9% (P < 0.001), splanchnic Vb decreased from 28.3 +/- 1.9 to 19.3 +/- 1.2 ml/kg (P < 0.01), and splanchnic V0 decreased from 19.6 +/- 1.4 to 6.3 +/- 2.1 ml/kg (P < 0.001). Splanchnic Rv and tau v also decreased, whereas splanchnic Cv increased. Phentolamine at low Pcs only partially reversed the decrease in splanchnic capacitance, whereas hexamethonium completely abolished it. In conclusion, changes in splanchnic Rv and blood flow distribution are important components of the carotid sinus reflex, and alpha-adrenergic receptor activation is only partially responsible for the changes in vascular capacitance by the baroreceptor reflex.

Adrenergic alpha-Antagonists↗
PubMed1983

Effects of stimulation of aortic chemoreceptors on abdominal vascular resistance and capacitance in anaesthetized dogs.

1. Dogs were anaesthetized with chloralose, ventilated artificially, and the regions of the aortic arch and carotid sinuses were isolated vascularly and perfused with blood. The abdominal circulation was isolated vascularly, perfused at constant flow and drained from the inferior vena cava at constant venous pressure. Changes in vascular resistance were determined by calculating changes in abdominal aortic perfusion pressure, and changes in capacitance by integrating the changes in venous outflow. 2. Stimulation of aortic body chemoreceptors, either by changing the aortic arch perfusate from arterial to venous blood at constant perfusion pressure or by injection of sodium cyanide into the aortic arch, resulted in an increase in abdominal vascular resistance and a decrease in abdominal vascular capacitance. 3. After both cervical vagosympathetic trunks had been cut, stimulation of aortic chemoreceptors no longer resulted in resistance or capacitance responses. 4. These results indicate that stimulation of aortic chemoreceptors, like carotid chemoreceptors, results in reflex constriction of both resistance and capacitance vessels in the abdominal circulation.

Abdomen↗
PubMed1990

Starling resistor versus compliance. Which explains the zero-flow pressure of a dynamic arterial pressure-flow relation?

Arterial pressure at zero flow (Pz = 0) that is higher than venous pressure (Pv) in dynamic pressure-flow relations has been explained by the presence of an arteriolar Starling resistor (SR) mechanism (i.e., vascular waterfall) or the discharge of vascular capacitance. To determine which was predominant, I studied in vivo hind limbs of 18 anesthetized dogs in which femoral arteries were cannulated with in-line electromagnetic flow probes to measure inflow (Qin), Pv was controlled, and collateral flow was eliminated with a tourniquet. Pz = 0 was obtained by turning flow to zero. Three tests were applied: 1) Pv was raised in steps with either constant Qin or constant arterial pressure (Pa) to determine the pressure at which upstream vascular characteristics were affected by a change in Pv, 2) the time to reach Pz = 0 was varied to determine compliance effects, and 3) an equation was developed to determine if experimentally derived parameters could explain Pz = 0 without invoking an SR. With constant Qin and a Pz = 0 of 56.9 +/- 11.7 mm Hg (time to Pz = 0, 3 seconds), Pv could be raised by 9.6 +/- 6.2 to 16.3 +/- 6.0 mm Hg before Pa increased, and with constant Pa, Pv could be raised by 6.8 +/- 7.3 to 14.0 +/- 8.0 mm Hg before Qin decreased. With increasing times to reach Pz = 0, Pz = 0 initially dropped precipitously, but then decreased by only a small amount over the next 5-10 seconds even though arterial pressure was much above Pv. This could be explained by an SR mechanism with a critical pressure of 42.3 +/- 11.4 mm Hg and an arterial compliance of 0.0104 +/- 0.0023 ml.mm Hg-1 (n = 6). There was no value for the compliance that described the results when the arterial outflow pressure was Pv. Thus, this study supports the hypothesis that an SR mechanism is present in the vascular system. It is most likely precapillary, and in the resting limb, it has a value of 40-50 mm Hg. However, Pz = 0 in dynamic pressure-flow studies of less than 4 seconds is also greatly influenced by capacitance effects and the initial Pa.

Animals↗