Effect of sympathectomy on arterial and venous changes in renal hypertensive rats

1981 ◽  
Vol 241 (3) ◽  
pp. H449-H454
Author(s):  
G. Simon
Keyword(s):  
Arterial Pressure ◽  
Structural Changes ◽  
Venous Pressure ◽  
Vena Cava ◽  
Hypertensive Rats ◽  
Flow Curves ◽  
Pressure Flow ◽  
Pressure Axis ◽  
Arteries And Veins ◽  
Renal Hypertensive Rats

Arterial pressure-flow and venous pressure-volume relationships were measured at maximal vasodilatation in the denervated pump-perfused hindquarters of four groups of rats: 1) neonatally sympathectomized (guanethidine-injected and adrenal-demedullated), one-kidney, one-clip hypertensive (n = 9); 2) sympathectomized, sham-operated, unilaterally nephrectomized control (n = 10); 3) sham-sympathectomized, one-kidney, one-clip hypertensive (n = 8); and 4) sham-sympathectomized, sham-operated, unilaterally nephrectomized control (n = 9). Dry defatted weight of anatomically defined segments of the aorta and vena cava in the four groups of rats also was measured. Significant rises in arterial pressure developed in sympathectomized rats after clipping of the renal artery and contralateral nephrectomy. Arterial pressure-flow curves were shifted toward the pressure axis (P less than 0.01) in clipped rats whether sympathectomized or not. In sympathectomized clipped rats, there was also a shift of the venous pressure-volume curves toward the pressure axis (P less than 0.05). The same degree of hypertrophy of the aorta was found in sympathectomized and sham-sympathectomized clipped rats. The findings indicate that in renal hypertensive rats structural changes of both large arteries and veins may develop in the absence of an intact sympathoadrenergic system.

Effect of hypoxic hypoxia on systemic vasculature

1984 ◽  
Vol 56 (5) ◽  
pp. 1403-1410 ◽  
Author(s):  
J. Malo ◽  
H. Goldberg ◽  
R. Graham ◽  
H. Unruh ◽  
C. Skoog
Keyword(s):  
Arterial Pressure ◽  
Inferior Vena ◽  
Superior Vena ◽  
Venous Pressure ◽  
Vena Cava ◽  
Venous Drainage ◽  
Hypoxic Hypoxia ◽  
Venous Compliance ◽  
Flow Curves ◽  
Pressure Flow

Effects of hypoxic hypoxia (HH) on cardiac output (CO), CO distribution, arterial and venous pressure-flow curves, vascular compliance, vascular time constant (tau), and resistance to venous return (RVR) were evaluated on six dogs. The vascular bed was isolated into four compartments depending on venous drainage: superior vena cava (SVC), splanchnic, renal and adrenal, and the remainder of the inferior vena cava (IVC). Low arterial O2 content and PO2 produced a threefold increase in CO at the same mean arterial pressure and a significant redistribution of CO to the SVC. Arterial pressure-flow curves decreased their slope (i.e., flow resistance) by a factor of two in the IVC and renal beds and by a factor of three in the splanchnic and SVC beds. Venous pressure-flow curves for the animal also decreased their slope significantly. HH causes a twofold increase in venous compliance and in mean venous pressure; tau did not change, but RVR halved. Seventy percent of the CO increase is explained by the increase in mean venous pressure and 30% by the reduction in RVR.

Hepatic arterial and portal venous pressure-flow relationships in isolated, perfused liver

1962 ◽  
Vol 202 (6) ◽  
pp. 1090-1094 ◽  
Author(s):  
Robert E. Condon ◽  
Niles D. Chapman ◽  
Lloyd M. Nyhus ◽  
Henry N. Harkins
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Portal Vein ◽  
Venous Pressure ◽  
Perfused Liver ◽  
Perfusion Rate ◽  
Flow Curves ◽  
Pressure Flow ◽  
Pressure Axis ◽  
Blood Pressure Responses

Blood pressure responses to alteration in blood flow were studied in the completely isolated, excised liver of the calf during perfusion of the hepatic artery or portal vein. The pressure-flow curves in both of the afferent vessels of the liver are curvilinear, with concavity toward the pressure axis. Resistance increases progressively with increases in perfusion rate; resistance increases are proportionately of greater magnitude than the increases in blood flow demonstrating autoregulation in both hepatic arterial and portal venous systems. The autoregulatory nature of pressure-flow responses is not affected by prolonged perfusion or marked acidosis.

Effect of pulsatile pressure and metabolic rate on intestinal autoregulation

1982 ◽  
Vol 242 (5) ◽  
pp. H769-H775 ◽  
Author(s):  
A. P. Shepherd ◽  
G. L. Riedel
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Metabolic Rate ◽  
Venous Pressure ◽  
Systematic Effect ◽  
Flow Curves ◽  
Pressure Flow ◽  
Pulsatile Pressure ◽  
Series Of Experiments ◽  
Pressure Autoregulation

In the intestine, raising venous pressure elicits a precapillary vasoconstriction that has been ascribed to a myogenic mechanism. Such myogenic responses occur more frequently and have a greater magnitude if arterial pressure is pulsatile. This laboratory reported that the ability of the gut to autoregulate blood flow in response to perfusion pressure manipulations is enhanced if metabolic rate is stimulated by transportable intraluminal solutes. Since both myogenic and metabolic mechanisms may participate in local control, we attempted to delineate the relative contributions the two mechanisms make to autoregulation. In one set of experiments, pulse pressures of 20 and 40 mmHg evoked a slight but statistically significant vasoconstriction. In a second series of experiments, pressure-flow curves were determined in isolated canine small bowel. The ability of the gut to autoregulate was compared at pulse pressures of 0, 20, and 40 mmHg and at basal and elevated metabolic rates. Altering pulse pressure had no systematic effect on the ability of the intestine to autoregulate blood flow. In contrast, increasing metabolic rate consistently enhanced autoregulation at each of the pulse pressures studied. Therefore, these results indicate that although a myogenic mechanism may best account for the response to elevated venous pressure, autoregulation as expressed in pressure-flow curves is more strongly influenced by the prevailing metabolic rate than by stretch stimuli such as arterial pressure pulsations.

Relative Influence of Variations in Arterial and Venous Pressures on Resistance to Flow

1957 ◽  
Vol 192 (1) ◽  
pp. 164-170 ◽  
Author(s):  
Matthew N. Levy
Keyword(s):  
Arterial Pressure ◽  
Pressure Gradient ◽  
Venous Pressure ◽  
The Other ◽  
Relative Influence ◽  
Curvilinear Relationship ◽  
Flow Curves ◽  
Flow Axis ◽  
Pressure Axis ◽  
Arterial Inflow

Arterial inflow and arterial and venous pressures were measured in the hind legs of dogs under conditions of variations in arterial or in venous pressures. When the arteriovenous pressure gradient was reduced by continuous or stepwise diminutions of arterial pressure, a curvilinear relationship, convex to the pressure axis, was observed when flow was plotted as a function of pressure gradient. With elevations of venous pressure, on the other hand, the pressure-flow curves were invariably linear over the range studied, and the extrapolated curve usually intersected the flow-axis at a low, positive value. The calculated value of resistance fluctuated markedly with variations in arterial pressure, but usually decreased only slightly with elevations of the venous pressure.

Functional and structural changes with hypoxia in pulmonary circulation of spontaneously hypertensive rats

1994 ◽  
Vol 77 (3) ◽  
pp. 1101-1107 ◽  
Author(s):  
S. P. Janssens ◽  
B. T. Thompson ◽  
C. R. Spence ◽  
C. A. Hales
Keyword(s):  
Pulmonary Hypertension ◽  
Arterial Pressure ◽  
Vascular Remodeling ◽  
Spontaneously Hypertensive Rats ◽  
Structural Changes ◽  
Chronic Hypoxia ◽  
Acute Hypoxia ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto

Chronic hypoxic pulmonary hypertension involves both vasoconstriction and vascular remodeling. Spontaneously hypertensive rats (SHR) have an increased systemic vascular resistance and a greater responsiveness to constricting stimuli. We hypothesized that, in contrast to age-matched normotensive Wistar-Kyoto rats (WKY), SHR also display spontaneous pulmonary hypertension in normoxia and increased vascular response to acute and chronic hypoxia. Baseline mean pulmonary arterial pressure (PAP) and total pulmonary resistance (TPR) were higher in SHR than in WKY. With acute hypoxia (10% O2 for 15 min), PAP increased to the same extent in SHR and WKY and cardiac output (CO) was unchanged in WKY but increased in SHR. Thus, the rise in PAP in the SHR might be accounted for by the rise in CO, as TPR did not rise, but not that in the WKY, as TPR increased. After 12 days in hypoxia (10% O2), mean arterial pressure was unchanged in WKY but decreased significantly in SHR without a change in CO. PAP increased by 59% in SHR and 54% in WKY when the rats were taken from the hypoxic chamber for 1 h. Acute hypoxic challenge caused a further increase in PAP only in WKY. Medial wall thickness of alveolar duct and terminal bronchial vessels was similar in WKY and SHR after chronic hypoxia. We conclude that SHR exhibit mild baseline pulmonary hypertension in normoxia and that chronic hypoxia does not produce a disproportionate increase in SHR pulmonary vascular remodeling and pulmonary hypertension.

Cardiovascular reflexes during abdominal ischemia in cats

1994 ◽  
Vol 267 (1) ◽  
pp. R97-R106 ◽  
Author(s):  
H. S. Huang ◽  
J. C. Longhurst
Keyword(s):  
Blood Pressure ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Femoral Vein ◽  
Venous Pressure ◽  
Vena Cava ◽  
Left Ventricular ◽  
Mesenteric Arteries ◽  
Cardiovascular Reflexes ◽  
Group 3

The cardiovascular effects of regional abdominal ischemia and reperfusion were studied in cats anesthetized with alpha-chloralose. In group 1 (n = 9), central venous pressure was kept constant by a servo-controller while the celiac and superior mesenteric arteries were occluded by loop snares for 10 min. In group 2 (n = 9), a constant-perfusion circuit to the celiac and superior mesenteric arteries that could divert flow to the femoral vein was used to induce abdominal ischemia. In group 3 (n = 7), venous return from the inferior vena cava was controlled, and a constant-perfusion circuit was used to induce abdominal ischemia. Abdominal ischemia significantly (P < 0.05) increased portal venous blood lactate from 4.3 +/- 0.6 to 6.0 +/- 0.6 mM in group 3. The early increases in blood pressure caused by passive volume shifts in groups 1 and 2 were abolished in group 3. The late, i.e., 10 min, response to abdominal ischemia consisted of significant (P < 0.05) increases in mean arterial pressure (29 +/- 7, 24 +/- 7, and 33 +/- 8 mmHg in groups 1, 2, and 3, respectively). Abdominal ischemia also significantly (P < 0.05) increased the first derivative of left ventricular pressure at 40 mmHg developed pressure from 4,355 +/- 377 to 4,839 +/- 407 mmHg/s in group 3. Celiac and superior mesenteric ganglionectomy abolished the late but not the early hemodynamic changes. Ganglionectomy also significantly (P < 0.05) enhanced the decrease in mean arterial pressure during reperfusion in all groups. We conclude that the pressor and contractile responses during 10 min of abdominal ischemia and the relative maintenance of blood pressure during reperfusion after ischemia are reflex in nature.

Decreased hexokinase activity in paraventricular nucleus of adult SHR and renal hypertensive rats

1988 ◽  
Vol 254 (3) ◽  
pp. R508-R512 ◽  
Author(s):  
T. L. Krukoff
Keyword(s):  
Arterial Pressure ◽  
Paraventricular Nucleus ◽  
Metabolic Activity ◽  
Central Nucleus ◽  
Hypothalamic Nucleus ◽  
Sprague Dawley ◽  
Hypertensive Rats ◽  
Medial Nucleus ◽  
Wistar Kyoto ◽  
Renal Hypertensive Rats

Metabolic activity was assessed in the brains of spontaneously hypertensive rats (SHR) using the histochemical hexokinase (HK) technique and photodensitometric analysis. Of eight regions known to play a role in cardiovascular regulation, only the paraventricular nucleus of the hypothalamus (PVH) exhibited alterations in HK activity. Significantly lower levels of HK activity in SHR than in control Sprague-Dawley and Wistar-Kyoto rats were measured in both the parvo- and magnocellular divisions of the PVH. No differences in HK activity were found in the anterior hypothalamic nucleus, posterior hypothalamic nucleus, supraoptic nucleus, subfornical organ, central nucleus of the amygdala, or the medial nucleus of the tractus solitarius of SHR. Similar results were obtained in renal hypertensive rats; furthermore, a positive correlation was found between levels of arterial pressure and densitometric readings. These latter results strongly suggest that metabolic alterations in the PVH of SHR are directly related to the increases in arterial pressure and are not due to the genetic makeup of SHR. In light of studies by others, the data from the present study have been interpreted to suggest that the decreases in metabolic activity in the PVH of the adult SHR are the result of a central attempt to bring the level of the arterial pressure down to normal levels and not to the altered activity of a region that might be acting to keep arterial pressure elevated.

Reversal of cardiac hypertrophy in renal hypertensive rats: medical vs. surgical therapy

1981 ◽  
Vol 240 (3) ◽  
pp. H408-H412
Author(s):  
S. Sen ◽  
R. C. Tarazi ◽  
F. M. Bumpus
Keyword(s):  
Drinking Water ◽  
Surgical Treatment ◽  
Arterial Pressure ◽  
Cardiac Hypertrophy ◽  
Converting Enzyme ◽  
Hypertensive Rats ◽  
Sham Control ◽  
Captopril Treatment ◽  
Renal Hypertensive Rats ◽  
Catecholamine Concentration

Cardiac hypertrophy consequent to renovascular hypertension was investigated in two-kidney one-clip Goldblatt rats. Ventricular weight in renal hypertensive rats correlated closely with level of arterial pressure (r = 0.93, P less than 0.001). DNA, RNA and hydroxyproline contents of the hypertrophied hearts were higher than sham control, but there was no significant change in myocardial concentration of any of them. Surgical treatment (removal of clipped kidney) as well as medical therapy (inhibition of converting enzyme with orally administered captopril, 150 mg/l drinking water) led to reduction of ventricular weight (2.70 +/- 0.01 and 2.78 +/- 0.06, respectively, vs. 3.4 +/- 0.05 mg/g in controls, P less than 0.01 for both). Reduction of cardiac weight was associated with increase in both myocardial concentration and content of hydroxyproline in surgically treated rats and in medically treated animals. Ventricular catecholamine concentration was increased after nephrectomy but was unchanged by captopril treatment.

Quantitative study of intramyocardial compression in the fibrillating heart

1979 ◽  
Vol 237 (2) ◽  
pp. H191-H196 ◽  
Author(s):  
J. M. Downey ◽  
R. W. Chagrasulis ◽  
V. Hemphill
Keyword(s):  
Blood Flow ◽  
Left Ventricle ◽  
Coronary Blood Flow ◽  
Quantitative Study ◽  
Coronary Arteries ◽  
Venous Pressure ◽  
Beating Heart ◽  
Flow Curves ◽  
Pressure Flow ◽  
Zero Flow

Extravascular compression inhibits coronary blood flow in fibrillating hearts. Pressure-flow curves from spontaneously fibrillating hearts whose coronary arteries were maximally dilated were examined to see whether this inhibition involves a vascular waterfall mechanism as has been found in the beating heart. Waterfall behavior is indicated when pressure-flow curves are linear and experience a zero-flow intercept at pressures greater than venous pressure. Regional pressure-flow curves revealed a zero flow intercept of 28.4 mmHg for the inner quarter of the left ventricle, indicating that compression is quite high in that region. A zero-pressure intercept of only 15.1 was found at the outer quarter, which was not significantly different from venous pressure. We conclude that the spontaneously fibrillating heart experiences a gradient of compression falling from 28 mmHg at the subendocardium to near zero at the subepicardium.

Effective Vascular Compliance of Dogs in Acute Heart Failure

1975 ◽  
Vol 53 (1) ◽  
pp. 129-136 ◽  
Author(s):  
Pierre Larochelle ◽  
Richard I. Ogilvie
Keyword(s):  
Arterial Pressure ◽  
Left Atrial ◽  
Circulatory Arrest ◽  
Venous Pressure ◽  
Vena Cava ◽  
Plasma Catecholamine ◽  
Vascular Compliance ◽  
Plasma Catecholamine Concentrations ◽  
Circulating Volume ◽  
Effective Vascular Compliance

Effective vascular compliance was measured repeatedly in dogs without circulatory arrest utilizing a closed-circuit venous bypass system and constant cardiac output. Compliance, determined by the ΔV/ΔP relationship at the end of a 1-min infusion of 5% of the circulating volume into the inferior vena cava, was independent of the initial venous pressure, total circulating volume and systemic arterial pressure. It remained constant over a 3 h experimental period at 1.55 ± 0.05 ml (mm Hg)−1 kg−1 body weight. Elevation of mean left atrial pressure and mean pulmonary arterial pressure by gradual aortic constriction was associated with a large and significant reduction in vascular compliance to a value of 1.14 ± 0.06 ml (mm Hg)−1 kg−1 after 2 h. This reduction was independent of the initial venous pressure and total circulating volume but was associated with the changes in left atrial and pulmonary artery pressures and an increase in plasma catecholamine concentrations. The mechanism responsible for the reduction in effective compliance is not clear from the present experiments. Increased circulating catecholamines and sympathetic nerve traffic resulting from baro- and volume receptor stimulation in the vascular tree may be the causative mechanism.

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