Distribution of cardiac output and nutritional blood flow in the unanesthetized rat: alterations during experimental renal hypertension

1973 ◽  
Vol 343 (3) ◽  
pp. 257-266 ◽  
Author(s):  
A. M. Bralet ◽  
J. Wepierre ◽  
J. Bralet
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Renal Hypertension ◽  
Experimental Renal Hypertension ◽  
Distribution Of Cardiac Output

scholarly journals Increased Cardiac Output as a Contributory Factor in Experimental Renal Hypertension in Dogs

1970 ◽  
Vol 27 (5) ◽  
pp. 799-810 ◽  
Author(s):  
CARLOS M. FERRARIO ◽  
IRVINE H. PAGE ◽  
JAMES W. McCUBBIN
Keyword(s):  
Cardiac Output ◽  
Renal Hypertension ◽  
Contributory Factor ◽  
Experimental Renal Hypertension

Distribution of cardiac output during induced isometric exercise in dogs

1979 ◽  
Vol 236 (2) ◽  
pp. H218-H224 ◽  
Author(s):  
S. C. Crayton ◽  
R. Aung-Din ◽  
D. E. Fixler ◽  
J. H. Mitchell
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Adrenergic Receptor ◽  
Isometric Exercise ◽  
Peripheral Resistance ◽  
Minute Volume ◽  
Adrenergic Blockade ◽  
Limb Muscles ◽  
Anesthetized Dogs ◽  
Distribution Of Cardiac Output

Studies were designed to characterize the distribution of cardiac output during induced isometric exercise in anesthetized dogs. The response to isometric exercise involved significant increases in heart rate (+12 +/- 3%(SE)), mean arterial pressure (+13 +/- 2%), cardiac output (+26 +/- 8%), and respiratory minute volume (+75 +/- 26%); total peripheral resistance did not change significantly. Significant changes in blood flow were observed during isometric exercise in kidneys (-18 +/- 6%) and contracting limb muscles (+453 +/- 154%). Flow to liver (hepatic artery), spleen, brain, and myocardium remained near control values. Section of spinal dorsal roots L6-L7 abolished the responses to isometric exercise except for the increase in flow to exercising limb muscles. Alpha-adrenergic receptor blockade abolished the decrease in renal blood flow during isometric exercise; however, the increase in flow to exercising limb muscles was not affected by either alpha- or beta-adrenergic blockade.

Development of chronic perinephritic hypertension in dogs without volume expansion

1977 ◽  
Vol 233 (4) ◽  
pp. F278-F281 ◽  
Author(s):  
R. H. Freeman ◽  
J. O. Davis ◽  
B. E. Watkins
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Volume Expansion ◽  
Left Kidney ◽  
Renal Hypertension ◽  
Control Level ◽  
Whole Body ◽  
Sodium Balance ◽  
Contralateral Kidney ◽  
Experimental Renal Hypertension

The theory of whole body autoregulation to explain the pathogenesis of experimental renal hypertension states that hypertension is initiated in response to an early increase in salt and water retention and a subsequent elevation of the cardiac output. This hypothesis was evaluated in the present study. Dogs (n,5) were made hypertensive by wrapping the left kidney in cellophane and removing the contralateral kidney 3 wk later. One week prior to right nephrectomy, the dogs were volume depleted by placing them on a low sodium intake (less than 3 meq of sodium/day) and giving them a mercurial diuretic for the first 3 days of the diet. This superimposed sodium depletion (negative sodium balance of 137 +/- 17 meq) increased plasma renin activity 3-5 times but did not change arterial pressure or heart rate. Within 2 days after nephrectomy, the mean arterial pressure increased from the control level of 105 +/- 1 to 135 +/- 6 mmHg (P less than 0.005) and pressure remained elevated throughout an additional 4-wk period in which volume depletion was enforced. The present study suggests, therefore, that initial blood volume expansion with such possible consequences as elevated cardiac output are not essential to the pathogenesis of experimental renal hypertension.

Cardiac output and organ blood flow in warm- and cold-acclimated rats exposed to cold

1968 ◽  
Vol 46 (4) ◽  
pp. 653-659 ◽  
Author(s):  
L. Jansky ◽  
J. S. Hart
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Skeletal Muscles ◽  
Organ Blood Flow ◽  
Internal Organs ◽  
Exposure To Cold ◽  
Brown Adipose ◽  
Production Increase ◽  
Distribution Of Cardiac Output ◽  
Fractional Distribution

Cold acclimation increased the cardiac output of unanesthetized rats when measured at 30 °C. After exposure to 9 °C for 70 min cardiac output further increased by 46% in both warm- and cold-acclimated rats. From the changes in the fractional distribution of cardiac output after cold exposure it was shown that the blood flow increased significantly in muscular organs (heart, diaphragm, skeletal muscles) and in the adrenals of warm-acclimated rats. In cold-acclimated rats the blood flow to the brown and white adipose tissues, pancreas, kidney, intestine, liver, and other internal organs was also increased in a cold environment, and accounted for 65% of the increase in blood flow during exposure to cold compared with only 36% in warm-acclimated rats. It is estimated that the extramuscular thermogenesis can account for a greater proportion of the total nonshivering thermogenesis in cold-acclimated rats. The contribution of brown adipose tissue is estimated not to exceed about 6% of the total heat production increase in cold-acclimated rats during exposure to cold.

Comparison of microspheres and 86Rb+ as tracers of the distribution of cardiac output in rats indicates invalidity of 86Rb+-based measurements

1978 ◽  
Vol 56 (1) ◽  
pp. 97-109 ◽  
Author(s):  
David O. Foster ◽  
M. Lorraine Frydman
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Cardiac Output ◽  
Valid Measure ◽  
White Rats ◽  
Direct Measurements ◽  
Brown Adipose ◽  
Valid Data ◽  
Distribution Of Cardiac Output ◽  
Fractional Distribution

The technique of using γ-labeled plastic microspheres (15 ± 5 μm) to measure cardiac output (CO) and its fractional distribution (FD) to individual tissues and organs was judged by various criteria to give valid data when applied to barbital-sedated warm-acclimated or cold-acclimated (CA) white rats, which were either resting or responding calorigenically to infused noradrenaline (NA). The FD of CO to each of 16 tissues or organs of CA rats at rest or responding to NA was then estimated both with 86Rb+ and with microspheres, the two tracers being injected simultaneously. For only seven of the tissues examined in resting rats and only one in NA-infused rats was the FD of CO estimated with 86Rb+ not significantly different from that estimated with microspheres. 86Rb+ to microsphere ratios of the FD of CO to individual tissues ranged from 3.5 and 3.0 for liver and skeletal muscle, respectively, down to 0.09 and 0.07 for brown adipose tissue (BAT) and brain. Since microsphere-based estimates of blood flow to the interscapular BAT of CA rats responding to NA were corroborated by direct measurements of venous efflux from the tissue, it is unequivocal that the 86Rb+-based estimate of the fraction of CO directed to interscapular BAT was highly erroneous. When considered along with data from the literature, the present findings support a conclusion that the uptake of 86Rb+ by a tissue frequently does not provide a valid measure of the FD of CO to the tissue. Some of the factors that are likely responsible for this situation are discussed, and it is suggested that only by a fortuitous combination of circumstances does the uptake of 86Rb+ by a tissue sometimes match the FD of CO to the tissue.

Analysis of myocardial and total body integral extraction ratios of rubidium-86

1978 ◽  
Vol 235 (6) ◽  
pp. H794-H802
Author(s):  
P. F. McDonagh ◽  
A. F. Salel ◽  
K. A. Krohn ◽  
E. A. Rhode ◽  
D. T. Mason
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Coronary Blood Flow ◽  
Animal Experiments ◽  
Clinical Use ◽  
Right Heart ◽  
Preliminary Study ◽  
Total Body ◽  
Distribution Of Cardiac Output ◽  
Right Heart Bypass

Coronary blood flow (QM) measurement with radiorubidium (Rb) assumes that Rb distributes to the myocardium in proportion to flow. This assumption is correct if the integral myocardial Rb extraction ratio (ERM) equals total body extraction (ERTB). A right-heart-bypass preparation was employed to test the hypothesis that ERM = ERTB and to examine the determinants of Rb extraction. Dogs were anesthetized with pentobarbital, and arterial, coronary venous, and total body venous Rb concentrations were continuously measured for 4 min after injection. We found that ERM (0.56 +/- 0.01) was significantly less than ERTB (0.70 +/- 0.01), P less than 0.01 (n = 29) and concluded that Rb did not distribute in proportion to flow. We do not recommend this method for clinical use. ERM is flow dependent and ERRB is a function of the total cardiac output and the distribution of cardiac output. Before employing Rb in animal experiments, it is recommended that a preliminary study be performed comparing flow measured with Rb to an independent measure of blood flow.

Effects of protoveratrine on coronary blood flow of the renal hypertensive dog

1963 ◽  
Vol 204 (5) ◽  
pp. 895-898 ◽  
Author(s):  
James W. West ◽  
Elwood L. Foltz
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Oxygen Saturation ◽  
Coronary Blood Flow ◽  
Arterial Oxygen Saturation ◽  
Renal Hypertension ◽  
Peripheral Resistance ◽  
Arterial Oxygen ◽  
Arterial Blood ◽  
Venous Oxygen Saturation

In renal hypertension, protoveratrine decreased coronary blood flow, cardiac oxygen consumption, arterial and venous oxygen saturation, coronary arteriovenous oxygen difference, mean arterial blood pressure, cardiac output, cardiac work, cardiac efficiency, cardiac rate, total peripheral resistance, coronary resistance, respiratory rate, and minute volume. The decrease was significant in all functions except coronary blood flow, coronary venous oxygen saturation, and cardiac output. The results of these experiments indicate that in the renal hypertensive animal, a therapeutically beneficial effect was derived from protoveratrine on the circulation by its ability to decrease the work of the heart (lowering the elevated mean arterial pressure) and the coronary vascular resistance while maintaining coronary blood flow and cardiac output within normal levels. The less advantageous effect of protoveratrine on circulation resulted from its respiratory inhibiting effect which reduced the arterial blood oxygen saturation. Although a small decline in coronary venous oxygen saturation was noted, the coronary flow and oxygen delivery in face of the reduced arterial oxygen saturation was apparently adequate to maintain a normal cardiac activity.

DISTRIBUTION OF BLOOD FLOW IN COLD STRESSED PIGLETS

1979 ◽  
Vol 59 (4) ◽  
pp. 721-726 ◽  
Author(s):  
P. E. V. WILLIAMS ◽  
R. O. PARKER ◽  
B. A. YOUNG ◽  
F. X. AHERNE
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Cold Stress ◽  
Rectal Temperature ◽  
Cold Exposure ◽  
Alimentary Tract ◽  
Distribution Of Cardiac Output

Radioactive ruthenium labelled microspheres 15 ± 3 μm in diameter were used to determine distribution of cardiac output in unfed control (35 °C) and unfed cold stressed (5 °C) piglets 3.5 h of age. The cold stress produced an average 7.1 °C drop in rectal temperature and a redistribution of blood flow. In cold exposed piglets the adrenal fraction of cardiac output was significantly (P < 0.05) lower: 0.56% in the control compared with 0.29% in the cold exposed piglets; however, the relative blood flow to the adrenals was higher than for other tissues. The fractions of cardiac output reaching the psoas and biceps muscles increased (P < 0.05) by 148 and 260%, respectively, during cold exposure, while that reaching the heart, brain, alimentary tract, skin and fat was not significantly (P > 0.05) affected by cold exposure.

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