LOW DOSE L-NAME DECREASES CARDIAC OUTPUT AND RENAL BLOOD FLOW IN PIGLETS

Increasing renal blood flow (RBF) by the administration of low-dose dopamine is one mechanism to increase urine output in oliguric patients. This response is mediated in part by stimulation of dopaminergic receptors in the kidney, which could be attenuated by the dopamine blocker haloperidol. We evaluated this interaction by administering both drugs in clinically used doses to six anesthetized mongrel dogs. A dopamine regimen of 2.5 μg/kg/min significantly increased RBF along with cardiac output and stroke volume. Simultaneous administration of haloperidol 50 μg/kg iv did not influence the ability of low-dose dopamine to increase RBF. Although haloperidol is an antagonist of dopaminergic receptors, the increase in RBF associated with low-dose dopamine is maintained when intravenous haloperidol is concurrently administered to dogs.

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Low-dose dopamine preserves renal blood flow in endotoxin shocked dogs treated with ibuprofen

Journal of Surgical Research ◽

10.1016/0022-4804(85)90079-4 ◽

1985 ◽

Vol 38 (6) ◽

pp. 582-591 ◽

Cited By ~ 23

Author(s):

Mitchell P. Fink ◽

Ronald Nelson ◽

Rudolph Roethel

Keyword(s):

Blood Flow ◽

Renal Blood Flow ◽

Low Dose

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The Relationship of Renal Blood Flow to Cardiac Output in Normal Individuals as Determined by Concomitant Radioisotopic Measurements

Cardiovascular Research ◽

10.1093/cvr/2.3.243 ◽

1968 ◽

Vol 2 (3) ◽

pp. 243-246 ◽

Cited By ~ 9

Author(s):

R. E. Botti ◽

M. A. Razzak ◽

W. J. MacIntyre ◽

W. H. Pritchard

Keyword(s):

Blood Flow ◽

Cardiac Output ◽

Renal Blood Flow ◽

Normal Individuals ◽

Relationship Of ◽

The Relationship

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Circulatory and renal control by prostaglandins and renin in low cardiac output in dogs

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1989.256.4.h1079 ◽

1989 ◽

Vol 256 (4) ◽

pp. H1079-H1086 ◽

Cited By ~ 5

Author(s):

G. A. Riegger ◽

D. Elsner ◽

E. P. Kromer

Keyword(s):

Blood Flow ◽

Cardiac Output ◽

Glomerular Filtration Rate ◽

Renal Blood Flow ◽

Plasma Levels ◽

Filtration Rate ◽

Sympathetic Nerve Activity ◽

Peripheral Vascular ◽

Nerve Activity ◽

Low Cardiac Output

Changes of neurohumoral factors including vasodilatory prostaglandins (PGs) were investigated in an experimental model of moderate low-cardiac-output status induced by rapid right ventricular pacing (240 beats/min). After 7 days of pacing, we studied the response of renal, hormonal, and hemodynamic parameters to cyclooxygenase inhibition by indomethacin and the effects of the renin system by converting-enzyme blockade in addition to the inhibition of PG synthesis. Lowering cardiac output increased plasma levels of norepinephrine and atrial natriuretic peptide. Plasma renin concentration was suppressed, despite a fall in cardiac output and blood pressure and a stimulation of sympathetic nerve activity. Urinary excretion of PGE2 was increased (P less than 0.04); plasma levels of PGE2 and 6-keto-PGF1 alpha were unchanged as measured in blood from the renal vein, pulmonary artery, and aorta. During low cardiac output, we found a significant decrease of glomerular filtration rate, whereas renal blood flow and renal and peripheral vascular resistances were unchanged. Administration of indomethacin decreased plasma and urinary PGs significantly, markedly reduced renal blood flow, and increased renal vascular resistance without affecting peripheral vascular resistance. The additional blockade of the renin-angiotensin system by captopril showed mainly a vasodilator effect on peripheral arterial resistance vessels, resulting in an increase of cardiac output. Our results suggest that, in moderate low-cardiac-output status, renal blood flow is maintained by renal vasodilator PGs, which counterbalance vasoconstrictor mechanisms like the activated sympathetic nerve activity. We indirectly showed the importance of angiotensin II in preserving glomerular filtration rate, which declines when renin secretion is suppressed, as it may be the case in moderate heart failure.(ABSTRACT TRUNCATED AT 250 WORDS)

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The effect of mannitol infusion on cardiac output and renal blood flow after graded hemorrhage

Journal of Thoracic and Cardiovascular Surgery ◽

10.1016/s0022-5223(19)33178-2 ◽

1965 ◽

Vol 50 (4) ◽

pp. 561-566 ◽

Cited By ~ 5

Author(s):

Worthington G. Schenk ◽

N. Anders Delin ◽

Lawrence Pollock ◽

Kjartan B. Kjartansson ◽

John W. Boylan

Keyword(s):

Blood Flow ◽

Cardiac Output ◽

Renal Blood Flow

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Renal hemodynamics and fatty acid uptake: effects of obesity and weight loss

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.00135.2019 ◽

2019 ◽

Vol 317 (5) ◽

pp. E871-E878 ◽

Cited By ~ 6

Author(s):

Eleni Rebelos ◽

Prince Dadson ◽

Vesa Oikonen ◽

Hidehiro Iida ◽

Jarna C. Hannukainen ◽

...

Keyword(s):

Bariatric Surgery ◽

Weight Loss ◽

Blood Flow ◽

Cardiac Output ◽

Fatty Acid ◽

Renal Blood Flow ◽

Renal Hemodynamics ◽

Renal Volume ◽

Obese Subjects ◽

Total Renal Blood Flow

Human studies of renal hemodynamics and metabolism in obesity are insufficient. We hypothesized that renal perfusion and renal free fatty acid (FFA) uptake are higher in subjects with morbid obesity compared with lean subjects and that they both decrease after bariatric surgery. Cortical and medullary hemodynamics and metabolism were measured in 23 morbidly obese women and 15 age- and sex-matched nonobese controls by PET scanning of [15O]-H2O (perfusion) and 14( R,S)-[18F]fluoro-6-thia-heptadecanoate (FFA uptake). Kidney volume and radiodensity were measured by computed tomography, cardiac output by MRI. Obese subjects were re-studied 6 mo after bariatric surgery. Obese subjects had higher renal volume but lower radiodensity, suggesting accumulation of water and/or lipid. Both cardiac output and estimated glomerular filtration rate (eGFR) were increased by ~25% in the obese. Total renal blood flow was higher in the obese [885 (317) (expressed as median and interquartile range) vs. 749 (300) (expressed as means and SD) ml/min of controls, P = 0.049]. In both groups, regional blood perfusion was higher in the cortex than medulla; in either region, FFA uptake was ~50% higher in the obese as a consequence of higher circulating FFA levels. Following weight loss (26 ± 8 kg), total renal blood flow was reduced ( P = 0.006). Renal volume, eGFR, cortical and medullary FFA uptake were decreased but not fully normalized. Obesity is associated with renal structural, hemodynamic, and metabolic changes. Six months after bariatric surgery, the hemodynamic changes are reversed and the structural changes are improved. On the contrary, renal FFA uptake remains increased, driven by high substrate availability.

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EFFECT OF MANNITOL ON RENAL BLOOD FLOW AND CARDIAC OUTPUT IN HEMORRHAGIC SHOCK

Survey of Anesthesiology ◽

10.1097/00132586-196606000-00015 ◽

1966 ◽

Vol 10 (3) ◽

pp. 230???231

Author(s):

R. C. CAMISHION ◽

N. H. FISHMAN ◽

Hebbel E. Hoff

Keyword(s):

Blood Flow ◽

Cardiac Output ◽

Hemorrhagic Shock ◽

Renal Blood Flow

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Hemodynamic responses to dopamine and to isoproterenol following acute myocardial injury

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y69-005 ◽

1969 ◽

Vol 47 (1) ◽

pp. 25-32 ◽

Cited By ~ 9

Author(s):

Keith L. MacCannell

Keyword(s):

Blood Flow ◽

Cardiac Output ◽

Renal Blood Flow ◽

Myocardial Injury ◽

Left Renal Artery ◽

Arterial Blood ◽

Acute Myocardial Injury ◽

Cardiac Slowing ◽

Anesthetized Dogs ◽

Higher Doses

Severe myocardial injury was produced in eight anesthetized dogs by the injection of microspheres into the coronary circulation. Cardiac output and renal blood flow were monitored continuously with electromagnetic flow probes around the ascending thoracic aorta and left renal artery respectively. Intravenous infusions of isoproterenol and of dopamine (0.01–0.64 and 0.4–32.0 μg/kg per minute respectively) produced an increase in the cardiac output. Renal blood flow increased with small doses of isoproterenol but tended to decrease with higher doses; in contrast, all doses of dopamine increased renal blood flow. Dopamine was more effective in raising the systemic arterial blood pressure, but also increased cardiac work. Occasional extrasystoles were induced at higher doses of both amines. In three unanesthetized dogs sensitized by prior ligation of a coronary artery, the largest doses of dopamine tested (24–64 μg/kg per minute) did not produce cardiac arrhythmias. However, when dopamine was given to anesthetized dogs during vagal-induced cardiac slowing (a condition conducive to the emergence of ventricular automaticity), arrhythmias were induced. These data suggest that dopamine can increase both cardiac output and renal blood flow after severe myocardial injury, and may be a rational agent in the treatment of cardiogenic shock. Its arrhythmogenic properties would not appear to restrict its use.

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