Hemodynamic responses to dopamine and to isoproterenol following acute myocardial injury

1969 ◽  
Vol 47 (1) ◽  
pp. 25-32 ◽  
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.

Renal vascular and excretory responses to prostaglandin endoperoxides in the dog

1979 ◽  
Vol 236 (3) ◽  
pp. H427-H433
Author(s):  
J. A. Oliver ◽  
R. R. Sciacca ◽  
P. J. Cannon
Keyword(s):  
Blood Flow ◽  
Renal Artery ◽  
Renal Blood Flow ◽  
Biologically Active ◽  
Direct Effects ◽  
Cortical Areas ◽  
Anesthetized Dogs ◽  
Renal Vascular ◽  
Higher Doses

To determine whether the prostaglandin endoperoxides PGG2 and PGH2 have direct effects in the kidney, PGG2 and PGH2 were administered into the renal artery of anesthetized dogs and their effects were compared to those of PGE2. Like PGE2, PGG2 and PGH2 induced a dose-related renal vasodilation. A 50% increase in the renal blood flow was observed with 0.05 microgram/kg body wt of PGE2 and with four- and sixfold higher doses of PGH2 and PGG2, respectively. Infusion of all three compounds at doses inducing a 50% increase in the renal blood flow resulted in 1) increases in blood flow to all cortical areas, with the greatest increase occurring in the juxtamedullary area, 2) diuresis with no change in the glomerular filtration rate, and 3) natriuresis and kaliuresis. In vitro incubation of PGH2, a maneuver known to result in its conversion to other prostaglandins, had no influence on its renal effects. The data indicate that PGH2 and PGG2 are biologically active when infused into the renal artery of the anesthetized dog and suggest that the endoperoxides exert their effects after bioconversion to other prostaglandins.

Effects of albumin infusion on renal function in the dog

1963 ◽  
Vol 205 (1) ◽  
pp. 153-161 ◽  
Author(s):  
Mary Jo Elpers ◽  
Ewald E. Selkurt
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Renal Plasma Flow ◽  
Venous Pressure ◽  
Venous Blood ◽  
Urine Volume ◽  
Albumin Infusion ◽  
Arterial Blood ◽  
Vasa Recta ◽  
Anesthetized Dogs

Serum albumin (25%) was infused into anesthetized dogs undergoing a saline diuresis. No significant effect was seen on arterial pressure, but renal venous pressure was elevated slightly. GFR remained unchanged, while Cpah, renal plasma flow, total renal blood flow, and flow to medullary tissue increased significantly. Accompanying these changes were marked declines in PAH and creatinine extraction ratios. Urine volume, Cna, and Cosm declined appreciably during albumin infusion; TcHH2O tended to decrease. The ratio of Na and osmolar constituents in renal venous blood to that in arterial blood increased above unity, and calculations indicated that at this time Na was washed from the kidney. Tmpah remained unchanged during albumin infusion. It is concluded that during albumin infusion, there is an increase in plasma volume and renal blood flow accompanied by a diversion of part of this blood through aglomerular regions, possibly through A-V anastomoses, as evidenced by the accompanying decrease in Ecr and Epah. This could involve increased perfusion of the medullary papillary zone, including the vasa recta vessels, supported by the observations that during albumin infusion there is a washout of osmotic constituents, primarily Na, presumably from a zone of high Na concentration.

scholarly journals Nitric oxide–endothelin-1 interaction in humans

1997 ◽  
Vol 82 (5) ◽  
pp. 1593-1600 ◽  
Author(s):  
Gunvor Ahlborg ◽  
Jan M. Lundberg
Keyword(s):  
Nitric Oxide ◽  
Heart Rate ◽  
Blood Flow ◽  
Cardiac Output ◽  
Renal Blood Flow ◽  
Metabolic Effects ◽  
Endothelin 1 ◽  
Arterial Blood ◽  
Glucose Output ◽  
Change In Mean

Ahlborg, Gunvor, and Jan M. Lundberg. Nitric oxide–endothelin-1 interaction in humans. J. Appl. Physiol. 82(5): 1593–1600, 1997.—Healthy men received N G-monomethyl-l-arginine (l-NMMA) intravenously to study cardiovascular and metabolic effects of nitric oxide synthase blockade and whether this alters the response to endothelin-1 (ET-1) infusion. Controls only received ET-1.l-NMMA effects were that heart rate (17%), cardiac output (17%), and splanchnic and renal blood flow (both 33%) fell promptly (all P < 0.01). Mean arterial blood pressure (6%), and systemic (28%) and pulmonary (40%) vascular resistances increased ( P < 0.05 to 0.001). Arterial ET-1 levels (21%) increased due to a pulmonary net ET-1 release ( P < 0.05 to 0.01). Splanchnic glucose output (SGO) fell (26%, P < 0.01). Arterial insulin and glucagon were unchanged. Subsequent ET-1 infusion caused no change in mean arterial pressure, heart rate, or cardiac output, as found in the present controls, or in splanchnic and renal blood flow or splanchnic glucose output as previously found with ET-1 infusion (G. Ahlborg, E. Weitzberg, and J. M. Lundberg. J. Appl. Physiol. 79: 141–145, 1995). In conclusion, l-NMMA like ET-1, induces prolonged cardiovascular effects and suppresses SGO.l-NMMA causes pulmonary ET-1 release and blocks responses to ET-1 infusion. The results indicate that nitric oxide inhibits ET-1 production and thereby interacts with ET-1 regarding increase in vascular tone and reduction of SGO in humans.

A novel method for infusing drugs continuously into the renal artery of rats

1995 ◽  
Vol 268 (5) ◽  
pp. F967-F971 ◽  
Author(s):  
N. Parekh
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Renal Artery ◽  
Renal Blood Flow ◽  
Kidney Volume ◽  
Membrane Pump ◽  
Arterial Blood ◽  
Novel Method ◽  
Kidney Functions ◽  
Higher Doses

A method is described to achieve a homogeneous intravascular distribution of drugs infused into the renal artery of anesthetized rats. The device for intrarenal infusion consisted of a multiple-catheter system with a cannula inserted into the renal artery, which was connected to different lines for drug infusions and to one line for oscillating blood back and forth in the renal cannula with a magnetic membrane pump. The blood oscillation served to mix the drugs with renal arterial blood. To verify the usefulness of this procedure, Lissamine green was infused into the renal artery; without the mixing pump the dye was located on a small portion of the kidney surface, whereas the dye could be visualized evenly distributed and less concentrated over the entire kidney with the pump. With the mixing device, intrarenal infusion of angiotensin II, 5 pmol.kg-1.min-1, or norepinephrine, 150 pmol.kg-1.min-1, reduced renal blood flow by approximately 25% without affecting blood pressure. Tenfold higher doses given intravenously had comparable renal effects, but these increased systemic pressure. Without the mixing pump, vasoactive drugs given into the renal artery had a distinctly smaller effect on renal blood flow than with the pump (angiotensin II, 39%; norepinephrine, 49%; and acetylcholine, at 5 nmol.kg-1.min-1, 33%). The results show that intrarenally infused drugs, without a mixing device, have access to an unpredictably small kidney volume, and estimation of their effects on kidney functions can be equivocal. The present device ensures an adequate mixing of drugs with renal blood.

Effects of endothelin on renal function in dogs and rats

1990 ◽  
Vol 258 (4) ◽  
pp. F775-F780 ◽  
Author(s):  
R. O. Banks
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Renal Function ◽  
Renal Blood Flow ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Left Renal Artery ◽  
Ang Ii ◽  
Arterial Blood ◽  
Entire Experiment

Endothelin was infused for 20 min into the left renal artery of pentobarbital-anesthetized dogs at 1 (n = 6) and 10 (n = 5) ng.min-1.kg-1. Renal blood flow (flow probe) increased 6 +/- 2 (SE) and 29 +/- 2% during the first 5 min of endothelin infusion and then slowly decreased to 86 +/- 3 and 29 +/- 2% of control at 20 min, respectively; the low renal blood flow persisted for at least 30 min after endothelin infusion, and there were no systemic effects of the peptide at either dose. These effects of endothelin on renal function were not altered by the angiotensin (ANG) II receptor antagonist, [Sar1,Thr8]ANG II. In the rat, endothelin was infused intravenously into three groups of pentobarbital-anesthetized females for 30 min at 0.1 microgram.min-1.kg-1; five had endothelin only, six had either endothelin + [Sar1,Thr8]ANG II (n = 4, 1.0 micrograms.min-1.kg-1) or endothelin + saralasin (n = 2, 1 and 2 micrograms.kg-1.min-1), and five had endothelin + captopril (5 mg.h-1.kg-1). The inhibitors were infused throughout the entire experiment. During infusion of endothelin alone mean arterial blood pressure increased from 106 +/- 2 to 136 +/- 4 mmHg and the glomerular filtration rate decreased from 2.7 +/- 0.2 to 0.7 +/- 0.3 ml/min. Captopril attenuated the endothelin-induced changes in renal function but not the increase in mean arterial blood pressure, whereas the competitive ANG II receptor antagonists had no effect on either the systemic or renal actions of the peptide. These data demonstrate that endothelin is a potent renal vasoconstrictor with transient vasodilator effects and that the inhibition of kinin degradation may attenuate the renal actions of the peptide.

Decreased renal blood flow in the baboon during mild dynamic leg exercise

1979 ◽  
Vol 236 (1) ◽  
pp. H141-H150 ◽  
Author(s):  
A. R. Hohimer ◽  
O. A. Smith
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Rapid Onset ◽  
Whole Body ◽  
Left Renal Artery ◽  
Papio Cynocephalus ◽  
Flow Transducer ◽  
Arterial Blood ◽  
Leg Exercise ◽  
Renal Vascular

Twelve chair-restrained baboons (Papio cynocephalus) were conditioned with operant techniques and a food reward to perform 4 min of dynamic leg exercise. During the last minute of exercise, blood flow through the left renal artery, measured by an electromagnetic flow transducer, was decreased 19 +/- 2% SEM with respect to the minute of rest preceding the exercise. This response occurred within 1.5 min, was maintained throughout the exercise, and recovered to control within 2 min. Mean arterial blood pressure rose 17 +/- 2%; renal vascular resistance, 46 +/- 6%; heart rate, 42 +/- 4%; and whole-body oxygen consumption, 233 +/- 19%. Behavioral situations simulating the arousal and feeding components of the exercise task, but not requiring muscular exertion, did not alter renal blood flow. In four animals, blood flow to the contralateral but surgically denervated kidney was measured; it increased transiently at the onset of exercise, but returned to control by the last minute of work. Thus, the baboon, like man, shows a decrease in renal blood flow during exercise. This response has a rapid onset and recovery and is primarily neurally mediated.

Relationship of pyruvate and lactate during anaerobic metabolism. V: Coronary adequacy

1961 ◽  
Vol 200 (6) ◽  
pp. 1169-1176 ◽  
Author(s):  
William E. Huckabee
Keyword(s):  
Blood Flow ◽  
Coronary Flow ◽  
Cardiac Tissue ◽  
Anaerobic Metabolism ◽  
Constant Ratio ◽  
Blood Concentrations ◽  
Arterial Blood ◽  
Anesthetized Dogs ◽  
Relationship Of ◽  
The Relationship

Veno-arterial differences of pyruvate and lactate across the myocardium in chloralose-anesthetized dogs were very variable; in any one animal they changed continually with time despite constant blood flow and arterial blood concentrations. There was a systematic tendency of v-a lactate to vary with v-a pyruvate, as expressed in the calculated "Δ excess lactate," which remained nearly constant (or, if blood flow changed, bore a constant ratio to (a-v)O2). No change in Δ excess lactate from control values occurred in nonhypoxic experiments despite marked changes in v-a differences, arterial blood composition, and coronary flow. Cardiac Δ excess lactate became positive in most animals breathing 10% O2 in N2; output of excess lactate was also observed in all those in which moderate muscular exercise was induced. This anaerobic metabolism, or change in the relationship between pyruvate and lactate exchanges, was interpreted as an indication that O2 delivery response was not adequate to meet cardiac tissue requirements during such mild stresses when judged by the standards of adequacy of the basal state.

Effects of l-arginine on systemic and renal haemodynamics in conscious dogs

1991 ◽  
Vol 81 (6) ◽  
pp. 727-732 ◽  
Author(s):  
Marohito Murakami ◽  
Hiromichi Suzuki ◽  
Atsuhiro Ichihara ◽  
Mareo Naitoh ◽  
Hidetomo Nakamoto ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Renal Blood Flow ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Renal Haemodynamics ◽  
Conscious Dogs ◽  
Arginine Infusion ◽  
Arterial Blood

1. The effects of l-arginine on systemic and renal haemodynamics were investigated in conscious dogs. l-Arginine was administered intravenously at doses of 15 and 75 μmol min−1 kg−1 for 20 min. 2. Mean arterial blood pressure, heart rate and cardiac output were not changed significantly by l-arginine infusion. However, l-arginine infusion induced a significant elevation of renal blood flow from 50 ± 3 to 94 ± 12 ml/min (means ± sem, P < 0.01). 3. Simultaneous infusion of NG-monomethyl-l-arginine (0.5 μmol min−1 kg−1) significantly inhibited the increase in renal blood flow produced by l-arginine (15 μmol min−1 kg−1) without significant changes in mean arterial blood pressure or heart rate. 4. Pretreatment with atropine completely inhibited the l-arginine-induced increase in renal blood flow, whereas pretreatment with indomethacin attenuated it (63 ± 4 versus 82 ± 10 ml/min, P < 0.05). 5. A continuous infusion of l-arginine increased renal blood flow in the intact kidney (55 ± 3 versus 85 ± 9 ml/min, P < 0.05), but not in the contralateral denervated kidney (58 ± 3 versus 56 ± 4 ml/min, P > 0.05). 6. These results suggest that intravenously administered l-arginine produces an elevation of renal blood flow, which may be mediated by facilitation of endogenous acetylcholine-induced release of endothelium-derived relaxing factor and vasodilatory prostaglandins.

Tubuloglomerular feedback dynamics and renal blood flow autoregulation in rats

1991 ◽  
Vol 260 (1) ◽  
pp. F53-F68 ◽  
Author(s):  
N. H. Holstein-Rathlou ◽  
A. J. Wagner ◽  
D. J. Marsh
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Renal Blood Flow ◽  
Slow Component ◽  
Broad Band ◽  
Experimental Results ◽  
Tubuloglomerular Feedback ◽  
Single Frequency ◽  
Vascular Control ◽  
Arterial Blood

To decide whether tubuloglomerular feedback (TGF) can account for renal autoregulation, we tested predictions of a TGF simulation. Broad-band and single-frequency perturbations were applied to arterial pressure; arterial blood pressure, renal blood flow and proximal tubule pressure were measured. Data were analyzed by linear systems analysis. Broad-band forcings of arterial pressure were also applied to the model to compare experimental results with simulations. With arterial pressure as the input and tubular pressure, renal blood flow, or renal vascular resistance as outputs, the model correctly predicted gain and phase only in the low-frequency range. Experimental results revealed a second component of vascular control active at 100-150 mHz that was not predicted by the simulation. Forcings at single frequencies showed that the system behaves linearly except in the band of 33-50 mHz in which, in addition, there are autonomous oscillations in TGF. Higher amplitude forcings in this band were attenuated by autoregulatory mechanisms, but low-amplitude forcings entrained the autonomous oscillations and provoked amplified oscillations in blood flow, showing an effect of TGF on whole kidney blood flow. We conclude that two components can be detected in the dynamic regulation of renal blood flow, i.e., a slow component that represents TGF and a faster component that most likely represents an intrinsic vascular myogenic mechanism.

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