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

1965 ◽  
Vol 50 (4) ◽  
pp. 561-566 ◽  
Author(s):  
Worthington G. Schenk ◽  
N. Anders Delin ◽  
Lawrence Pollock ◽  
Kjartan B. Kjartansson ◽  
John W. Boylan
1989 ◽  
Vol 256 (4) ◽  
pp. H1079-H1086 ◽  
Author(s):  
G. A. Riegger ◽  
D. Elsner ◽  
E. P. Kromer

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)


2019 ◽  
Vol 317 (5) ◽  
pp. E871-E878 ◽  
Author(s):  
Eleni Rebelos ◽  
Prince Dadson ◽  
Vesa Oikonen ◽  
Hidehiro Iida ◽  
Jarna C. Hannukainen ◽  
...  

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.


1966 ◽  
Vol 10 (3) ◽  
pp. 230???231
Author(s):  
R. C. CAMISHION ◽  
N. H. FISHMAN ◽  
Hebbel E. Hoff

1969 ◽  
Vol 47 (1) ◽  
pp. 25-32 ◽  
Author(s):  
Keith L. MacCannell

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.


Nephron ◽  
1989 ◽  
Vol 53 (4) ◽  
pp. 353-357 ◽  
Author(s):  
T. Kishimoto ◽  
W. Sakamoto ◽  
T. Nakatani ◽  
T. Ito ◽  
K. Iwai ◽  
...  

1992 ◽  
Vol 76 (5) ◽  
pp. 812-821 ◽  
Author(s):  
Douglas S. DeWitt ◽  
Donald S. Prough ◽  
Carol L. Taylor ◽  
John M. Whitley

✓ The authors investigated the effects of transient, mild hemorrhagic hypotension after fluid-percussion traumatic brain injury on intracranial pressure, cerebral blood flow (CBF), cerebral oxygen delivery (CBF × arterial O2 content), and electroencephalographic (EEG) activity. Adult mongrel cats were anesthetized with 1.6% isoflurane in N2O:O2 (70:30) and prepared for trauma and for radioactive microsphere CBF measurement. Isoflurane concentration was decreased to 0.8%, and the cats were randomly assigned to one of four control groups or to an experimental group. Animals in the four control groups underwent either mild hemorrhage (18 ml · kg−1) immediately followed by resuscitation with equal volumes of 10% Hetastarch (eight cats), mild hemorrhage followed by replacement of shed blood (six cats), isovolemic hemodilution with 18 ml · kg−1 of Hetastarch (six cats), or moderate (2.2 atm) trauma alone (eight cats). The experimental group received a combination of trauma and mild hemorrhage followed by resuscitation with Hetastarch (eight cats). Mild hemorrhage produced no significant changes in CBF, renal blood flow, or cardiac output. Following resuscitation from mild hemorrhage, mean arterial blood pressure, cardiac output, renal blood flow, and CBF were not significantly different from baseline; cardiac output and renal blood flow did not differ significantly from baseline 2 hours after Hetastarch resuscitation. Neither hemorrhage nor trauma alone produced significant decreases in CBF or in EEG activity, but trauma followed by hemorrhage and resuscitation produced significant (p < 0.01) decreases in CBF, cerebral oxygen delivery, and EEG score. These data demonstrate that, following traumatic brain injury, even mild hemorrhagic hypotension is associated with significant deficits in cerebral oxygen availability and neurological function.


1992 ◽  
Vol 13 (6) ◽  
pp. 394
Author(s):  
H. Kynaston ◽  
M. O??Driscoll ◽  
S. Grime ◽  
J. Yates ◽  
B. Taylor ◽  
...  

1995 ◽  
Vol 269 (1) ◽  
pp. H62-H71 ◽  
Author(s):  
B. J. Janssen ◽  
J. Oosting ◽  
D. W. Slaaf ◽  
P. B. Persson ◽  
H. A. Struijker-Boudier

In conscious resting rats, beat-to-beat fluctuations in systemic mean arterial pressure (MAP) were compared with those in cardiac output and those in blood flow in the renal, mesenteric, and hindquarter vascular beds. Spontaneous oscillations (lability) in MAP were observed in frequency bands centered about 1.6 Hz (high: HF), 0.4 Hz (mid: MF), and 0.13 Hz (low: LF). Lability of MAP was confined within the LF (approximately 8 s) band. Lability of cardiac output, on the other hand, showed primary HF oscillations. LF oscillations in regional blood flow were most prominent in the mesenteric and renal vascular beds. In these beds, LF oscillations in blood flow showed negative phase angles with MAP, whereas those between MAP and hindquarter blood flow were positive. Cross correlation analysis indicated that approximately 2 s following a LF change in MAP, LF changes in mesenteric and renal blood flow occurred opposite to those of MAP. Changes in hindquarter flow were negatively correlated with those in MAP about zero time delay. Admittance gains were > or = 1 across all frequencies for all vascular beds, indicating the absence of autoregulation. This hemodynamic pattern suggests that myogenic mechanisms predominantly control mesenteric and renal blood flow in a nonautoregulatory but rather superregulatory manner, while autonomic mechanisms regulate hindquarter blood flow. Thus, in conscious resting rats, spontaneous fluctuations in systemic arterial pressure predominantly exhibit slow (approximately 8 s) oscillations, which do not arise from fluctuations in cardiac output, but originate from regionally specific myogenic oscillatory mechanisms contributing to resistance to flow.


1997 ◽  
Vol 273 (5) ◽  
pp. H2452-H2457 ◽  
Author(s):  
Till Neumann ◽  
Gerd Heusch

The present study characterizes the hemodynamic and neurohumoral responses to moderate treadmill exercise in conscious dogs with pacing-induced heart failure. Seven dogs were instrumented with a left ventricular micromanometer, ultrasonic crystals for the measurement of systolic wall thickening, left atrial and aortic catheters for the injection of colored microspheres and reference withdrawal, respectively, and ventricular pacing leads with a subcutaneous pacemaker. Dogs were run on a treadmill at a speed of 5 km/h. After control studies, heart failure was induced by rapid left ventricular pacing at 250 beats/min for (mean ± SD) 23 ± 6 days. In the control state, cardiac output was increased from 4.5 ± 1.5 to 7.9 ± 1.4 l/min ( P < 0.05 vs. rest). With heart failure, cardiac output was decreased to 2.5 ± 0.5 l/min at rest ( P < 0.05 vs. control state) and was only 3.0 ± 0.3 l/min during exercise ( P < 0.05 vs. control state; not significant vs. rest). Myocardial and, more so, skeletal muscle blood flows at rest were reduced in heart failure; their increases with exercise were attenuated. An increase in renal blood flow during exercise in the control state was no longer seen in heart failure. Increases in plasma catecholamines and lactate during exercise were more pronounced in heart failure. In conclusion, in heart failure, the increase in cardiac output during exercise was largely attenuated. Increased catecholamine levels may have contributed to splanchnic vasoconstriction and preferential distribution of cardiac output into the working skeletal muscle.


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