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

1966 ◽  
Vol 10 (3) ◽  
pp. 230???231
Author(s):  
R. C. CAMISHION ◽  
N. H. FISHMAN ◽  
Hebbel E. Hoff
1956 ◽  
Vol 186 (1) ◽  
pp. 74-78 ◽  
Author(s):  
E. D. Frank ◽  
H. A. Frank ◽  
S. Jacob ◽  
H. A. E. Weizel ◽  
H. Korman ◽  
...  

Norepinephrine infusion did not prolong the survival or effect the recovery of dogs in hemorrhagic shock unresponsive to replacement transfusion. During its pressor action in shock, either before or after replacement transfusion, norepinephrine infusion increased coronary, cerebral and adrenal blood flow, reduced renal blood flow, and did not change hepatic blood flow. Cardiac output was increased in oligemic shock but not after blood replacement. Pulmonary arterial pressure and right and left auricular pressures were raised by norepinephrine infusion in all phases of hemorrhagic shock, and calculated pulmonary vascular resistance was reduced.


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)


1992 ◽  
Vol 262 (1) ◽  
pp. G92-G98 ◽  
Author(s):  
P. Wang ◽  
Z. F. Ba ◽  
J. Burkhardt ◽  
I. H. Chaudry

Although Ringer lactate (RL) is routinely used for resuscitation, it is not known whether the volume of RL that restores cardiac output after severe hemorrhagic shock also restores the depressed effective hepatic blood flow (EHBF). To study this, a 5-cm midline laparotomy was performed in rats (i.e., trauma induced), and the animals were then bled to and maintained at a mean arterial pressure of 40 mmHg until 40% of maximum bleedout volume was returned in the form of RL. Animals were then resuscitated with four or five times the volume of maximum bleedout with RL. EHBF was determined during hemorrhage and at various intervals thereafter by an in vivo indocyanine green (ICG) clearance technique and corrected by the appropriate hepatic extraction ratio for ICG. Cardiac output was determined by ICG dilution, and hepatic microvascular blood flow (HMBF) was measured with laser Doppler flowmetry. In addition, hepatic blood flow was assessed by using radioactive microspheres. Results indicate that resuscitation markedly improved but did not restore the depressed EHBF after trauma and hemorrhagic shock despite the fact that cardiac output was restored. Similar changes in EHBF, HMBF, and hepatic blood flow as determined by microspheres were observed, suggesting that the in vivo ICG clearance is a reliable method to assess effective hepatic perfusion. Thus the lack of restoration of EHBF may be responsible for the subsequent hepatocellular dysfunction after trauma and severe hemorrhage.


1965 ◽  
Vol 50 (4) ◽  
pp. 561-566 ◽  
Author(s):  
Worthington G. Schenk ◽  
N. Anders Delin ◽  
Lawrence Pollock ◽  
Kjartan B. Kjartansson ◽  
John W. Boylan

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.


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 ◽  
...  

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