ALLOPURINOL PLUS STANDARD RESUSCITATION PRESERVES HEPATIC BLOOD FLOW AND FUNCTION FOLLOWING HEMORRHAGIC SHOCK

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.

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Hepatic Blood Flow and Function in Elderly Patients Undergoing Laparoscopic Cholecystectomy

Anesthesia & Analgesia ◽

10.1097/00000539-200005000-00037 ◽

2000 ◽

Vol 90 (5) ◽

pp. 1198-1202 ◽

Cited By ~ 54

Author(s):

Kinya Sato ◽

Takae Kawamura ◽

Reiji Wakusawa

Keyword(s):

Blood Flow ◽

Laparoscopic Cholecystectomy ◽

Elderly Patients ◽

Hepatic Blood Flow ◽

And Function

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Hepatic blood flow in experimental hemorrhagic shock

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1962.202.1.7 ◽

1962 ◽

Vol 202 (1) ◽

pp. 7-11 ◽

Cited By ~ 17

Author(s):

Edward D. Frank ◽

Howard A. Frank ◽

Stanley W. Jacob ◽

Jacob Fine

Keyword(s):

Blood Flow ◽

Arterial Pressure ◽

Portal Vein ◽

Hemorrhagic Shock ◽

Hepatic Vein ◽

Hepatic Blood Flow ◽

Marked Reduction ◽

Blood Replacement ◽

Transient Improvement ◽

Experimental Hemorrhagic Shock

In dogs in hemorrhagic shock, the blood flow and oxygenation of the liver were measured with a catheter in a hepatic vein. There is a marked reduction in hepatic blood flow and oxygenation throughout hemorrhagic shock. There is transient improvement following blood replacement and additional transfusions. Arterial shunts into the portal vein may restore hepatic oxygenation to preshock levels. Norepinephrine does not increase hepatic blood flow even though arterial pressure is restored to normal. Dibenamine pretreatment sustains the hepatic flow to some extent during hypovolemia; antibiotic pretreated animals do not differ from controls.

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Effects of N-Acetylcysteine on Hepatic Blood Flow and Function

Critical Care Medicine ◽

10.1097/00003246-199802000-00048 ◽

1998 ◽

Vol 26 (2) ◽

pp. 415 ◽

Cited By ~ 3

Author(s):

Peter Ott

Keyword(s):

Blood Flow ◽

Hepatic Blood Flow ◽

And Function

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Regulation of hepatic blood flow during resuscitation from hemorrhagic shock: role of NO and endothelins

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1997.272.6.h2736 ◽

1997 ◽

Vol 272 (6) ◽

pp. H2736-H2745 ◽

Cited By ~ 7

Author(s):

B. H. Pannen ◽

M. Bauer ◽

G. F. Noldge-Schomburg ◽

J. X. Zhang ◽

J. L. Robotham ◽

...

Keyword(s):

Blood Flow ◽

Hemorrhagic Shock ◽

Receptor Antagonist ◽

Hepatic Blood Flow ◽

Vehicle Group ◽

Venous Flow ◽

Systemic Hemodynamic ◽

Eta Receptor ◽

Eta Receptor Antagonist

We determined the role of nitric oxide (NO) and endothelins (ETs) in the regulation of hepatic blood flow during resuscitation from hemorrhagic shock (HS) in anesthetized rats. Volume resuscitation restored systemic hemodynamics and increased hepatic arterial and portal venous flow above baseline in the vehicle group. Presence of N omega-nitro-L-arginine methyl ester (L-NAME, 1 mg/kg) during resuscitation increased systemic vascular resistance (SVR) above baseline, prevented the restoration of hepatic arterial flow, and abolished portal hyperemia. Although the ETA+B-receptor antagonist bosentan (10 mg/kg) did not alter the systemic hemodynamic response, it abolished the hepatic arterial and portal hyperemia. The ETA-receptor antagonist BQ-610 (150 micrograms/kg) reduced SVR below baseline, allowed hepatic arterial hyperemia to occur, and further enhanced the portal venous hyperemia. This indicates that 1) NO reduces SVR and acts to preserve hepatic blood flow during resuscitation from HS; 2) ETA-receptor-mediated vasoconstriction counteracts the systemic and portal hemodynamic effects of NO; and 3) simultaneous ETB-receptor stimulation enhances blood flow to the liver and may serve to modulate the ETA-receptor-mediated vasoconstrictive effects of ETs.

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