HEPATIC ARTERIAL AND PORTAL FLOW IN CARDIOGENIC AND HEMORRHAGIC-SHOCK IN AWAKE DOGS

  • 1 January 1982
    • journal article
    • research article
    • Vol. 9  (1) , 17-26
Abstract
The changes in liver blood flow produced by experimental cardiogenic and hemorrhagic shock are relatively unexplored. Fifteen unanesthetized dogs in which electromagnetic blood flow transducers were implanted on the common hepatic artery and portal vein were subjected to acute myocardial infarction by Hg embolization of the circumflex coronary artery. Another group of 10 dogs were bled to an arterial pressure of 40 mm Hg and maintained at that level for 2 h before reinfusion. Six additional dogs in which blood flow transducers were implanted on the superior mesenteric artery and portal vein also were subjected to hemorrhage. In 3 of the 6, phenoxybenzamine was infused directly into the superior mesenteric artery 45 min prior to bleed-out. During cardiogenic shock, both hepatic arterial and portal venous flows fell. While portal flow continued to fall, eventually stabilizing at values 36 .+-. 3% of control, hepatic arterial flow subsequently rose, reaching values 93 .+-. 9% above control. Total liver blood flow, after an initial decline to 53 .+-. 4% of control levels, rose as a result of the increased hepatic arterial flow to 73 .+-. 4% of control values. During hemorrhage, both hepatic arterial and portal venous flows decreased as aortic pressure fell. Within 5 min of reinfusion, hepatic arterial flow surpassed its control values. Portal flow also increased but, on a percentage basis, not to so great an extent. Flow in hepatic artery remained high for 40 min after reinfusion, while portal flow rapidly decreased to levels seen at the end of hemorrhage. In hemorrhage without .alpha.-adrenergic receptor blockade, the superior mesenteric bed constricted, thereby supporting systemic pressure. With .alpha.-adrenergic blockade, mesenteric flow became pressure-dependent and no longer acted as a homeostatic mechanism.

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