Profile of Circulating Vasoactive Substances in Hemorrhagic Shock and Their Pharmacologic Manipulation

Abstract

A B S T R A C T (a)Hemorrhage(b) Plasma catecholamines (CA) steadily increased during hemorrhage and peaked during compensation (a 100-fold increase). The CA decreased progressively during decompensation.(c) Prostaglandin (PG) E-like material was observed in arterial blood for 15-60 min (after hemorrhage); the peak arterial concentration was 2.6 ng/ml blood. Indomethacin (i.v., before 80% of maximum bleedout): (i) confirmed the presence of PGE, (ii) increased blood pressure, and (iii) increased blood loss.(d) Thus: peripheral resistance during hemorrhagic shock seems temporally correlated with blood CA levels (and not PRA), and the renin-AII system contributes to the maintenance of vascular resistance and may markedly decrease perfusion of organs, such as kidney; the administration of the proper combination of specific antagonists of vasoconstrictor humoral substances may radically improve organ perfusion and could contribute to ultimate recovery from hemorrhagic shock.Preliminary results of this study were presented at the

Short‐term hormonal control of hepatic carbohydrate and lipid catabolism

“…As would be expected, they have a role in the maintenance of blood pressure, especially in haemorrhagic states [52]. The circulating concentrations of adrenaline, vasopressin and angiotensin II also increase in other conditions (e.g., starvation, hypoglycaemia, Na' depletion) to levels which will affect the liver (see discussion in ref.…”

Mechanisms of Renin Secretion during Hemorrhage in the Dog

“…The enhancement ofthe activity ofthe renin-angiotensin system during hemorrhage is a well-accepted phenomena (18)(19)(20) that has stimulated physiologic investigation for a number of years. Studies in the nonfiltering kidney suggest that hemorrhage may provide a multifactorial stimulus for renin release (9 Although Romero et al (11) found that inhibition of prostaglandin synthesis abolished the renin response to hemorrhage in the conscious rabbit, this was not found to be the case in the present study in the anesthetized dog.…”

Anesthetic Influences on Myocardial and Hepatic Energy Metabolism in Hemorrhaged Spontaneous Hypertensive Rats.

“…However, hepatic glycogen content in the SHRs receiving enflurane was significantly lower than that in those receiving pentobarbital, and both myocardial and hepatic L/P ratios in the SHRs receiving enflurane were significantly higher than those receiving none. It is well established that circulating cathecolamines are raised during hemorrhage and this increases glycogenolysis and hyperglycemia (Jakschick et al 1974). It is also stated that the elevation in L/P ratio frequently observed in the shock state reflects decreased cell phosphorylation rather than the cell hypoxia (Yoshitake et al 1983).…”