Mechanism of Microcirculatory Failure in Shock.
Abstract
A prolonged reduction of visceral organ blood flow has been clearly demonstrated in our laboratory in primates after resuscitation from hemorrhagic shock. This is consistent with observations on visceral function and blood volume changes in humans after successful resuscitation from shock. The background for this hypothesis is discussed in detail. The present proposal using both a primate shock model and a pig hind limb perfusion system begins to evaluate these possible mechanisms and investigates empirical treatment mechanisms as follows: (1) Studies are undertaken on the effects of controlled vasodilator therapy on our primate shock model. (2) Determinations of hormone levels relative to production of catecholamines, renin and angiotensin II and Thromboxane A2 and prostacyclin are undertaken over an 18-hour period in our primate shock model. (3) Hemodynamic and metabolic effects of hind limb perfusion with blood from an animal 8 hours after resuscitation from hypovolemic shock. Finally, hypertonic glucose is investigated as a stop-gap measure for preserving life in primates in hemorrhagic shock. The rationale for this concept is well supported from recent research on the benefits of supplying high dose glucose as an acute energy substrate in shock states in man.
Document Details
- Document Type
- Technical Report
- Publication Date
- Jun 01, 1980
- Accession Number
- ADA134406
Entities
People
- J. Judson Mcnamara
Organizations
- The Queen's Medical Center