Mackway-Jones K, Foëx B A, Kirkman E, Little R A
North Western Injury Research Centre, University of Manchester, United Kingdom.
J Trauma. 1999 Sep;47(3):481-5. doi: 10.1097/00005373-199909000-00008.
Tissue injury modifies heart rate and blood pressure responses to hemorrhage. The effect of concomitant injury on the hemorrhage-induced redistribution of cardiac output is much less clear. However, if injury elicits the visceral alerting response of the defense reaction, then a change in this redistribution of peripheral blood flow might be expected. If such a change compromised the gut circulation, then it might explain the deleterious effects of injury on the ability to withstand hemorrhage.
Immature pigs anesthetized with Saffan were bled 30% of blood volume with or without concomitant somatic afferent (brachial) nerve stimulation (to mimic injury). In addition to global cardiovascular and oxygen transport variables, blood flow was measured in the cranial mesenteric (gut) and right femoral (skeletal muscle) arteries after a 60-minute stabilization period after surgery, at the end of the 30-minute hemorrhage, and after a 30-minute shock period.
Hemorrhage induced the expected cardiovascular and oxygen transport changes accompanied by a reduction in skeletal muscle blood flow and a 55% increase in skeletal muscle vascular resistance, but gut blood flow and vascular resistance were unchanged. However, in the presence of brachial nerve stimulation, the pattern of response to hemorrhage was modified, such that gut blood flow was now reduced and gut vascular resistance increased.
The sparing of the gut circulation after hemorrhage was abolished in the presence of "injury." This finding is consistent with injury eliciting the defense reaction and may help explain the deleterious effects of injury on resistance to hypovolemia.
