Microvascular responses of intact and adrenal medullectomized rats to hemorrhagic shock

Evidence indicates that during the later stages of hemorrhagic shock there appears to be a loss of response to the control systems that would normally maintain an adequate peripheral resistance. Therefore, the reactivity of the cremaster muscle microcirculation of pentobarbital-anesthetized Wistar rats, intact and adrenal medullectomized, was studied using videomicroscopy. The left cremaster muscle was spread over an optical port in a bath filled with modified Krebs solution (pH 7.4, 34 degrees C). The right femoral artery was cannulated for determination of mean arterial pressure (Pm) and for hemorrhage of the rat. Following control measurements of Pm and microvessel diameters, cumulative dose-response curves of arteriolar and venular diameters to topical norepinephrine (NE) (10(-9) - 10(-4) M) were obtained. The protocols for intact and medullectomized groups were: 1) hypovolemic shock (shed blood not reinfused)--hemorrhage of 3.2 ml/100 g, compensation allowed, and NE dose-response curves repeated and obtained again during late shock as determined by Pm declining below 60 mmHg; and 2) normovolemic shock (condition after reinfusion of shed blood)--hemorrhage into a reservoir to Pm of 40 mmHg, maintenance at this level until 25% of the bled volume had been taken back (irreversible shock), and then reinfusion of the remainder of the blood. After blood reinfusion, the NE dose-response curves were repeated and obtained again during late shock, as determined by Pm below 60 mmHg. In all of the bled animals, the A1 arterioles were constricted posthemorrhage. The A2 arterioles were constricted only in the hypovolemic intact group. The A3 arterioles of all groups were not significantly changed from control. The constricted arterioles remained so. However, the other arterioles in all groups were unchanged during the several hours until death. The threshold concentration of NE for constriction of arterioles (10% or greater) was significantly increased (decreased sensitivity) during shock in all four groups. The response of the medullectomized rats to normovolemic shock was similar to that of the intact group, indicating that the circulating catecholamines were not essential. The response of medullectomized rats to hypovolemic shock was more severe and indicated the need for circulating catecholamines to compensate for the blood volume loss.