DEVELOPMENT OF CIRCULATORY AND METABOLIC SHOCK FOLLOWING TRANSIENT PORTAL TRIAD OCCLUSION

Liver ischemia is purposefully induced by portal triad occlusion (PTO) in several clinical situations including liver surgery for trauma, tu mor, and transplantation. Despite significant morbidity from PTO, the hemodynamic and metabolic effects of PTO have not been evaluated relat ive to duration of ischemia. We investigated this using a total hepati c ischemia model. Rats received isoflurane anesthesia, carotid artery and jugular vein cannulation, and serial measurements of cardiac outpu t (GO), mean arterial pressure (MAP), heart rate (HR), central venous pressure (CVP), stroke volume (SV), systemic vascular resistance (SVR) , superior mesenteric artery blood flow (SMAF), intestinal vascular re sistance (IVR), pH, pCO(2), pO(2), lactate, glucose, hematocrit (HCT), white blood cell count (WBC), and total neutrophils. Each group recei ved 0, 15, 30, 45, or 60 min of PTO followed by 2 hr of reperfusion. A ll sham ischemia animals remained hemodynamically stable throughout th e study. However, in the ischemic groups, there were significant time- dependent decreases in MAP, HR, CO, CVP, SV, SMAF, and pH, and increas es in SVR, IVR, HCT, and lactate, while pCO(2), pO(2), glucose, and WB C remained stable. All of the ischemic animals survived except those t hat received 60 min of PTO. In this group, all of the animals survived the ischemic period; however, only one animal survived beyond 60 min of reperfusion. These data demonstrate a time-dependent circulatory an d metabolic shock following PTO heralded by intestinal venous pooling and loss of intravascular fluid, and culminating in death. Careful hem odynamic monitoring and restoration of blood volume in the trauma pati ent may reduce morbidity and mortality.