The Journal of surgical research
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Effective hepatic blood flow is thought to play a critical role in outcome following portal decompressive procedures. We have shown previously that hepatic arterialization occurs soon after shunting, preserving nutrient flow, but the remote effects of shunting are unknown. The purpose of this study was to determine the effect of small-diameter prosthetic H-graft portacaval shunt (HGPCS) on effective hepatic blood flow (EHF) and portal pressures 1 year from shunt placement. ⋯ Recollateralization of varices and progression of cirrhosis may account for the observed reductions in EHF at 1 year. Regardless of the cause, diminution of EHF at 1 year is well compensated as demonstrated by minimal encephalopathy and ascites, improved hepatic function reflected in blood chemistry profiles, and good survival.
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We studied the hemodynamic effects of delayed initiation (6 h postburn) of antioxidant therapy with high-dose vitamin C in second-degree thermal injuries. Seventy percent body surface area burns were produced by subxiphoid immersion of 12 guinea pigs into 100 degrees C water for 3 s. The animals were resuscitated with Ringer's lactate solution (R/L) according to the Parkland formula (4 ml/kg/% burn during the first 24 h) from 6 h postburn, after which the resuscitation fluid volume was reduced to 25% of the Parkland formula volume. ⋯ The vitamin C group showed significantly (P < 0.05) lower hematocrits 8 and 24 h postburn, and higher cardiac outputs after 7 h postburn. At 24 h postburn, the burned skin in the vitamin C group had a significantly (P < 0.05) lower water content (73.1 +/- 1.1) than that of the control group (76.0 +/- 0.8). In conclusion, delayed initiation of high-dose vitamin C therapy beginning 6 h postburn with 25% of the Parkland formula volume significantly reduced edema formation in burned tissue, while maintaining stable hemodynamics.
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Effects of different durations of total warm ischemia of the gut on rat mesenteric microcirculation.
Gut injury due to ischemia and reperfusion (I/R) plays a pivotal role in many clinical conditions, such as small bowel transplantation, heart or aortic surgery in adults, and necrotizing enterocolitis in neonates. The influence of ischemic events on microcirculatory mechanisms is not well understood. Therefore, we studied, in vivo, local perfusion and leukocyte-vessel wall interactions before and after different periods of total warm ischemia of the whole gut and subsequent reperfusion in mesenteric microvessels. ⋯ Even short periods of total warm ischemia of the whole gut induce severe attenuation of venular blood flow with an increase in leukocyte-vessel wall interactions. These changes increase with prolongation of the ischemic period. A 60-min period of total warm ischemia is fatal during the early reperfusion phase.
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Postischemic reperfusion injury is caused by microcirculatory disturbances, including both nutritive perfusion failure (no reflow) and leukocyte activation (reflow paradox). Recent studies brought evidence that pentoxifylline (PTX) reduces tissue injury, decreases enzyme release, and improves survival after normothermic liver ischemia/reperfusion. The mechanisms of action, however, by which PTX protects postischemic tissue from injury have not been elucidated yet. ⋯ Microvascular reperfusion after 20 min portal triad cross-clamping was characterized by the cessation of blood flow within individual sinusoids (no reflow) and accumulation of leukocytes within the hepatic microvasculature, with stasis in sinusoids and rolling and firm adherence in postsinusoidal venules. PTX (20 mg/kg x hr i.v.) significantly (P < 0.05) attenuated microvascular leukocyte accumulation (44,600 +/- 1833 mm(-3) vs 67,684 +/- 2620 mm(-3) in saline-treated controls) and firm adherence of leukocytes in postsinusoidal venules (316.9 +/- 40.9 mm(-2) vs 522.9 +/- 95.0 mm(-2)); however, PTX did not influence manifestation of individual sinusoidal perfusion failure. Since reperfusion-induced parenchymal cell damage was found reduced in treated animals, we conclude that PTX attenuates postischemic injury in rat liver by reduction of leukocytic/inflammatory response but not by prevention of nutritive perfusion failure.
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Gut and hepatic dysfunction, during and after hypovolemic shock, have been implicated as causative mechanisms in the development of multiple system organ failure in the trauma patient. Current techniques of assessment of perfusion only detect changes in systemic oxygen transport. We designed an animal model that can measure changes in oxygen transport in the liver and gut during hypovolemic shock and resuscitation. ⋯ These data show that hepatic and gut vascular beds are better perfused when resuscitation from hemorrhage is guided by systemic oxygen transport measurements compared to resuscitation guided by blood pressure.