Resuscitation · 2007
Hemodynamic changes in visceral organs following closed head trauma in rats.
СтатьяНазвание и аннотация: Перевод в очереди
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Kirshtein Boris, Hilzenrat Nir, Yaari Arie, Souter Karen J, Artru Alan A, Shapira Yoram, Sikuler Emanuel
Аннотация
BACKGROUND: Gastrointestinal (GI) tract dysfunction is well documented following head injury. Our study sought to determine whether head injury causes an immediate impairment of the splanchnic circulation which may contribute to later GI sequelae.
METHODS: Three groups of eight rats each received either no closed head trauma (CHT) (group 1) or CHT (groups 2 and 3) immediately following baseline measurements at time 0. The primary measures of interest - individual organ blood flows and cardiac output (radioactive microspheres), and individual organ and systemic vascular resistances - were determined in the control group, at 5 min after CHT in group 2, and at 15 min after CHT in group 3.
RESULTS: CHT caused no significant change in portal venous inflow (flows were 2.40+/-0.36, 2.38+/-0.54, and 2.33+/-0.62 ml min(-1) 100g(-1)bw, mean+/-S.D., in groups 1, 2, and 3, respectively). Individual organ and total hepatic blood flow, cardiac index, splanchnic, portal, and total peripheral resistance, and mean arterial or portal venous pressure also did not differ significantly among groups.
CONCLUSION: We found no significant changes in splanchnic circulation immediately after CHT in this rat model. Our results do not support the hypothesis that the splanchnic circulation is impaired immediately after head injury and that splanchnic blood flow impairment immediately after head injury may contribute to post-head injury GI dysfunction.
METHODS: Three groups of eight rats each received either no closed head trauma (CHT) (group 1) or CHT (groups 2 and 3) immediately following baseline measurements at time 0. The primary measures of interest - individual organ blood flows and cardiac output (radioactive microspheres), and individual organ and systemic vascular resistances - were determined in the control group, at 5 min after CHT in group 2, and at 15 min after CHT in group 3.
RESULTS: CHT caused no significant change in portal venous inflow (flows were 2.40+/-0.36, 2.38+/-0.54, and 2.33+/-0.62 ml min(-1) 100g(-1)bw, mean+/-S.D., in groups 1, 2, and 3, respectively). Individual organ and total hepatic blood flow, cardiac index, splanchnic, portal, and total peripheral resistance, and mean arterial or portal venous pressure also did not differ significantly among groups.
CONCLUSION: We found no significant changes in splanchnic circulation immediately after CHT in this rat model. Our results do not support the hypothesis that the splanchnic circulation is impaired immediately after head injury and that splanchnic blood flow impairment immediately after head injury may contribute to post-head injury GI dysfunction.