Waxman K, Clark L, Soliman M H, Parazin S
Department of Surgery, University of California, Irvine, Orange 92668.
Crit Care Med. 1991 May;19(5):728-31. doi: 10.1097/00003246-199105000-00021.
Pentoxifylline improves survival in animal models of hemorrhagic shock. The purpose of this study was to determine the physiologic effects of pentoxifylline in hemorrhagic shock that may be responsible for improved survival.
Randomized, prospective, blinded trials in Sprague-Dawley rats subjected to hemorrhage and resuscitation, with or without pentoxifylline.
Pentoxifylline had no effect on BP or cardiac output. However, tissue oxygenation and oxygen consumption were increased with pentoxifylline resuscitation. Pentoxifylline resuscitation also significantly decreased polymorphonuclear leukocyte adhesiveness.
Pentoxifylline improves tissue oxygenation and oxygen consumption posthemorrhage and this effect is not due to increased cardiac output. Therefore, it must be due to improved microcirculatory blood flow. This effect may be due to decreased polymorphonuclear leukocyte adhesiveness induced by pentoxifylline resuscitation.
己酮可可碱可提高失血性休克动物模型的生存率。本研究的目的是确定己酮可可碱在失血性休克中的生理作用，这些作用可能是其提高生存率的原因。
对接受出血和复苏的Sprague-Dawley大鼠进行随机、前瞻性、盲法试验，分为使用或不使用己酮可可碱两组。
己酮可可碱对血压或心输出量无影响。然而，己酮可可碱复苏可增加组织氧合和氧消耗。己酮可可碱复苏还显著降低了多形核白细胞的黏附性。
己酮可可碱可改善出血后的组织氧合和氧消耗，且这种作用并非由于心输出量增加。因此，其作用必定归因于微循环血流的改善。这种作用可能是由于己酮可可碱复苏诱导多形核白细胞黏附性降低所致。
