Wang W, Wang P, Chaudry I H
Center for Surgical Research, Department of Surgery, Brown University School of Medicine and Rhode Island Hospital, Providence 02903, USA.
Crit Care Med. 1998 Jan;26(1):101-7. doi: 10.1097/00003246-199801000-00023.
Although pentoxifylline produces various beneficial effects following adverse circulatory conditions, it is not known whether this agent has any effects on gut lipid metabolism after trauma-hemorrhage and resuscitation. The aim of this study, therefore, was to determine whether or not administration of pentoxifylline after trauma-hemorrhagic shock has any salutary effects on gut ketogenesis.
A prospective, controlled animal study.
A university research laboratory.
Fifty-six male Sprague-Dawley rats.
Rats underwent a midline laparotomy (i.e., trauma-induced) and were bled to and maintained at a mean arterial pressure of 40 mm Hg until 40% of the shed blood volume was returned in the form of lactated Ringer's solution. The animals were then resuscitated with four times the volume of maximal bleedout with lactated Ringer's solution over 60 mins. Pentoxifylline (50 mg/kg body weight) or an equivalent volume of normal saline was infused intravenously over 100 mins during and after resuscitation. For in vivo lipid loading, one milliliter of olive oil was given intraduodenally on the completion of resuscitation. Blood samples from portal vein and carotid artery, as well as enterocytes from proximal small intestine, were obtained at 1.5 hrs after fat feeding.
Mitochondrial fatty acid beta-oxidation enzyme (i.e., palmitoyl-coenzyme A dehydrogenase) activity, as well as portal and arterial plasma beta-hydroxybutyrate values, were determined. Palmitoyl-coenzyme A dehydrogenase activity in villus tip cells and plasma beta-hydroxybutyrate values in portal vein and carotid artery were significantly reduced after trauma-hemorrhage and resuscitation. Pentoxifylline administration, however, significantly increased mitochondrial fatty acid beta-oxidation enzyme activity and portal plasma beta-hydroxybutyrate concentration without significantly affecting arterial concentrations under such conditions.
Pentoxifylline promotes gut ketogenesis following trauma-hemorrhage and resuscitation.
尽管己酮可可碱在不良循环状况下会产生多种有益作用，但尚不清楚该药物在创伤性出血和复苏后对肠道脂质代谢是否有任何影响。因此，本研究的目的是确定创伤性失血性休克后给予己酮可可碱是否对肠道生酮作用有任何有益影响。
一项前瞻性对照动物研究。
大学研究实验室。
56只雄性斯普拉格 - 道利大鼠。
大鼠接受中线剖腹手术（即创伤诱导），放血至平均动脉压为40mmHg并维持该水平，直到以乳酸林格氏液的形式回输40%的失血量。然后在60分钟内用四倍于最大失血量的乳酸林格氏液对动物进行复苏。在复苏期间及复苏后100分钟内静脉输注己酮可可碱（50mg/kg体重）或等量的生理盐水。为进行体内脂质负荷实验，在复苏完成后经十二指肠给予1毫升橄榄油。在喂食脂肪后1.5小时采集门静脉和颈动脉血样以及近端小肠的肠上皮细胞。
测定线粒体脂肪酸β - 氧化酶（即棕榈酰辅酶A脱氢酶）活性以及门静脉和动脉血浆β - 羟基丁酸值。创伤性出血和复苏后，绒毛顶端细胞中的棕榈酰辅酶A脱氢酶活性以及门静脉和颈动脉中的血浆β - 羟基丁酸值均显著降低。然而，在此种情况下，给予己酮可可碱可显著增加线粒体脂肪酸β - 氧化酶活性和门静脉血浆β - 羟基丁酸浓度，而对动脉浓度无显著影响。
己酮可可碱可促进创伤性出血和复苏后的肠道生酮作用。
