Effects of Fructose-1,6-Diphosphate, Glucose, and Saline on Cardiac Resuscitation
Effects of Fructose-1,6-Diphosphate, Glucose, and Saline on Cardiac Resuscitation
复制标题
1,6-二磷酸果糖、葡萄糖和盐水对心脏复苏的影响
DOI：
10.1097/00000542-198612000-00006
复制
发表时间：
1986
期刊：
影响因子：
8.8
通讯作者：
G. Gregory
中科院分区：
文献类型：
--
作者：
L. A. Farias;M. Willis;G. Gregory
严重低氧血症导致呼吸和心脏骤停，部分原因是由于乳酸诱导的磷酸果糖激酶和甘油醛-3-P脱氢酶活性降低导致糖酵解和三磷酸腺苷（ATP）产生减少。果糖-1，6-二磷酸（FDP）的管理增加血液中的ATP浓度。作者推测FDP可能会增加从低氧性心脏骤停中复苏耳蜗的家兔数量。为了检验这一假设，在28只成年、白色、用戊巴比妥麻醉的新西兰兔中，在正常氧血症（FIO 2 =0.21）和低氧血症（FIO 2 =0.04）期间测量心率、动脉压、左心室舒张压、血气和pH值。低氧血症发生后，静脉注射5%FDP（n = 10）、5%葡萄糖（n = 11）或等体积生理盐水（n=7），并开始以2.0mg· kg-1 · min-1的速度持续输注5%FDP（n = 10）、5%葡萄糖（n = 11）或等体积生理盐水（n=7）。FDP组家兔呼吸时间为20.9 ± 4.9低氧血症开始后（平均值± SEM）min;葡萄糖处理的兔呼吸1.4 ± 0.2分钟，生理盐水处理的兔呼吸10.3 ± 4分钟。FDP处理的兔在呼吸骤停开始后2.5 ± 0.5分钟发生心脏骤停，葡萄糖处理的兔为4.1 ± 0.2分钟，生理盐水组为2.9 ± 0.4min。我们可以使所有10只FDP治疗的兔子复苏; 11只葡萄糖治疗的两只（FDP vs.葡萄糖，P < 0.001）; 7只盐水治疗的兔子中的一只（FDP vs.盐水，P < 0.001）心脏骤停。得出的结论是，FDP延长了严重低氧血症成年兔呼吸骤停的时间，并增加了心脏骤停的立即抢救。
Severe hypoxemia causes respiratory and cardiac arrest, in part, because severe hypoxemia decreases glycolysis and adenosine triphosphate (ATP) production by a lactic acid-induced decrease in the activity of phosphofructokinase and glyceraldehyde-3-P dehydrogenase. Fructose-1,6-diphosphate (FDP) administration increases the ATP concentration of blood. The authors hypothesized that FDP might increase the number of rabbits that coicular euld be resuscitated from hypoxemic cardiac arrest. To test this hypothesis, heart rate, arterial pressure, left ventrnd-diastolic pressure, and blood gases and pH were measured during normoxemia (FIO2=0.21) and again during hypoxemia (FIO2 =0.04) in 28 adult, white, New Zealand rabbits anesthetized with pentobarbital. With the onset of hypoxemia, we gave either 40 mg/kg of 5% FDP (n = 10), 5% glucose (n = 11), or an equal volume (2.5 ml) of normal saline (n=7) intravenously and began a continuous infusion of 2.0 mg · kg-1 · min-1 of the same sugar or 0.12 ml/min of saline. FDP-treated rabbits breathed for 20.9 ± 4.9 (mean ± SEM) min after initiation of hypoxemia; glucose-treated rabbits breathed for 1.4 ± 0.2 min, and saline-treated rabbits breathed 10.3 ± 4 min. Cardiac arrest occurred 2.5 ± 0.5 min after the onset of respiratory arrest in FDP-treated rabbits, 4.1 ± 0.2 min in glucose-treated rabbits, and 2.9 ± 0.4 min in saline-treated rabbits. We could resuscitate all ten FDP-treated rabbits; two of 11 glucose-treated (FDP vs. glucose, P < 0.001); and one of seven saline-treated rabbits (FDP vs. saline, P < 0.001) from cardiac arrest. It is concluded that FDP prolongs the time to respiratory arrest and increases immediate salvage from cardiac arrest in severely hypoxemic, adult rabbits.