Lathers C M, Tumer N, Schoffstall J M
Department of Pharmacology, Medical College of Pennsylvania/EPPI, Philadelphia 19129.
Resuscitation. 1989 Oct;18(1):59-74. doi: 10.1016/0300-9572(89)90113-5.
This study examined plasma epinephrine (E) and norepinephrine (NE) concentrations, pH, and mean arterial blood pressure (MAP) in a cardiac arrest model. Twenty-three domestic swine (15-26 kg) were anesthetized with ketamine 20 mg/kg, i.m. and alpha-chloralose 25 mg/kg, i.v. and ventilated with a respirator. Catheters were placed in the right ventricle, left ventricle and femoral arteries for MAP recordings and blood pH sampling every 2 min. Catecholamine samples were taken from the femoral artery every 2 min. Cardiac arrest was induced by endocardial stimulation with a Grass S88 stimulator. Five minute post arrest resuscitation was initiated with a mechanical resuscitator. Ten minute post arrest NaHCO3 1 mEq/kg was administered by the peripheral i.v. (P; n = 6), central (CE; n = 5), or intraosseous, via the tibia, (I; n = 6), route. Controls (C; n = 6) did not receive NaHCO3. MAP (mean +/- S.D.) prior to arrest was: C 144 +/- 16, P 139 +/- 11, CE 137 +/- 13 and I 133 +/- 11 mmHg. Five and 25 min post arrest it was: C 21 +/- 5 and 17 +/- 6, P 34 +/- 8 and 23 +/- 7, CE 17 +/- 7 and 14 +/- 10 and I 26 +/- 6 and 11 +/- 3 mmHg, respectively. A 2-way analysis of variance did not reveal any difference in MAP values in the four groups. In all groups the blood pH from the femoral artery demonstrated a respiratory alkalosis that peaked at approximately 7.48 5 min after initiation of mechanical resuscitation. In the groups receiving NaHCO3, it peaked at 7.77 +/- 0.09 CE and 7.65 +/- 0.06 P 2 min post infusion and at 7.71 +/- 0.06 I 8 min post infusion. An analysis of variance revealed that the CE and I routes were significantly different (P less than 0.05) from the P group and that all three groups were different (P less than 0.05) from the C. Plasma E and NE concentrations at 0, 6, 10, 12, 20 and 30 min post arrest in the C group were, respectively: 3 and 10, 94 and 327, 119 and 329, 92 and 234, 33 and 135, and 127 and 62 ng/ml, respectively. All 3 groups receiving NaHCO3 demonstrated similar patterns and were not significantly different from C when compared with a 2-way analysis of variance.(ABSTRACT TRUNCATED AT 400 WORDS)
本研究在心脏骤停模型中检测了血浆肾上腺素(E)和去甲肾上腺素(NE)浓度、pH值及平均动脉血压(MAP)。23头家猪(体重15 - 26千克),肌肉注射20毫克/千克氯胺酮及静脉注射25毫克/千克α-氯醛糖进行麻醉,并用呼吸机通气。将导管置于右心室、左心室和股动脉,每2分钟记录一次MAP并采集血样检测pH值。每2分钟从股动脉采集儿茶酚胺样本。用Grass S88刺激器进行心内膜刺激诱导心脏骤停。心脏骤停5分钟后用机械复苏器开始复苏。心脏骤停10分钟后,经外周静脉(P组,n = 6)、中心静脉(CE组,n = 5)或经胫骨骨髓腔(I组,n = 6)途径给予1毫当量/千克的碳酸氢钠。对照组(C组,n = 6)未给予碳酸氢钠。心脏骤停前MAP(平均值±标准差)为:C组144±16、P组139±11、CE组137±13、I组133±11毫米汞柱。心脏骤停后5分钟和25分钟时分别为:C组21±5和17±6、P组34±8和23±7、CE组17±7和14±10、I组26±6和11±3毫米汞柱。双向方差分析未显示四组MAP值有任何差异。所有组股动脉血pH值均显示呼吸性碱中毒,在机械复苏开始后约5分钟达到峰值,约为7.48。在接受碳酸氢钠的组中,输注后2分钟CE组峰值为7.77±0.09、P组为7.65±0.06,输注后8分钟I组为7.71±0.06。方差分析显示,CE组和I组与P组有显著差异(P<0.05),且这三组与C组均有差异(P<0.05)。C组心脏骤停后0、6、10、12、20和30分钟时血浆E和NE浓度分别为:3和10、94和327、119和329、92和234、33和135、127和62纳克/毫升。接受碳酸氢钠的所有三组显示出相似模式,经双向方差分析与C组相比无显著差异。(摘要截断于400字)