充气温控毯用于神经外科手术患者的控温效果

目的评价充气温控毯用于神经外科手术患者的控温效果。方法40例择期行平卧位脑肿瘤切除术患者,年龄16—65岁,体重41-72 kg,ASAⅠ-Ⅲ级,随机分为2组(n=20):A组,术中充气温控毯24℃风档进行降温,肿瘤切除完毕前30 min进行复温;B组,术中充气温控毯维持中心温度正常(35．2—36．60℃)。均采用气管内静吸复合麻醉,静脉注射异丙酚1．5～2 mg／kg、芬太尼4-6μg／kg、维库溴铵0．1～0．2 mg／kg诱导,吸入0．6％-1．2％异氟醚维持;吸入氧浓度40％;异丙酚1．5～2 mg·kg-1·h-1持续输注;维库溴铵1～2 mg间断静脉注射。每5分钟记录1次中心温度(鼻咽温),观察围术期不良反应及并发症。结果A组2例患者因手术时间超过24 h剔除,共38例进行统计。A组患者降温速率(1．11±0．05)℃／h,复温速率(0．74±0．09)℃／h。A组患者89％(16/18)在硬脑膜打开前达到目标温度34℃,平台期平均中心温度(34．3±0．5)℃,距34℃最大升幅0．52℃,最大降幅为0．23℃。A组患者67％(12／18)手术结束时中心温度恢复正常。返回ICU后A组患者中心温度(返回ICU时实测温度的均值)(35．8±0．6)℃低于B组(36．6±0．4)℃(P<0．05)。A组患者4例术后出现寒颤、3例发热、1例死亡。结论神经外科手术中应用充气温控毯可较理想地降低体温,相对于降温效率其复温效率偏低。     

Effect of pindolol on endocrine and temperature responses to buspirone in healthy volunteers

Ten healthy subjects received buspirone (30 mg orally) with and without pre-treatment with the 5-HT1A receptor antagonist, pindolol (80 mg over 3 days). Following pindolol treatment the growth hormone and hypothermic responses to buspirone were significantly decreased. There was also a delay in the onset of the prolactin response to buspirone but the total amount of prolactin secretion, calculated as area under the curve, was not significantly reduced. The data suggest that the growth hormone and hypothermic responses to buspirone in humans are mediated by 5-HT1A receptors, but an explanation founded on pharmacokinetic factors cannot presently be excluded. Both this latter possibility and the lack of selectivity of pindolol for 5-HT receptors indicate the need for the further neuroendocrine studies of the mode of action of buspirone, preferably with more selective 5-HT1A receptor antagonists.     

亚低温对大鼠脑损伤后脑组织炎性反应的影响

目的探讨颅脑外伤后早期应用亚低温治疗对脑组织炎性反应的影响。方法采用Feeney自由落体改良模型,设定对照组、颅脑外伤模型组及亚低温组,每组再根据伤后不同生存时间随分为3个亚组。取伤灶脑组织检测髓过氧化酶(MPO)活性,做细胞间黏附子-1(ICAM-1)免疫组化染色,光镜下计数ICAM-1阳性血管数。结果亚低温组各时间点伤灶区ICAM-1阳性血管数明显低于颅脑外伤模型相应时间点(P<0.01)。亚低温组各时间点MPO活性均明显低于颅脑外伤模型组相应时间点(P<0.01)。结论亚低温治疗能明显减少伤灶区白细胞浸润及ICAM-1的表达,有助于改善颅脑外伤后脑组织炎性反应引起的继发性脑损伤。     

深低温对吸入麻醉药的MAC,心脏麻醉指数和心肌稳定性的影响

目的:研究深低温对吸入麻醉药MAC、心脏麻醉指数和心肌稳定性的影响。方法:新西兰白兔40只,随机分为氟烷、安氟醚、异氟醚和七氟醚组。采用夹尾试验法测定常温下(38℃±0.5℃)的最低肺泡有效浓度(MAC)。行体表降温后测定深低温下(23℃±0.5 ℃)的MAC。维持深低温增加吸入性麻醉药的浓度,同时用50Hz、25V电压胸外电击心脏。记录出现室颤或室性心律失常时的肺泡呼气末吸入麻醉药浓度。结果:从38℃到23℃兔体温每降低1℃,MAC下降值为:氟烷5.1％、安氟醚3.6％、异氟醚4.4％、七氟醚4.3％;氟烷、安氟醚、异氟醚和七氟醚心脏麻醉指数分别为4.4、3.18、6.25和4.6,异氟醚明显高于其它麻醉药;麻醉药浓度8MAC以内安氟醚和氟烷发生室颤的机率(100％)明显高于七氟醚和异氟醚(40％)。结论:异氟醚是深低温麻醉的最佳选择用药,而安氟醚则不宜用于低温麻醉。     

Normothermic cardiopulmonary bypass: effect on the incidence of persistent postoperative neurological dysfunction following coronary artery bypass graft surgery

We retrospectively reviewed the records of 250 consecutive patients undergoing coronary artery bypass graft surgery (CABG) from January 1994 through January 1996 to determine the incidence of persistent postoperative neurological dysfunction after CABG and to compare normothermic and moderate hypothermic cardiopulmonary bypass (CPB). Normothermic CPB was used in 128 patients (36°–37°C) and hypothermic CPB (27°–28°C) in 122 patients. Postoperative neurological dysfunction included focal motor deficits, delayed recovery of consciousness (>24h) after surgery, and seizures within 1 week postoperatively. Persistent neurological dysfunction was diagnosed if complete resolution had not occurred within 10 days of surgery. The incidence of persistent postoperative neurological dysfunction was 4.1% in the hypothermic CPB group and 2.3% in the normothermic CPB group. There were no statistically significant differences between the two groups (P=NS). These results suggest that normothermic CPB did not increase the incidence of persistent postoperative neurological dysfunction compared to hypothermic CPB.     

Thrombocytopenia after therapeutic hypothermia in severe traumatic brain injury

Objective: To investigate the clinical characteristics and significance of thrombocytopenia after therapeutic hypothermia in severe traumatic brain injury (TBI). Methods:Ninety-six inpatients with severe brain injury were randomized into three groups: SBC (selective brain cooling) group (n=24), MSH (mild systemic hypothermia ) group (n=30), and control (normothermia) group (n=42). The platelet counts and prognosis were retrospectively analyzed. Results: Thrombocytopenia was present in 18 (75%), 23 (77%) and 15 (36%) patients in SBC group, MSH group and control group, respectively (P<0. 01). Thrombocytopenia, in which the minimum platelet count was seen 3 days after hypothermia, showed no significant difference between SBC and MSH group (P>0.05). Most platelet counts (37 cases, 90 %) in hypothermia group were returned to normal level after 1 to 2 days of natural rewarming. The platelet count in SBC group reduced by 16%, 27% and 29% at day 1, 3 and 5 respectively compared with the baseline value. Good recovery ( GOS score 4-5) rate of thrombocytopenia 1 year after injury for hypothermia group (17 cases, 37%) was significantly lower than that of control group (P < 0.01). Conclusions: Therapeutic hypothermia increases the incidence of thrombocytopenia in severe TBI, and patients with thrombocytopenia after therapeutic hypothermia are associated with unfavorable neurological prognosis.     

Post-traumatic brain hypothermia reduces histopathological damage following concussive brain injury in the rat

The purposes of this study were (1) to document the histopathological consequences of moderate traumatic brain injury (TBI) in anesthetized Sprague-Dawley rats, and (2) to determine whether posttraumatic brain hypothermia (30°C) would protect histopathologically. Twenty-four hours prior to TBI, the fluid percussion interface was positioned over the right cerebral cortex. On the 2nd day, fasted rats were anesthetized with 70% nitrous oxide, 1% halothane, and 30% oxygen. Under controlled physiological conditions and normothermic brain temperature (37.5°C), rats were injured with a fluid percussion pulse ranging from 1.7 to 2.2 atmospheres. In one group, brain temperature was maintained at normothermic levels for 3 h after injury. In a second group, brain temperature was reduced to 30°C at 5 min post-trauma and maintained for 3 h. Three days after TBI, brains were perfusion-fixed for routine histopathological analysis. In the normothermic group, damage at the site of impact was seen in only one of nine rats. In contrast, all normothermic animals displayed necrotic neurons within ipsilateral cortical regions lateral and remote from the impact site. Intracerebral hemorrhagic contusions were present in all rats at the gray-white interface underlying the injured cortical areas. Selective neuronal necrosis was also present within the CA3 and CA4 hippocampal subsectors and thalamus. Post-traumatic brain hypothermia significantly reduced the overall sum of necrotic cortical neurons (519±122 vs 952±130, mean ±SE, P=0.03, Kruskal-Wallis test) as well as contusion volume (0.50±0.14 vs 2.14±0.71 mm³, P=0.004). These data document a consistent pattern of histopathological vulnerability following normothermic TBI and demonstrate hypothermic protection in the post-traumatic setting.Supported by USPHS Grants NS30291 and NS27127     

Pharmacological effects of epibatidine optical enantiomers

The pharmacology of synthetic - and -epibatidine, an alkaloid originally characterized from frog skin, were studied in different behavioral tests in mice and rats. The two enantiomers have potent antinociceptive activity in mice using the tail-flick test, with an ED₅₀ of 6.1 and 6.6 μg/kg for - and -epibatidine respectively. Epibatidine enantiomers were 200 × more potent than -nicotine as an antinociceptive agent in mice after s.c. administration. Their analgesic effect was blocked by mecamylamine but not naloxone, an opiate antagonist. Both - and -epibatidine have high affinity (K_i 54.7 and 55.0 pM, respectively) for [³H]nicotine binding site in rat brain. In addition, they reduced mice locomotor activity and body temperature in a dose-dependent manner. In rats trained with nicotine (0.4 mg/kg), epibatidine enantiomers engendered nicotine-like responding in a dose-related manner with an ED₅₀ of 1.00 and 0.93 μg/kg for and , respectively. The discriminative effect of - and -epibatidine in rats was blocked by mecamylamine but not by hexamethonium. As in binding results, there was no significant enantioselectivity for these effects in our study.     

Differences in the hypothermic response to ethanol in rats selectively bred for oral ethanol preference and nonpreference

The duration of retention of tolerance to ethanol was tested in the alcohol-preferring (P) and alcohol-nonpreferring (NP) rats lines, using ethanol-induced hypothermia as a measure of tolerance. Rats received two injections of ethanol (3.5 g/kg) body wt, IP) and the time between the injections was 1, 2, or 3 days. When one day separated the two injections, tolerance to the hypothermic effect of a second “test” injection was found in both lines. When 2 or 3 days separated the two injections, the P line showed a loss of tolerance and the NP line showed sensitization to ethanol. Sensitization in the NP line grew stronger when the interval between injections was increased from 2 to 3 days. The duration of retention of tolerance to ethanol-induced hypothermia in the P line was shorter than has previously been reported for motor impairment in this line. It appears that the duration of tolerance retention in the P line depends on the test used to measure tolerance. Sensitization to ethanol in the NP line may be associated with low oral ethanol intake. This research was supported, in part, by grants AA08312, AA03243, and AA07611 from the PHS     

低温对缺血再灌流心肺脂质过氧化的影响

用犬心脏停跳再复跳模型，观察低温对缺血再灌流心肺脂质过氧化和乳酸脱氢酶的影响。结果显示，再灌期低温３４～３６℃组和３０～３２℃组心肌丙二醛（ＭＤＡ）含量明显增加，低温３０～３２℃组乳酸脱氢酶（ＬＤＨ）明显降低（Ｐ＜０．０５）。肺组织ＭＤＡ、ＬＤＨ变化不明显（Ｐ＞０．０５）。表明低温下心肌脂质过氧化损伤仍然明显。低温对肺再灌流损伤有一定的保护作用。