非体外循环冠状动脉搭桥手术的麻醉

目的对非体外循环下冠状动脉搭桥手术(OPCAB)的麻醉方法和效果进行总结和探讨。方法回顾分析笔者进修期间连续实施OPCAB麻醉40例及我院2004年1月～2005年10月30例,共计70例。多数病人心功能差并伴有其他器官功能不全,麻醉诱导用小剂量咪唑安定和氯胺酮以及中小剂量芬太尼,麻醉维持以异氟醚复合小剂量异丙酚,术中随手术操作出现血流动力学的骤然变化,应用血管活性药物及时处理。结果麻醉效果满意,术中血压心率调控基本稳定。本组病人术后苏醒时间(2.3±0.8)小时,拔管时间术后(3.2±1.2)小时。ICU停留时间0.5天～1.0天,术后(7.0±1.6)天出院。无脑血管意外、心肌梗死等并发症,无住院期间死亡。结论对于OPCAB麻醉,合理应用麻醉药物和血管活性药物维持循环稳定,对于保证手术实施和病人安全至关重要。     

分离的胰腺腺泡的制备方法

作者参照国外的方法,结合国内的特点,介绍采用化学消化,机械分离和离心提纯的方法制备胰腺腺泡的过程,并对每一过程的意义和注意点进行了讨论。     

大剂量地塞米松及SOD在实验性脑损伤中的治疗作用

大剂量地塞米松和ＳＯＤ是外伤性脑继发性损害药物治疗的新方案。本实验在豚鼠局灶性脑损伤模型上试用该两种药物，通过脑含水量、灶周伊文斯兰渗出、血ＣＫ、Ｃａ和ＬＤＨ含室及光镜和电镜病理检查等指标。     

替米沙坦治疗原发性高血压的疗效和安全性

目的 :观察替米沙坦治疗原发性高血压的疗效和安全性。方法 :进行随机、双盲、双模拟、平行分组对照试验。符合条件的轻中度高血压患者随机分为 2组 :替米沙坦组和氯沙坦组。每天一次口服替米沙坦 40mg或氯沙坦 5 0mg ,每 2周随访 1次。 4周后 ,如患者舒张压 (DBP)≥ 90mmHg则增加剂量 ,每天一次口服替米沙坦 80mg或氯沙坦 10 0mg。治疗前后分别查心电图 ,血、尿常规 ,血生化检查和常规查体。 结果 :(1)治疗 8周末 ,替米沙坦组和氯沙坦组患者的DBP均显著降低 ,2组下降幅度相似 (11.9mmHgvs 10 .4mmHg) ;(2 )治疗8周末 ,替米沙坦组收缩压 (SBP)下降幅度稍大于氯沙坦组 (9.5mmHgvs 6.2mmHg) ;(3 )替米沙坦降压有效率为 83 .3 % ,稍高于氯沙坦组 69.2 % ,无统计学差异 ;(4 ) 2组的不良事件发生率相似 (替米沙坦组 3 3 .3 % ,氯沙坦组 3 4.6% )。最常见的不良事件是头晕、头痛 ,多为轻度 ,可迅速缓解。结论 :替米沙坦 40mg～ 80mg ,每天一次口服治疗轻中度高血压安全有效     

外源性一氧化氮抗日本血吸虫的实验研究

目的观察外源性一氧化氮(NO)抗日本血吸虫的效果。方法以蜂蜡为NO的吸收剂,在不同条件下用逆转乳化法制备NO乳状液,测定其中NO的含量,选择乳状液中NO含量最大的用于抗日本血吸虫试验。在小鼠感染日本血吸虫尾蚴后22天起灌服,剂量为0.5ml/d,连续灌服5d,心脏灌注法收集虫体计数,研究外源性NO抗日本血吸虫的效果。结果外源性NO中NO的最大含量为536.2μmol/L;对小鼠日本血吸虫有一定的杀虫效果,减虫率达45.0%,减卵率达42.7%。结论外源性NO对日本血吸虫有一定的抗虫作用。     

Variation of Apolipoprotein A-I in Cirrhosis and its Clinical Value

The serum apolipoprotein A- I (apo A-I) Concentrations in 39 patients with posthepatitis cirrhosis were reported to be 0.87±0.27 g/L lower than that of controls 1.15±0.14 g/L P<0.01. The, decrease of apo. A-I was correlated with the severityof impaired liver function. Apo A- I concentrations in serum correlated positively with decrease of serum albumin (r=0.503 P< 0.01) and negatively with serum bilirubin increase (r=- 0.508 P <0.01) . The data indicate that decreasing of apo A- I concentration may be regarded as one of the reliable indices reflecting the degree of liver function impairment.     

Protective effects of amiloride on the ischemic reperfused rat heart. Relation to mitochondrial function.

We examined the effect of amiloride on mechanical, electrical and mitochondrial function as well as ultrastructural integrity, in isolated rat hearts subjected to 30 min low-flow ischemia and 30 min reperfusion. In control hearts, ischemia produced a rapid loss of contractility and a concomitant elevation in resting tension which were associated with a 100% incidence in arrhythmic activity. Reperfusion produced a 22 and 54% recovery in force and rate of force (dF/dt) development, respectively. In control hearts the incidence of arrhythmias was 100% within 5 min of reperfusion which then declined to 50% by 30 min. Ultrastructural defects in these hearts were restricted primarily to mitochondrial damage. Amiloride significantly attenuated the elevation in resting tension at the end of ischemia. Postischemic recovery was significantly increased to 38 and 86% for force and dF/dt, respectively and the incidence of arrhythmias was reduced to 30%. No ultrastructural defects were ever observed in amiloride-treated reperfused hearts. Both interfibrillar and subsarcolemmal mitochondria exhibited depressed respiratory function and adenine nucleotide translocase activity. Although virtually all parameters tended to be elevated in mitochondria isolated from amiloride-treated hearts, a significant increase was seen in only one case. Our results therefore demonstrate an ability of amiloride to enhance postischemic contractile recovery and reduce the incidence of arrhythmias, particularly during reperfusion, an effect associated with virtual total prevention of ultrastructural defects. Although the salutary effect was not significantly correlated to improved mitochondrial function, this dissociation may have been due to removal of damaged mitochondria during the isolation process, in view of diminished mitochondrial damage as viewed by transmission electron microscopy.(ABSTRACT TRUNCATED AT 250 WORDS)     

SD大鼠肺中降钙素基因相关肽的分布及缺氧对其含量的影响

本研究用免疫细胞化学方法(ABC法)观察了降钙素基因相关肽(CGRP)在SD大鼠肺中的分布,缺氧对肺中神经内分泌细胞内CGRP含餐的影响。结果表明:含CGRP的神经纤维分布在肺血管平滑肌层中及其周围、气管-支气管树的粘膜下层;含CGRP的神经内分泌细胞位于气管一支气管树的上皮层、粘液腺中和肺实质内。缺氧不引起火鼠肺的神经内分泌细胞数目改变,但可使这些细胞内的CGRP含量增加。