Abstract：
It is a well-known fact that general anesthesia leads to cerebral hemorrhage in patients with spontaneous hypertension apart of the fact that the hypertension is under control. The literature is already flooded with this debate, and still, there appears a lag regarding the effects of high blood pressure on pathological changes in the brain after cerebral hemorrhage. They are still not well recognized. Furthermore, it is the stage of anesthesia resuscitation which is known to have adverse effects on the body during cerebral hemorrhage. Owing to the lag of knowledge in the above said facts, the objectives of this study were to evaluate the effects of propofol combined with sufentanil on the expression of Bax, BCL-2, and caspase-3 genes in spontaneously hypertensive rats suffering with cerebral hemorrhage. The initial sample consisted of 54 male Wrister rats. All were of the age of 7 to 8 months with a weight of 500 ± 100 gm. All the rats were evaluated by the investigators before enrolment. A total of 0.5 mg/kg ketamine followed by a 10 mg/kg intravenous injection of propofol was introduced to each included rat. It was followed by a total of 1 μG/kg/h of sufentanil which was administered to rats who had cerebral hemorrhage (n = 27). The rest 27 normal rats were not administered with sufentanil. Hemodynamic parameters, biochemistry, western blot assay, and immunohistochemical staining were performed. The results were statistically analyzed. Heart rate (p < 0.0001) was higher for rats who had a cerebral hemorrhage. The cytokine levels of rats who had cerebral hemorrhage were higher than those of normal rats (p < 0.01 for all). Bacl-2 (p < 0.01), bax (p < 0.01), and caspase-3 (p < 0.01) expressions were reported to be disturbed in rats who had cerebral hemorrhage. Urine volume was reduced in rats who had cerebral hemorrhage (p < 0.01). It was concluded that in spontaneously hypertensive rats with cerebral hemorrhage, propofol combined with sufentanil target-controlled intravenous anesthesia increased hemodynamic parameters and cytokine levels. Furthermore, cerebral hemorrhage disturbs the expression of bacl-2, Bax, and caspase-3 expressions.
摘要：
众所周知,除了高血压得到控制之外,全身麻醉导致自发性高血压患者的脑出血。文学已经充斥着这场辩论，而且仍然,高血压对脑出血后脑部病理变化的影响存在滞后性。他们仍然没有得到很好的认可。此外，这是麻醉复苏阶段，已知在脑出血期间对身体有不利影响。由于对上述事实的认识滞后,本研究的目的是评价异丙酚复合舒芬太尼对Bax表达的影响,自发性高血压脑出血大鼠的BCL-2和caspase-3基因。初始样品由54只雄性Wrister大鼠组成。所有年龄为7至8个月，体重为500±100gm。所有大鼠在登记前由研究者评估。将总共0.5mg/kg氯胺酮和随后10mg/kg静脉内注射的丙泊酚引入每只纳入的大鼠。随后是总共1μG/kg/h的舒芬太尼,其被给予患有脑出血的大鼠(n=27)。其余27只正常大鼠均未给予舒芬太尼。血流动力学参数,生物化学,westernblot检测,进行免疫组织化学染色。对结果进行统计学分析。脑出血大鼠的心率较高(p<0.0001)。脑出血大鼠的细胞因子水平高于正常大鼠（均p<0.01）。Bacl-2（p<0.01），bax(p<0.01)，据报道，脑出血大鼠的caspase-3表达受到干扰（p<0.01）。脑出血大鼠尿量减少(p<0.01)。结论自发性高血压大鼠脑出血,丙泊酚复合舒芬太尼靶控静脉麻醉可提高血流动力学参数和细胞因子水平。此外，脑出血干扰bacl-2,bax,和caspase-3表达。
