Hameroff S R, Otto C W, Kanel J, Weinstein P R, Blitt C D
Crit Care Med. 1981 Dec;9(12):855-7. doi: 10.1097/00003246-198112000-00011.
Dimethylsulfoxide (DMSO) has been advocated as a central nervous system (CNS) protectant against ischemia and trauma. The present study was performed to evaluate acute cardiovascular effects of DMSO which might complicate the clinical treatment of CNS compromised patients. Intravenously administered DMSO in doses which reportedly provide CNS protection, 2 g/kg, were infused in 6 dogs; hemodynamic variables were measured and compared to infusion of equal volumes of 0.9% sodium chloride. Immediately after infusion, DMSO caused increases in cardiac index, heart rate, pulmonary capillary wedge pressures (WP), and pulmonary arterial (systolic, mean, and diastolic) pressures which were significantly greater than changes induced by saline. DMSO decreased systematic diastolic pressure and systemic vascular resistance at the end of infusion. Most DMSO induced changes returned toward pre-infusion values 10 min after the end of infusion. These results suggest transient DMSO effects different from equal volumes of saline, possibly due to hyperosmotic expansion of plasma volume. A decrease in systemic vascular resistances was also observed. Although neither CNS production, intracranial pressure or blood flow were studied, these data suggest that DMSO used for CNS protection would not have adverse acute hemodynamic consequences. This may be particularly relevant in traumatized, hypovolemic patients.
二甲基亚砜(DMSO)已被提倡作为一种针对缺血和创伤的中枢神经系统(CNS)保护剂。本研究旨在评估DMSO可能使中枢神经系统受损患者临床治疗复杂化的急性心血管效应。以据报道可提供中枢神经系统保护作用的剂量2 g/kg,对6只犬静脉注射DMSO;测量血流动力学变量,并与输注等量0.9%氯化钠进行比较。输注后立即发现,DMSO使心脏指数、心率、肺毛细血管楔压(WP)以及肺动脉(收缩压、平均压和舒张压)压力升高,这些升高显著大于盐水引起的变化。输注结束时,DMSO使体循环舒张压和全身血管阻力降低。输注结束10分钟后,大多数DMSO诱导的变化恢复到输注前的值。这些结果表明,DMSO的效应短暂,与等量盐水不同,可能是由于血浆容量的高渗性扩张所致。还观察到全身血管阻力降低。尽管未对中枢神经系统的生成、颅内压或血流进行研究,但这些数据表明,用于中枢神经系统保护的DMSO不会产生不良急性血流动力学后果。这对于创伤性、低血容量患者可能尤为重要。