Denda S, Sakuma K, Satomi K, Fujiwara N, Fukuda S, Shimoji K
Department of Anesthesiology, School of Medicine, Niigata University.
Masui. 1991 Jun;40(6):972-7.
We had five cases of surgical removal of pheochromocytoma by continuous intravenous injection of prostaglandin E1. During anesthesia, we used Swan-Ganz catheter for circulatory monitoring and measured plasma catecholamines. When PGE1 dose was increased from 0.05 to 0.1 and 0.15 microgram.kg-1.min-1, total systemic vascular resistance and mean arterial pressure were decreased but heart rate and cardiac output were not significantly altered from the preanesthetic values. Plasma catecholamines were also similar to the preanesthetic values. Therefore, the results suggest that the mechanism of suppression of hypertension by PGE1 is by affecting vascular beds directly rather than by diminishing catecholamine excretion from sympathetic nerve and adrenal medulla. During manipulation of pheochromocytoma, mean arterial blood pressure increased extremely. Although PGE1 was injected at a rate of 0.3 to 0.5 microgram.kg-1.min-1 in some cases, we could not suppress the elevation of blood pressure. PGE1 alone could not normalize blood pressure and heart rate, and other cardiovascular agents were necessary.
我们有5例通过持续静脉注射前列腺素E1进行嗜铬细胞瘤手术切除的病例。麻醉期间,我们使用 Swan-Ganz 导管进行循环监测并测量血浆儿茶酚胺。当前列腺素E1剂量从0.05增加到0.1和0.15微克·千克-1·分钟-1时,总全身血管阻力和平均动脉压降低,但心率和心输出量与麻醉前值相比无明显变化。血浆儿茶酚胺也与麻醉前值相似。因此,结果表明前列腺素E1抑制高血压的机制是直接影响血管床,而不是通过减少交感神经和肾上腺髓质的儿茶酚胺排泄。在处理嗜铬细胞瘤期间,平均动脉血压极度升高。尽管在某些情况下以0.3至0.5微克·千克-1·分钟-1的速率注射前列腺素E1,但我们无法抑制血压升高。仅前列腺素E1不能使血压和心率恢复正常,还需要其他心血管药物。