Huval W V, Lelcuk S, Feingold H, Valeri C R, Shepro D, Hechtman H B
Department of Surgery, Brigham and Women's Hospital, Boston, Massachusetts 02115.
Surg Gynecol Obstet. 1988 Jun;166(6):527-34.
Increased hydrostatic pressure and microvascular permeability after acid aspiration as causes of pulmonary and tracheobronchial edema were studied. Eighteen dogs were anesthetized and 3.0 milliliters per kilogram of 0.1 normal hydrochloride instilled into the trachea. After one hour, the platelet count decreased 47,500 per cubic millimeter (p less than 0.05) from base line levels of 221,400 per cubic millimeter and platelet serotonin stores decreased from 2.09 to 1.65 micrograms per 10(9) platelets (p less than 0.05). Mean pulmonary arterial pressure increased progressively from a base line value of 11 to 21 millimeters of mercury four hours after acid instillation (p less than 0.05). Mean arterial pressure fluctuated from a high of 143 millimeters of mercury to the final value, at four hours, of 119 millimeters of mercury. Ketanserin, a serotonin receptor antagonist, infused one hour after acid injury did not prevent release of platelet 5 hydroxytryptamine but led to a 24 per cent decrease in mean pulmonary arterial pressure from 13 to 10 millimeters of mercury (p less than 0.05) and an 11 per cent decrease in mean arterial pressure from 135 to 120 millimeters of mercury (p less than 0.05). Nitroprusside produced a 30 per cent decrease in mean arterial pressure, but only a 20 per cent decline in mean pulmonary arterial pressure (p less than 0.05). Four hours after acid was instilled, untreated dogs produced 129 milliliters of edema fluid from the endotracheal tube. In proportion to the relative decline in mean pulmonary arterial pressure, nitroprusside therapy reduced the volume of edema to 72 milliliters (p less than 0.05) and ketanserin to 52 milliliters (p less than 0.05). These results suggest that 5 hydroxytryptamine contributes to the pulmonary hypertension associated with acid injury and that the volume of edema formed may be directly related to the increase in the hydrostatic pressure.
研究了酸吸入后增加的流体静压和微血管通透性作为肺和气管支气管水肿成因的情况。对18只狗进行麻醉，并将每千克3.0毫升的0.1当量盐酸滴入气管。1小时后，血小板计数从每立方毫米221,400的基线水平下降了47,500（p<0.05），血小板5-羟色胺储存量从每10(9)个血小板2.09微克降至1.65微克（p<0.05）。酸滴入4小时后，平均肺动脉压从基线值11毫米汞柱逐渐升至21毫米汞柱（p<0.05）。平均动脉压在4小时内从143毫米汞柱的高位波动至最终值119毫米汞柱。在酸损伤1小时后输注5-羟色胺受体拮抗剂酮色林，虽不能阻止血小板5-羟色胺的释放，但导致平均肺动脉压从13毫米汞柱降至10毫米汞柱，降幅达24%（p<0.05），平均动脉压从135毫米汞柱降至120毫米汞柱，降幅达11%（p<0.05）。硝普钠使平均动脉压下降30%，但平均肺动脉压仅下降20%（p<0.05）。酸滴入4小时后，未治疗的狗从气管内管产生了129毫升水肿液。与平均肺动脉压的相对下降成比例，硝普钠治疗使水肿量减少至72毫升（p<0.05），酮色林治疗使其减少至52毫升（p<0.05）。这些结果表明，5-羟色胺促成了与酸损伤相关的肺动脉高压，并且形成的水肿量可能与流体静压的增加直接相关。
