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新生羔羊实验性青紫型心脏病中局部血流和氧输送的重新分布

Redistribution of regional blood flow and oxygen delivery in experimental cyanotic heart disease in newborn lambs.

作者信息

Bernstein D, Teitel D, Sidi D, Heymann M A, Rudolph A M

机构信息

Cardiovascular Research Institute, University of California, San Francisco 94143.

出版信息

Pediatr Res. 1987 Oct;22(4):389-93. doi: 10.1203/00006450-198710000-00004.

Abstract

Redistribution of regional blood flow is an important compensatory response to acute hypoxemia which preserves oxygen delivery to the most vital organs. It is not known if this change in blood flow persists when hypoxemia is prolonged, as occurs in cyanotic congenital heart disease. Chronic hypoxemia was produced in newborn lambs by creating pulmonary stenosis and an atrial septal defect. Oxygen saturation was maintained at 60-70% of control for 2 wk. Distribution of cardiac output was then measured with radionuclide-labeled microspheres. As compared with control, chronic hypoxemia did not alter total cardiac output. Regional blood flow was redistributed, however, the pattern of this redistribution was different from that seen during acute hypoxemia. Myocardial and cerebral blood flows, which increase during acute hypoxemia, return to control levels during chronic hypoxemia. Renal, splenic, gastrointestinal, carcass, and skin blood flows remain decreased. Hemoglobin gradually increases so that after 2 wk of hypoxemia total systemic oxygen delivery returns toward control. However, oxygen delivery to all organs except the heart and brain is reduced. Thus, although cardiac output and total systemic oxygen delivery return toward normal during chronic hypoxemia, these measurements may not reflect important regional variations in blood flow and oxygen delivery. Decreased oxygen and substrate delivery to the gastrointestinal tract, liver, and carcass may account for the alterations of metabolism and growth seen in the newborn with cyanotic congenital heart disease.

摘要

局部血流再分布是对急性低氧血症的一种重要代偿反应,可维持向最重要器官的氧输送。目前尚不清楚当低氧血症持续存在时(如在青紫型先天性心脏病中那样),这种血流变化是否依然持续。通过制造肺动脉狭窄和房间隔缺损,在新生羔羊中诱发慢性低氧血症。氧饱和度维持在对照值的60 - 70%达2周。然后用放射性核素标记的微球测量心输出量的分布。与对照相比,慢性低氧血症并未改变总心输出量。然而,局部血流发生了再分布,不过这种再分布模式与急性低氧血症时所见不同。在急性低氧血症时增加的心肌和脑血流,在慢性低氧血症时恢复到对照水平。肾、脾、胃肠道、躯体和皮肤血流仍减少。血红蛋白逐渐增加,因此在低氧血症2周后,全身总氧输送量趋于恢复到对照水平。然而,除心脏和脑外,所有器官的氧输送均减少。因此,尽管在慢性低氧血症期间心输出量和全身总氧输送量趋于正常,但这些测量结果可能无法反映血流和氧输送方面重要的局部差异。向胃肠道、肝脏和躯体输送的氧和底物减少,可能是青紫型先天性心脏病新生儿出现代谢和生长改变的原因。

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