胎儿豚鼠体外肺产生肺液:精氨酸加压素和精氨酸催产素的影响。

Journal of developmental physiology Pub Date : 1993-05-01
A M Perks, P M Kindler, J Marshall, B Woods, M Craddock, I Vonder Muhll
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引用次数: 0

摘要

近期胚胎豚鼠的肺在体外支撑3小时;用染料稀释法测定肺液产率。70种制剂用于研究精氨酸抗利尿激素(AVP)在体外生理盐水中放置1小时的效果,其浓度为出生时报告的浓度[胎儿妊娠61 +/- 2天;94.7±16.2 g (SD)体重]。在1200微u /ml时,AVP阻滞产液率(连续小时,3.03 +/- 0.60、0.50 +/- 0.14和0.02 +/- 0.08 ml/kg体重/ h);P < 0.01-0.0005)。在600、300和100微u /ml时,有显著但较小的减少。AVP浓度为600 ~ 1200微u /ml的8种制剂均有重吸收。10微u /ml AVP、AVP载体和对照生理盐水对AVP的影响不显著。反应(治疗期间减少的百分比)与AVP的对数浓度线性相关(r = 0.99);理论阈值为8微u /ml)。延长治疗至2h并没有增加最终疗效。体重> 120 g的5个胎儿的制剂反应显著高于(P < 0.025)[妊娠64 +/- 2天胎儿;135.1 +/- 18.6 g (SD)体重]。10(-6) M -阿米洛利可消除胎儿对AVP的反应[妊娠62 +/- 1天];93.4±18.5 g (SD)体重,n = 30;费率,随后的小时数;avon,仅1.78 + / - 0.22,0.48 + / - 0.09,0.16 + / - 0.99 (P < 0.01 - -0.0005);阿米洛利组AVP分别为1.15 +/- 0.07、0.93 +/- 0.10、0.86 +/- 0.08 ml/kg体重/ h(无显著下降)。精氨酸缩宫素(AVT, 10 ~ 600 μ u /ml)处理的36种制剂与AVP处理后的效果相近。这些研究将结果扩展到胎儿豚鼠,并表明AVP,在分娩时报告的浓度,可以通过直接作用于肺来减缓肺液的产生或引起重吸收。这种效应随着期限的临近而增加,这是由于活化了酰胺敏感的Na+通道。
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Lung liquid production by in vitro lungs from fetal guinea pigs: effects of arginine vasopressin and arginine vasotocin.

Lungs from near-term fetal guinea pigs were supported in vitro for 3 h; lung liquid production rates were measured by a dye dilution technique. Seventy preparations were used to study the effects of arginine vasopressin (AVP) placed in the outer saline for the middle hour, at concentrations reported at birth [fetuses 61 +/- 2 days of gestation; 94.7 +/- 16.2 g (SD) body weight]. At 1200 microU/ml, AVP arrested fluid production (rates, successive hours, 3.03 +/- 0.60, 0.50 +/- 0.14 and 0.02 +/- 0.08 ml/kg body weight per h; falls significant, P < 0.01-0.0005). At 600, 300 and 100 microU/ml there were significant but smaller reductions. Reabsorptions were seen in 8 preparations given 600-1200 microU/ml, AVP. Preparations given 10 microU/ml AVP, AVP carrier or control saline showed no significant change. The responses (% reductions during treatment), were linearly related to the log concentration of AVP (r = 0.99); theoretical threshold, 8 microU/ml). Increasing treatment to 2h did not increase final responses. Preparations from 5 fetuses > 120 g body weight showed significantly greater responses (P < 0.025) [fetuses 64 +/- 2 days of gestation; 135.1 +/- 18.6 g (SD) body weight]. 10(-6) M amiloride abolished responses to AVP [fetuses 62 +/- 1 days of gestation; 93.4 +/- 18.5 g (SD) body weight, n = 30; rates, succeeding hours; AVP alone, 1.78 +/- 0.22, 0.48 +/- 0.09, 0.16 +/- 0.99 (P < 0.01-0.0005); AVP with amiloride, 1.15 +/- 0.07, 0.93 +/- 0.10, 0.86 +/- 0.08 (no significant fall) ml/kg body weight per h]. Thirty-six preparations treated with arginine vasotocin (AVT, 10-600 microU/ml) showed closely similar responses to those from AVP. These studies extend results to fetal guinea pigs, and show that AVP, at concentrations reported at delivery, can slow lung liquid production or cause reabsorption by a direct action on the lung. The effect increases close to term, and is due to activation of amiloride-sensitive Na+ channels.

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