Epinephrine induces rapid deterioration in pulmonary oxygen exchange in intact, anesthetized rats: a flow and pulmonary capillary pressure-dependent phenomenon.
Epinephrine induces rapid deterioration in pulmonary oxygen exchange in intact, anesthetized rats: a flow and pulmonary capillary pressure-dependent phenomenon.
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DOI：
10.1097/aln.0b013e31826a7da7
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发表时间：
2012-10
期刊：
影响因子：
8.8
通讯作者：
Weinberg GL
中科院分区：
文献类型：
--
作者：
Krishnamoorthy V;Hiller DB;Ripper R;Lin B;Vogel SM;Feinstein DL;Oswald S;Rothschild L;Hensel P;Rubinstein I;Minshall R;Weinberg GL
先前的研究表明，在局部麻醉剂过量的大鼠模型中，肾上腺素对动脉氧合有不良影响。作者测试了肾上腺素是否单独在完整的动物中发挥类似的作用。麻醉大鼠接受肾上腺素（25、50或100 mcg/kg）单次静脉注射;匹配队列接受酚妥拉明（100 mcg/kg）预处理; 6个治疗组中，每组n = 5。在基线、肾上腺素给药后1分钟和10分钟测量动脉压和血气。在离体肺标本中测量了肾上腺素输注期间正常和增加流量时的肺毛细血管压力。在所有剂量下，在完整动物中注射肾上腺素引起低氧血症、高碳酸血症和酸中毒。动脉氧分压在注射后1分钟内降低。50和100 mcg/kg给药后10分钟出现高乳酸血症。100 mcg/kg肾上腺素给药后，心率血压乘积降低10分钟。除100 mcg/kg肾上腺素外，酚妥拉明预处理可减弱这些作用。在离体肺准备中，肾上腺素与增加的肺流量相结合增加了肺毛细血管压力和肺水。在完整的麻醉大鼠中推注肾上腺素在治疗的1分钟内损害肺氧交换。α-肾上腺素能受体阻滞剂可减弱这种作用。当肾上腺素治疗与肺流量增加相结合时，在高于阈值肺毛细血管压的离体肺中发生水肿。这些结果可能反对使用传统剂量的肾上腺素进行复苏，特别是在麻醉患者中。
Previous studies indicate epinephrine adversely affects arterial oxygenation when administered in a rat model of local anesthetic overdose. The authors tested whether epinephrine alone exerts similar effects in the intact animal. Anesthetized rats received a single intravenous injection of epinephrine (25, 50, or 100 mcg/kg); matched cohorts were pretreated with phentolamine (100 mcg/kg); n = 5 for each of the six treatment groups. Arterial pressure and blood gases were measured at baseline, 1 and 10 min after epinephrine administration. Pulmonary capillary pressures during epinephrine infusion with normal and increased flows were measured in an isolated lung preparation. Epinephrine injection in the intact animal caused hypoxemia, hypercapnia, and acidosis at all doses. Arterial oxygen tension was reduced within 1 min of injection. Hyperlactatemia occurred by 10 min after 50 and 100 mcg/kg. Rate pressure product was decreased by 10 min after 100 mcg/kg epinephrine. Pretreatment with phentolamine attenuated these effects except at 100 mcg/kg epinephrine. In the isolated lung preparation, epinephrine in combination with increased pulmonary flow increased pulmonary capillary pressure and lung water. Bolus injection of epinephrine in the intact, anesthetized rat impairs pulmonary oxygen exchange within 1 min of treatment. Effects were blunted by a-adrenergic receptor blockade. Edema occurred in the isolated lung above a threshold pulmonary capillary pressure when epinephrine treatment was coupled with an increase in pulmonary flow. These results potentially argue against using traditional doses of epinephrine for resuscitation, particularly in the anesthetized patient.