Guthrie S D, Murphy Q R
Can J Physiol Pharmacol. 1976 Jun;54(3):347-56. doi: 10.1139/y76-049.
The epinephrine-induced loss and subsequent uptake of K+ by the liver was studied by measuring hepatic arterio-venous K+ differences and splanchnic blood flows in anesthetized dogs with chronically implanted portal vein catheters and celiac and superior mesenteric artery flow probes. When epinephrine was administered intraportally, neither alpha- nor beta-adrenergic blockade, singly or in combination, had significant effects upon the hyperkalemic or the hypokalemic phases in either hepatic venous or systemic arterial blood. It was concluded that the movements of K+ into and out of the liver caused by epinephrine are not mediated by the classical adrenergic receptors as defined by inhibition by specific blocking agents.
通过测量慢性植入门静脉导管以及腹腔干和肠系膜上动脉血流探头的麻醉犬的肝动静脉钾差异和内脏血流量，研究了肾上腺素诱导的肝脏钾流失及随后的摄取情况。当经门静脉给予肾上腺素时，单独或联合使用α-或β-肾上腺素能阻滞剂，对肝静脉或体循环动脉血中的高钾血症或低钾血症阶段均无显著影响。得出的结论是，肾上腺素引起的钾进出肝脏的运动不是由特定阻滞剂抑制所定义的经典肾上腺素能受体介导的。
