Hiatt N, Chapman L W, Mack H, Hiatt J
Department of Surgery, Cedars-Sinai Medical Center, Los Angeles, CA 90048.
Biomed Biochim Acta. 1988;47(4-5):395-400.
In control ureter ligated dogs infused with 2 mEq KCl/kg.h until prelethal electrocardiographic changes of hyperkalemic cardiotoxicity appear, a kaluresis independent K homeostatic mechanism delays the development of hyperkalemia by transferring some 55% of administered K to intracellular fluid. In preparations with cervical trunk vagotomy the proportion increases to about 70%; but not if the adrenals are simultaneously removed or denervated. A dosage of atropine that crosses the blood-brain barrier is an exact substitute for cervical vagotomy. Our findings suggest that ureter ligated K loaded dogs, ureteral and/or renal afferent vagal fibres to the brain release a "muscarinic" neurotransmitter(s) that modulated neural traffic in rami of splanchnic nerves to the adrenal medulla.
在对照的输尿管结扎犬中,以2毫当量氯化钾/千克·小时的速度输注氯化钾,直至出现高钾血症心脏毒性的致死前心电图变化,一种与尿钾增多无关的钾稳态机制通过将约55%的输入钾转移至细胞内液,从而延迟高钾血症的发展。在颈干迷走神经切断的制备中,这一比例增加至约70%;但如果同时切除肾上腺或使其去神经支配,则比例不会增加。一种能穿过血脑屏障的阿托品剂量可完全替代颈迷走神经切断术。我们的研究结果表明,输尿管结扎且负荷钾的犬,输尿管和/或肾传入迷走神经纤维向脑释放一种“毒蕈碱样”神经递质,该递质调节内脏神经分支至肾上腺髓质的神经冲动传导。