Hohnloser S H, Verrier R L, Lown B
Cardiovasc Res. 1986 Dec;20(12):891-6. doi: 10.1093/cvr/20.12.891.
The influence of adrenergic and muscarinic receptor activation on cardiac electrical stability and on serum potassium concentrations was studied in 23 anaesthetised dogs. The ventricular fibrillation threshold was assessed using the single stimulus technique. Adrenaline (1.0 microgram X kg-1 X min-1) caused a brief rise and a subsequent prolonged fall in serum potassium concentration, which was accompanied by a decline in ventricular fibrillation threshold when baroreceptor activation was prevented. After pretreatment with the beta1 adrenoceptor blocking agent metoprolol (0.5 mg X kg-1), adrenaline did not alter vulnerability to ventricular fibrillation but still elicited hypokalaemia. In contrast, selective beta2 adrenoceptor blockade (ICI 118551, 100 micrograms X kg-1) prevented the adrenaline induced lowering of serum potassium concentration but not of ventricular vulnerability. Muscarinic receptor activation by methacholine (3.0 micrograms X kg-1 X min-1) had no effect on serum potassium concentration but increased the ventricular fibrillation threshold by 30%. When methacholine was administered concomitantly with adrenaline the decline in serum potassium concentration persisted, but the increase in ventricular vulnerability was completely prevented. It is concluded that in the normal canine myocardium adrenaline produces an increase in vulnerability that is mediated through beta 1 adrenoceptors and that the beta 2 adrenoceptor mediated hypokalaemia is dissociated from electrophysiological effects of adrenaline. Parasympathetic nervous system activation does not influence serum potassium concentrations but opposes the effects of adrenaline on susceptibility to ventricular fibrillation.
在23只麻醉犬中研究了肾上腺素能和毒蕈碱受体激活对心脏电稳定性及血清钾浓度的影响。采用单次刺激技术评估室颤阈值。肾上腺素（1.0微克·千克⁻¹·分钟⁻¹）使血清钾浓度短暂升高，随后持续下降，当压力感受器激活被阻断时，这伴随着室颤阈值降低。在用β1肾上腺素能受体阻断剂美托洛尔（0.5毫克·千克⁻¹）预处理后，肾上腺素未改变室颤易感性，但仍引起低钾血症。相反，选择性β2肾上腺素能受体阻断（ICI 118551，100微克·千克⁻¹）可防止肾上腺素诱导的血清钾浓度降低，但不能防止心室易损性降低。毒蕈碱受体被乙酰甲胆碱（3.0微克·千克⁻¹·分钟⁻¹）激活对血清钾浓度无影响，但使室颤阈值提高了30%。当乙酰甲胆碱与肾上腺素同时给药时，血清钾浓度持续下降，但心室易损性增加被完全防止。结论是，在正常犬心肌中，肾上腺素通过β1肾上腺素能受体介导使易损性增加，且β2肾上腺素能受体介导的低钾血症与肾上腺素的电生理效应无关。副交感神经系统激活不影响血清钾浓度，但对抗肾上腺素对心室颤动易感性的影响。
