Thompson K E, Adams M A
Department of Pharmacology and Toxicology, Queen's University, Kingston, Ontario, Canada.
J Hypertens. 1994 Apr;12(4):409-18.
To determine in rats the acute effect of ethanol on the activity of a marker of cardiac and vascular growth processes (ornithine decarboxylase) and on alpha 1-adrenergic-induced vascular trophic responses, and whether ethanol-induced sympathoadrenal hyperactivity stimulated vascular structural changes after a more prolonged treatment.
Acute treatment was as follows: ethanol (5 g/kg, intubation), alpha 1-adrenergic agonist (10 mg/kg methoxamine subcutaneously), methoxamine plus ethanol, or control. Left ventricular, aortic and mesenteric vascular ornithine decarboxylase activity was determined 4 h later by measuring 14CO2 evolved from [14C]-ornithine. Three-day treatment was as follows: ethanol (every 8 h, intubation, 5 g/kg initial dose, subsequent doses based on intoxication level) or isocaloric quantities of maltose dextrin. The left ventricular: body weight ratio, hindlimb vascular resistance properties and indices of cardiac and vascular hypertrophy were determined.
In the acute treatment methoxamine-induced pressor responses and the activation of vascular ornithine decarboxylase were both inhibited by ethanol treatment. Ethanol alone elevated the heart rate and decreased mean arterial pressure while stimulating left ventricular but not vascular ornithine decarboxylase activity. Methoxamine did not alter left ventricular ornithine decarboxylase activity. Three-day ethanol treatment induced cardiac hypertrophy but had no effect on the hindlimb vascular resistance properties measured at maximum dilation and maximum constriction.
Acute and short-term ethanol exposure induces cardiac growth processes. Ethanol prevents alpha 1-adrenergic activated vascular growth response by a mechanism that may be similar to the attenuation of alpha 1-adrenergic-induced elevation of arterial pressure.
确定乙醇对大鼠心脏和血管生长过程标志物（鸟氨酸脱羧酶）活性以及α1-肾上腺素能诱导的血管营养反应的急性影响，以及乙醇诱导的交感肾上腺功能亢进在更长时间治疗后是否会刺激血管结构变化。
急性处理如下：乙醇（5 g/kg，插管给药）、α1-肾上腺素能激动剂（10 mg/kg甲氧明皮下注射）、甲氧明加乙醇或对照。4小时后，通过测量从[14C]-鸟氨酸释放的14CO2来测定左心室、主动脉和肠系膜血管的鸟氨酸脱羧酶活性。三天处理如下：乙醇（每8小时，插管给药，初始剂量5 g/kg，后续剂量根据中毒程度调整）或等热量的麦芽糖糊精。测定左心室与体重比、后肢血管阻力特性以及心脏和血管肥大指标。
在急性处理中，乙醇处理抑制了甲氧明诱导的升压反应和血管鸟氨酸脱羧酶的激活。单独乙醇可提高心率并降低平均动脉压，同时刺激左心室而非血管的鸟氨酸脱羧酶活性。甲氧明未改变左心室鸟氨酸脱羧酶活性。三天乙醇处理诱导了心脏肥大，但对最大扩张和最大收缩时测量的后肢血管阻力特性无影响。
急性和短期乙醇暴露可诱导心脏生长过程。乙醇通过一种可能类似于减弱α1-肾上腺素能诱导的动脉压升高的机制，阻止α1-肾上腺素能激活的血管生长反应。
