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The effects of alcohol binge on vessel reactivity

Alcohol (ALC) consumption is associated with alterations in blood pressure and changes in vascular function. Chronic and excessive ALC consumption increases the risk for hypertension and stroke, while moderate daily intake has been shown to reduce incidence of coronary artery disease leading to a reduction in the risk of myocardial infarction. The underlying mechanism has been suggested to be altered endothelial function, with moderate ALC consumption enhancing endothelial function, while chronic excessive consumption impairs function. Previous studies have shown that acute ALC intoxication (AAI) decreases blood pressure, enhances hypotension following hemorrhagic shock, and impairs pressor response to fluid resuscitation. This study examined the effects of AAI on blood vessel reactivity to phenylephrine (PE), acetylcholine (Ach), and nitroprusside (NP) ex‐vivo. Chronically instrumented, conscious male Sprague‐Dawley rats (300–350 g) received a primed continuous 15 hour intragastric ALC infusion (1.75g/kg + 300 mg/kg/hr). Thirty minutes after discontinuing ALC, animals were sacrificed for isolation of thoracic aorta and mesenteric arteries. Aortic and mesenteric ring segments (1–2 mm) were suspended in myograph baths containing Krebs‐Henseleit bicarbonate buffer, pH 7.4, gassed with 95% O2: 5% CO2. Arterial rings from AAI rats had decreased PE‐induced tension (aorta: 2.28 ± 0.09 vs. 2.6 ± 0.13 g; mesenteric artery: 1.70 ± 0.06 vs. 1.91 ± 0.10), greater (21%) Ach‐mediated relaxation and similar NP‐mediated relaxation. These results indicate that AAI favors vasodilatation and are consistent with enhanced endothelial dilator function. (Supported by DOD PR‐054196).