Hemodynamic effects of the early and long-term administration of propranolol in rats with intrahepatic portal hypertension

Background and aims The aims of this study were to evaluate a preventive effect on collateral venous circulation of long-term administration of propranolol in intrahepatic portal hypertensive rats. Methods Eighty-six Sprague–Dawley rats were allocated to two models of hepatic fibrosis, bile duct-ligated (BDL) induced and carbon tetrachloride (CCl4) induced. Each model was divided into two groups: one receiving placebo and the other propranolol (75 mg kg−1 d−1). Mean arterial pressure (MAP), heart rate (HR), portal pressure (PP), cardiac index (CI), vascular systemic resistance, and splenorenal shunt blood flow (SRS-BF) were measured in anesthetized rats. Results In the BDL model, no significant hemodynamic changes were observed in the propranolol group compared with the placebo group. In CCl4-induced rats, HR (390 ± 50 vs. 329 ± 51 beats/min, P = .001), CI (44 ± 11 vs. 34 ± 10 ml/min, P = .004), PP (15.4 ± 3.0 vs. 13.4 ± 1.9 mmHg, P = .045), and SRS-BF (1.4 ± 1.1 vs. 1.0 ± 1.0 ml/min, P = .047) were significantly lower in the propranolol group. Conclusions This study showed that propranolol has a significant hemodynamic effect only in the CCl4 model and suggested a model-dependent effect of propranolol

Cardiovascular effects of electronic cigarettes

Cardiovascular safety is an important consideration in the debate on the benefits versus the risks of electronic cigarette (EC) use. EC emissions that might have adverse effects on cardiovascular health include nicotine, oxidants, aldehydes, particulates, and flavourants. To date, most of the cardiovascular effects of ECs demonstrated in humans are consistent with the known effects of nicotine. Pharmacological and toxicological studies support the biological plausibility that nicotine contributes to acute cardiovascular events and accelerated atherogenesis. However, epidemiological studies assessing Swedish smokeless tobacco, which exposes users to nicotine without combustion products, generally have not found an increased risk of myocardial infarction or stroke among users, but suggest that nicotine might contribute to acute cardiovascular events, especially in those with underlying coronary heart disease. The effects of aldehydes, particulates, and flavourants derived from ECs on cardiovascular health have not been determined. Although ECs might pose some cardiovascular risk to users, particularly those with existing cardiovascular disease, the risk is thought to be less than that of cigarette smoking based on qualitative and quantitative comparisons of EC aerosol versus cigarette smoke constituents. The adoption of ECs rather than cigarette smoking might, therefore, result in an overall benefit for public health