Insulin administration during beta receptor blockade in dogs exerted dose-dependent inotropic and vasodilator effects, significantly improving cardiac performance (P<0.01).
p-value: p=<0.01
Haemodynamic effects of small and high doses of insulin during beta receptor blockade were studied in nine dogs. Beta receptor blockade was induced by 0.5 mg/kg propranolol and caused depression of cardiac performance with a significant increase in left ventricular end-diastolic pressure (LVEDP) and a significant decrease in heart rate; maximum rate of left ventricular (LV) pressure rise (LVdP/dtmax), stroke volume and cardiac output. At 15 min, after beta receptor blockade, a bolus injection of 0.5 IU/kg of insulin, free of glucagon and calcium, was given followed by a continuous infusion of 0.5 IU/kg/h. After 30 min another bolus dose of 300 IU insulin was injected. Glucose and potassium were given to maintain physiological levels of these factors. Five minutes after a low dose of insulin there was a significant decrease in LVEDP (P less than 0.01), and a significant increase in LVdP/dtmax (P less than 0.01), in stroke volume (P less than 0.01) and in cardiac output (P less than 0.01). The other haemodynamic variables were not significantly changed. Administration of a high dose of insulin further, significantly, improved performance of the beta receptor blocked heart and caused a significant reduction in total peripheral resistance. In conclusion, insulin exerts inotropic and vasodilator effects which are dose-dependent and not related to adrenergic mechanisms.
Reikerås et al. (Tue,) conducted a other in Beta receptor blockade (n=9). Insulin vs. Baseline (post-beta blockade) was evaluated on Haemodynamic variables (LVEDP, LVdP/dtmax, stroke volume, and cardiac output) (p=<0.01). Insulin administration during beta receptor blockade in dogs exerted dose-dependent inotropic and vasodilator effects, significantly improving cardiac performance (P<0.01).