Introduction: Abrupt hyperglycemia induces unexpected cardiovascular responses; however, their underlying pathophysiological mechanisms remain unknown. We studied how hyperglycemia affects the cardiohemodynamic and electrophysiological variables.
Methods: Glucose in a dose of 3 g/6 mL/kg was intravenously infused over 30 min to the isoflurane-anesthetized intact dogs (n=4).
Results: Administration of glucose increased plasma glucose level and osmolality but decreased Na⁺, Cl⁻ and glucagon concentrations, whereas it tended to increase insulin level accompanied with decreased K⁺ concentration. Glucose decreased peripheral vascular resistance, but increased heart rate, left ventricular contractility and cardiac output along with increased preload to the left ventricle. Glucose infusion prolonged atrioventricular nodal and intraventricular conduction time as well as ventricular repolarization period.
Conclusion: Delay of ventricular repolarization might be partly caused by insulin-induced hypokalemia in the hyperglycemia dog model. Hyperosmolarity was reported to induce negative chronotropic, inotropic and dromotropic effects in vitro, which could be well counterbalanced by the reflex-mediated sympathetic tone in vivo, resulting in various phenotypes as shown in this study.