Glucose infusion suppresses acute restraint stress-induced peripheral and central sympathetic responses in rats

Background: Acute restraint stress (RS) induces sympathetic activation such as elevating plasma catecholamines, resulting in increase in blood glucose. We aimed to investigate whether glucose infusion affects the RS-induced sympathetic responses. Methods: Plasma catecholamines were measured by high-performance liquid chromatography with electrochemical detection. Blood glucose levels were measured with a glucometer and a glucose assay kit. Cardiac parameters were measured by echocardiographic and hemodynamic analysis. Prostanoid levels in the paraventricular nucleus of hypothalamus (PVN) microdialysates were measured by liquid chromatography-ion trap tandem mass spectrometry analysis. Results: RS significantly increased plasma noradrenaline and adrenaline. Intravenous infusion of a 5% glucose solution significantly attenuated the RS-induced elevation of plasma adrenaline but did not alter the plasma noradrenaline. Glucose administration during RS suppressed the progression of cardiac impairment by attenuating the decline rates in left ventricular diastolic, end-diastolic volume, stroke volume, fractional shortening, and ejection fraction. Both Intravenous and intracerebroventricular infusion of glucose solution significantly attenuated the RS-induced elevation of thromboxane B-2 (TxB(2)) (a metabolite of TxA(2)) levels in the PVN but did not alter prostaglandin E2 levels in the PVN. Conclusion: Our results demonstrate that glucose infusion suppresses RS-induced elevation of plasma adrenaline and left ventricular dysfunction. In the brain, glucose infusion suppresses RS-induced production of TxA(2) in the PVN.

Automated summary

Acute restraint stress induces sympathetic activation and increased blood glucose levels. Glucose infusion has been found to attenuate the stress-induced elevation of plasma adrenaline and prevent cardiac dysfunction. In addition, glucose infusion suppresses the production of TxA(2) in the PVN during stress.