Key result
Glucose infusion significantly attenuated acute restraint stress-induced elevation of plasma adrenaline, left ventricular dysfunction, and TxA2 production in the PVN in rats.
Why the study?
Acute restraint stress activates the sympathetic system and increases blood glucose, but whether glucose infusion affects these stress-induced sympathetic responses remained unknown.
Does glucose infusion suppress acute restraint stress-induced sympathetic responses and cardiac impairment in rats?
Does glucose infusion suppress acute restraint stress-induced sympathetic responses and cardiac impairment in rats?
In a rat model, glucose infusion suppresses acute restraint stress-induced elevation of plasma adrenaline, left ventricular dysfunction, and central production of TxA2.
Answers are grounded in this paper and cite their sources.
Hypothesis-generating in rats; leaves open any clinical role for glucose during acute stress.
BackgroundAcute 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.MethodsPlasma 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.ResultsRS 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 B2 (TxB2) (a metabolite of TxA2) levels in the PVN but did not alter prostaglandin E2 levels in the PVN.ConclusionOur 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 TxA2 in the PVN.
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Yamaguchi et al. (2022) studied Acute restraint stress. Glucose infusion was evaluated on Plasma catecholamines, cardiac parameters, and prostanoid levels in the PVN. Glucose infusion significantly attenuated acute restraint stress-induced elevation of plasma adrenaline, left ventricular dysfunction, and TxA2 production in the PVN in rats.
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