The effect of endogenously released glucose, insulin, glucagon-like peptide 1, ghrelin on cardiac output, heart rate, stroke volume, and blood pressure.
BACKGROUND
Ingestion of a meal increases the blood flow to the gastrointestinal organs and affects the heart rate (HR), blood pressure and cardiac output (CO), although the mechanisms are not known. The aim of this study was to evaluate the effect of endogenously released glucose, insulin, glucagon-like peptide 1 (GLP-1), ghrelin on CO, HR, stroke volume (SV), and blood pressure.


METHODS
Eleven healthy men and twelve healthy women ((mean ± SEM) aged: 26 ± 0.2 y; body mass index: 21.8 ± 0.1 kg/m(2))) were included in this study. The CO, HR, SV, systolic and diastolic blood pressure, antral area, gastric emptying rate, and glucose, insulin, GLP-1 and ghrelin levels were measured.


RESULTS
The CO and SV at 30 min were significantly higher, and the diastolic blood pressure was significantly lower, than the fasting in both men and women (P < 0.05). In men, significant correlations were found between GLP-1 level at 30 min and SV at 30 min (P = 0.015, r = 0.946), and between ghrelin levels and HR (P = 0.013, r = 0.951) at 110 min. Significant correlations were also found between the change in glucose level at 30 min and the change in systolic blood pressure (P = 0.021, r = -0.681), and the change in SV (P = 0.008, r = -0.748) relative to the fasting in men. The insulin 0-30 min AUC was significantly correlated to the CO 0-30 min AUC (P = 0.002, r = 0.814) in men. Significant correlations were also found between the 0-120 min ghrelin and HR AUCs (P = 0.007, r = 0.966) in men. No statistically significant correlations were seen in women.


CONCLUSIONS
Physiological changes in the levels of glucose, insulin, GLP-1 and ghrelin may influence the activity of the heart and the blood pressure. There may also be gender-related differences in the haemodynamic responses to postprandial changes in hormone levels. The results of this study show that subjects should not eat immediately prior to, or during, the evaluation of cardiovascular interventions as postprandial affects may affect the results, leading to erroneous interpretation of the cardiovascular effects of the primary intervention.


BACKGROUND
NCT01027507.
Center for Emergency, Department of Cardiology, Skåne University Hospital, Malmö, Lund University, Sweden. Joanna.hlebowicz@med.lu.se
Joanna
J
Hlebowicz
Sandra
S
Lindstedt
Ola
O
Björgell
Magnus
M
Dencker
D000328:Adult; D001786:Blood Glucose / Q000378:metabolism*; D001794:Blood Pressure / Q000502:physiology; D002302:Cardiac Output / Q000502:physiology; D003971:Diastole / Q000502:physiology; D004435:Eating / Q000502:physiology; D015150:Echocardiography, Doppler / Q000592:standards; D005215:Fasting / Q000502:physiology; D005260:Female; D054439:Ghrelin / Q000097:blood*; D052216:Glucagon-Like Peptide 1 / Q000097:blood*; D006334:Heart Function Tests / Q000592:standards*; D006339:Heart Rate / Q000502:physiology; D006439:Hemodynamics / Q000502:physiology*; D006801:Humans; D007328:Insulin / Q000097:blood*; D008297:Male; D019518:Postprandial Period / Q000502:physiology; D015203:Reproducibility of Results; D013318:Stroke Volume / Q000502:physiology; D013599:Systole / Q000502:physiology
D001786:Blood Glucose; D054439:Ghrelin; D007328:Insulin; D052216:Glucagon-Like Peptide 1