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Postprandial hypotension (PPH) is a unique clinical phenomenon in the elderly. But its underlying pathogenesis has not been elucidated. The aim of the study was to evaluate the effect of insulin, glucagon and neurotensin on postprandial hypotension.
From May 2014 to Feb 2016, 28 inpatients who were diagnosed with PPH at stable condition (PPH group), and 22 aged-matched cases without PPH (control group) were selected from the Department of Senior Ward, China-Japan Friendship Hostital. The changes in blood pressure, blood glucose, insulin, glucagon as well as neurotensin at fasting stage and at 30 min, 60 min, 90 min and 120 min after meal were measured. The differences between the two groups were compared.
The incidence of abnormal glucose metabolism (including diabetes and impaired glucose tolerance) were significantly higher in PPH group than in control group [78.6% vs.40.9%, P<0.05]. There were no significant differences in other clinical data between the two groups. The maximal fall of postprandial systolic blood pressure in PPH group was significantly larger compared with those in control group [(34.6±12.8) mmHg vs. (12.1±9.7) mmHg, P<0.05]. There was no significant difference in the maximal fall of postprandial diastolic blood pressure between the two groups [(12.1±9.7) mmHg vs. (10.9±7.9) mmHg, P>0.05]. The maximal increase of postprandial glucose, insulin and neurotensin were significantly larger in PPH group than in control group [(3.3±1.6) mmol/L vs. (2.5±0.5) mmol/L, (20.1±3.7) UIU/ml vs. (12.1±3.9) UIU/ml, (213.2±165.4) pg/ml vs. (143.3±112.6) pg/ml, P<0.05]. The maximal increase of glucagon was not statistically significant between PPH group and control group [(35.7±33.9) pg/ml vs. (43.3±30.3) pg/ml, P>0.05].
The postprandial insulin and neurotensin secretion are increased significantly in PPH, indicating that PPH formation is associated with abnormal secretion of some gastrointestinal hormones.