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  • 1
    ISSN: 1432-0428
    Keywords: Insulin-induced hypoglycaemia ; plasma volume ; heart rate ; cardiac output ; cardiac stroke volume ; blood pressure ; plasma catecholamines ; vascular resistance
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Haemodynamic variables (plasma volume, heart rate, blood pressure, cardiac output, stroke volume, pulmonary tissue volume, total peripheral vascular resistance, hepato-splanchnic vascular resistance, lower extremity vascular resistance and plasma catecholamines) were measured before and after insulin-induced hypoglycaemia in seven healthy men. Plasma volume decreased significantly at the nadir of glucose (mean decrease 222±41 ml) and subsequently increased to pre-hypoglycaemic values within 30 min. Cardiac output increased in response to hypoglycaemia (mean increase 2.8±0.61/min). The early rise in cardiac output was primarily due to an increase in heart rate, but later mainly due to increased stroke volume. Since pulmonary tissue volume was constant, the observed changes in cardiac output are unlikely to be due to a Frank-Starling mechanism but rather to increased sympatho-adrenal activity. Total peripheral vascular resistance as well as lower extremity vascular resistance decreased, whereas hepato-splanchnic vascular resistance was unaffected. Thus insulin-induced hypoglycaemia has marked transient effects on the circulation.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-0428
    Keywords: Insulin-dependent diabetes ; autonomic neuropathy ; graded exercise ; heart rate ; blood pressure ; cardiac output ; cardiac stroke volume ; plasma volume ; hepato-splanchnic blood flow ; body temperature ; plasma catecholamines
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Haemodynamic variables were measured during supine rest and during ergometer cycle exercise at two work loads (50 W and 100 W) in normal subjects (n = 7), in insulin-dependent diabetic subjects without neuropathy (n = 8), in insulin-dependent diabetic subjects with slight autonomic neuropathy (decreased beat-to-beat variation in heart rate, which is considered due to a cardiac parasympathetic defect; n = 8), and in insulin-dependent diabetic subjects with severe autonomic neuropathy, including orthostatic hypotension (n = 7). Compared with normal subjects, cardiac stroke volume was lower in the diabetic subjects with autonomic neuropathy, both at rest and during exercise (p 〈 0.025), whereas intermediate values were found in the diabetic subjects without neuropathy. The increase in cardiac output in response to exercise was smaller (p 〈 0.05) in both diabetic groups with autonomic neuropathy compared with the normal and diabetic subjects without autonomic neuropathy. The increase in hepato-splanchnic vascular resistance was smaller in the diabetic subjects with severe autonomic neuropathy than in the normal subjects and the diabetic subjects without autonomic neuropathy (p 〈 0.025), whereas intermediate values were found in the diabetic subjects with slight autonomic neuropathy. We conclude that, in diabetic patients with severe autonomic neuropathy, the responses of the heart and the splanchnic resistance vessels to exercise are impaired. While sympathetic neuropathy may be responsible for impaired function of splanchnic resistance vessels, both cardiac sympathetic neuropathy and diabetic cardiomyopathy may be involved in the impaired cardiac response to exercise in diabetic subjects with autonomic neuropathy.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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