Key result
Type II diabetes did not significantly alter overall peak reactive hyperaemia compared to controls, though in diabetics it was influenced by meal intake (fasting 51.2 vs non-fasting 42.8, P<0.05).
Why the study?
What are the determinants of post-ischaemic reactive hyperaemia in patients with type II diabetes mellitus compared to controls?
Cross-Sectional (n=161)
What are the determinants of post-ischaemic reactive hyperaemia in patients with type II diabetes mellitus compared to controls?
In patients with type II diabetes, post-ischaemic reactive hyperaemia is influenced by gender, actual blood glucose, and postprandial state, which should be considered when assessing resistance vessel function.
Answers are grounded in this paper and cite their sources.
Meal intake may confound reactive hyperaemia assessment in type II diabetes; hypothesis-generating for standardized microvascular protocols.
Dysfunction of resistance arteries is thought to be an early reversible stage in the development of atherosclerosis. Dynamics of post-ischaemic reactive hyperaemia are believed to constitute a useful tool for monitoring resistance vessel function. Patient characteristics influencing reactive hyperaemia, however, need to be defined more precisely. Since reactive hyperaemia is a dynamic process, yielding submaximal peak values after 5 min of ischaemia, this period was chosen to investigate the determinants of reactive hyperaemia in 100 type II diabetic patients as well as in 61 control subjects. Reactive hyperaemia was measured by venous-occlusion plethysmography; clinical and laboratory data were acquired by routine methods. Statistical comparison was performed with SYSTAT 5.0 for Apple Macintosh. Overall, no significant differences between diabetic patients and controls were observed by group comparison. In control subjects, only gender showed an influence on peak reactive hyperaemia (females 40.5 +/- 15.3; males 51.8 +/- 17.7 ml min-1 100 ml-1, P < 0.01). In diabetic patients, in addition to gender, actual blood glucose (r = 0.377, P < 0.05) and meal intake (non-fasting 42.8 +/- 19.2; fasting 51.2 +/- 19.5 ml min-1 100 ml-1, P < 0.05) were found to influence reactive hyperaemia. Further investigation revealed a loss of the correlation between peak reactive hyperaemia and actual blood glucose observed in the fasting state (P < 0.001) in non-fasting diabetic patients, indicating an influence of meal intake on resistance vessel reactivity. Our results suggest that, in diabetic subjects, in addition to gender actual blood glucose and the postprandial situation impacts on peak reactive hyperaemia.
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Francesconi et al. (1999) conducted a cross-sectional in Type II diabetes mellitus (n=161). Type II diabetes mellitus vs. Control subjects was evaluated on Peak reactive hyperaemia after 5 min of ischaemia. Type II diabetes did not significantly alter overall peak reactive hyperaemia compared to controls, though in diabetics it was influenced by meal intake (fasting 51.2 vs non-fasting 42.8, P<0.05).
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