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Randsbaek, F. et al.

Randsbaek, Lund, Kimose, Grove, Bøtker, Schmitz, Nielsen,

Angiotensin II inhibition increases cellular glucose transport during reperfusion but not ischemia in pig hearts.

OBJECTIVE: To study whether ACE inhibition and AT-II receptor blockade modulates myocardial glucose uptake during ischemia and reperfusion. DESIGN: We developed a method for in vivo sampling of large trans-myocardial tissue samples from beating pig hearts and in vitro measurement of sarcolemmal glucose transport, in a series of experiments in which hearts were exposed to stimuli (glucose-insulin and pacing) known to promote cellular glucose transport. In the subsequent study we compared three experimental groups: (i) ACE inhibition (ACE-I, n = 6): increasing oral doses of benazepril up to 40 mg daily for 3 weeks, (ii) angiotensin II receptor antagonist (AT II-A, n = 7): increasing oral doses of valsartan up to 320 mg for 3 weeks, (iii) control (n = 7). Samples were harvested at baseline, following 20 min of regional ischemia, and following 5 and 15 min of reperfusion. The samples were incubated with 3-O-methylglucose (MeGlu), and cellular MeGlu uptake was measured. RESULTS: Insulin-glucose, pacing, and ischemia increased cellular MeGlu transport two- to fourfold (p < 0.001). Cellular MeGlu transport was increased in ACE-I and AT II-A animals during reperfusion (p < 0.001), but not at baseline or during ischemia, compared with controls. CONCLUSION: Enhanced capacity for glucose transport during reperfusion may be a mechanism underlying the beneficial effects of ACE inhibition and AT II-antagonism in ischemic heart disease.[1]

References

Angiotensin II inhibition increases cellular glucose transport during reperfusion but not ischemia in pig hearts. Randsbaek, F., Lund, S., Kimose, H.H., Grove, E., Bøtker, H.E., Schmitz, O., Nielsen, T.T. Scand. Cardiovasc. J. (2003) [Pubmed]

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