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In our laboratory, we found in anesthetized goats that Godofredo Diéguez Castrillo
during partial occlusion of the left circumflex coronary
artery, coronary vascular conductance was reduced by effects of ET-1 in the coronary circulation. In this case, 15-
about 30%, and the coronary vasodilatation in response to or 60-min total occlusion of the left circumflex coronary
Achand sodium nitroprusside was decreased in animals artery was induced in anesthetized goats. In non-treated
non-treated or treated with L-NAME or with animals, during reperfusion after 15-min occlusion, the
meclofenamate; the vasoconstriction in response to ET- ET-1-induced coronary effects were lightly increased, and
1 was depressed in non-treated animals, and this the effects of Ach were unchanged. During reperfusion
depression was reversed by L-NAME and was accentuated after 60-min occlusion, the ET-1-induced effects were
by meclofenamate. At 30 min of reperfusion after this more pronounced, and the effects of Ach were decreased.
partial coronary occlusion, coronary vascular conductance L-NAME treatment did not modify the coronary effects of
remained decreased by about 25%, and the vasodilatation ET-1 during reperfusion after both occlusion durations.
in response to Achand sodium nitroprusside, as well as the This treatment inhibited the effects of Ach during
vasoconstriction with ET-1 were as in the control and were reperfusion after 15-min, and after 60-min occlusions.
comparable in treated and non-treated animals. These Meclofenamate treatment did not modify the coronary
results suggest: a) that during partial ischemia, effects of ET-1 and Ach during reperfusion after both
the coronary vasodilator reserve is greatly reduced, and the occlusion durations. Thus, ischemia-reperfusion could
vasoconstriction to ET-1 is blunted, with preservation of increase the coronary response to ET-1, which is more
the modulatory role of NO and involvement of pronounced during reperfusion after prolonged than after
vasoconstrictor prostanoids in this vasoconstriction, and 2) brief ischemia, and that this increased response to ET-1 is
that during its reperfusion, the coronary vasodilator reserve probably related to inhibition of NO release, without
and the coronary reactivity to Ach and ET-1 recover, but involvement of prostanoids (184). Figure 12 shows an
the modulatory role of NO in this reactivity may be estimation of the role played by NO in the regulation of
attenuated (183). the coronary circulation under normal conditions and after
ischemia-reperfusion (183, 184).
We also explored the effects of reperfusion after short
and prolonged, total ischemia on the role of NO and the
Figure 12. Estimation of the role played by NO in the regulation of the coronary circulation under normal conditions, after partial
coronary occlusion followed by reperfusion (PI+R), after 15 min of total coronary occlusion followed by reperfusion (TI15+R) and after
60 min of total coronary occlusion followed by reperfusion (TI60+R). These estimations are based on data obtained in experiments with
Ach and ET-1 in anesthetized goats (References 183, 184).
To compare the coronary response to ET-1 with the human plasma levels of AVP are augmented after
response to other vasoconstrictor after ischemia- myocardial infarction (187), and during reperfusion after
reperfusion, we explored the coronary effects of arginine– myocardial infarction (188). Studies performed in dogs
vasopressin (AVP). This hormone may be of significance show that the coronary effects of AVP are increased in the
in the regulation of coronary circulation as it can produce ischemic myocardium, which can worsen hypoperfusion of
coronary vasoconstriction (185), which can be severe collateral-dependent myocardium during exercise (189).
enough to cause myocardial ischemia (186). This peptide Sellke and Quillen (190) report that the coronary action of
also could be of interest for understanding the AVP is augmented after ischemia alone or followed by
pathophysiology of myocardial ischemia-reperfusion as reperfusion, and the authors suggest that this augmented
32 @Real Academia Nacional de Farmacia. Spain
