Myocardium tolerates intermittent ischemia lbllowed by short reperfusions better than continuous ischemia of the same dural:ion. We attempted to delineate the differential mechanism(is) inw~lved in intermittent t, continuous ischemia. Isolated, paced rabbit hearts were perfused tit 22 ml/min. Coronary flow was stopped iutermi/tently 12 x lbr 2 or 4 rain, with 3-rain reperfusions (tolat reperfusion period: 36 rain). /n two other groups, llow was stopped continuously for 24 or 36 rain followed by a fiat 36-rain reperfusiun. Following the first intermittent 2-rain ischemia, adenosine eft/ux increased ninefold; in all subsequent ischemia/reperfusion cycles, adenosine and total purine releases were substantially less despite identical heart rates, coronary flows and ischemic periods. The rate-pressure product prior to the intermittent ischemias exhibited exponential correlations with total purine efllux during the 3 rain of repeffusion. When intermittent ischemia was extended to 4 min, the initial attenuation of NFI:' breakdown during the prior 2-rain occlusions was overcome, but during subsequent 4-rain ischemia/reperfusion cycles, ATP breakdown was again attenuated relative to the first 4-min ischemia. After the prolonged continuous ischemias, purine eftlux was up to 6 x higher than with intermittent ischemias of the same total time of zero flow. l,actate release and hence cellular H + export after intermittent ischemias remained consislently elevated, but following the continuous ischemia of 36 rain, release of lactate, and thus H +, was subsequentially decreased. Glycogen mobilization occurred regardless of the ischemia's nature, but it was markedly enhanced during conlinuous ischemias, where no fall in proglycogen levels occurred. Similarly, myocardial norepinephrine release increased substantially only during the prolonged continuous ischemias. Thus short intermittent ischemia attenuates cardiac adenylate degradation and glycogen mobilization; such ischemic insult a/so provides for better lactate and tt ~ washouts immediately upon reperfusiun. Another beneticial effect of intermittent ischemia was lhe nearcomplete absence of free interstitial norepinephrine, which exacerbates myocardial ischemic insults. In addition, the exponential correlations between preischemic rate-pressure product and postischemic purine release suggest that preischemic energy demand may determine ATP breakdown in ischemic rabbit myocardium.

Intermittent v continuous ischemia decelerates adenylate breakdown and prevents norepinephrine release in reperfused rabbit heart.

CECONI, Claudio;FERRARI, Roberto
1995

Abstract

Myocardium tolerates intermittent ischemia lbllowed by short reperfusions better than continuous ischemia of the same dural:ion. We attempted to delineate the differential mechanism(is) inw~lved in intermittent t, continuous ischemia. Isolated, paced rabbit hearts were perfused tit 22 ml/min. Coronary flow was stopped iutermi/tently 12 x lbr 2 or 4 rain, with 3-rain reperfusions (tolat reperfusion period: 36 rain). /n two other groups, llow was stopped continuously for 24 or 36 rain followed by a fiat 36-rain reperfusiun. Following the first intermittent 2-rain ischemia, adenosine eft/ux increased ninefold; in all subsequent ischemia/reperfusion cycles, adenosine and total purine releases were substantially less despite identical heart rates, coronary flows and ischemic periods. The rate-pressure product prior to the intermittent ischemias exhibited exponential correlations with total purine efllux during the 3 rain of repeffusion. When intermittent ischemia was extended to 4 min, the initial attenuation of NFI:' breakdown during the prior 2-rain occlusions was overcome, but during subsequent 4-rain ischemia/reperfusion cycles, ATP breakdown was again attenuated relative to the first 4-min ischemia. After the prolonged continuous ischemias, purine eftlux was up to 6 x higher than with intermittent ischemias of the same total time of zero flow. l,actate release and hence cellular H + export after intermittent ischemias remained consislently elevated, but following the continuous ischemia of 36 rain, release of lactate, and thus H +, was subsequentially decreased. Glycogen mobilization occurred regardless of the ischemia's nature, but it was markedly enhanced during conlinuous ischemias, where no fall in proglycogen levels occurred. Similarly, myocardial norepinephrine release increased substantially only during the prolonged continuous ischemias. Thus short intermittent ischemia attenuates cardiac adenylate degradation and glycogen mobilization; such ischemic insult a/so provides for better lactate and tt ~ washouts immediately upon reperfusiun. Another beneticial effect of intermittent ischemia was lhe nearcomplete absence of free interstitial norepinephrine, which exacerbates myocardial ischemic insults. In addition, the exponential correlations between preischemic rate-pressure product and postischemic purine release suggest that preischemic energy demand may determine ATP breakdown in ischemic rabbit myocardium.
1995
J. W., De; A., Cargnoni; S., Bradamante; S., Curello; M., Janssen; E., Pasini; Ceconi, Claudio; R., Bünger; Ferrari, Roberto
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11392/524523
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