Four brief periods of myocardial ischemia cause no cumulative ATP loss or necrosis

Abstract

The effect of repetitive periods of coronary occlusion on myocardial adenine nucleotides, lactate, and infarct size was studied. In one series of dogs, the circumflex artery was occluded for one, two, or four 10-min episodes, each separated by 20 min of reperfusion. Hearts were excised and sampled for metabolic assays after one or more periods of ischemia before or after reperfusion. One 10-min period of ischemia caused a 61% loss of ATP and 41% loss of adenine nucleotides from the most severely ischemic subendocardial zone. Reperfusion resulted in rapid restoration of the adenylate charge but in only slight repletion of the adenine nucleotide pool. However, two or even four 10-min periods of ischemia caused no further adenine nucleotide loss. In contrast, 40 min of continuous coronary occlusion caused an 87% depletion of ATP and 67% of the adenine nucleotide pool from the same subendocardial region. Collateral blood flow was similar during all occlusions, but lactate accumulation was less during later occlusions. In a second series of experiments, myocardial necrosis was quantitated 4 days after four 10-min periods of ischemia. Necrosis was observed in only one of six dogs and, in this dog, was only 1.5% of the anatomic area at risk. Thus intermittent reperfusion prevents cumulative metabolic deficits and myocardial ischemic cell death, perhaps by restoring the capacity for high-energy phosphate (HEP) production and/or washing out deleterious catabolites. A first episode of ischemia also slows HEP utilization in subsequent episodes.

Glucose for the Heart

“…Preconditioning decreases glycogen breakdown as well as the accumulation of hexose 6-phosphates and lactate during no-flow ischemia. 119,120 Because the duration of protection by preconditioning is also related to the time course of postischemic glycogen recovery, 121 the data, when taken together, show that protection by ischemic preconditioning reduces glycogen breakdown, therefore attenuating the accumulation of metabolic end products and the development of intracellular acidosis. The slower decline of both pH i and highenergy phosphates in preconditioned hearts during no-flow ischemia 122 is in agreement with this hypothesis.…”

Pré-condicionamento isquêmico em diferentes tempos e seu efeito na translocação bacteriana induzida por isquemia e reperfusão intestinal em ratos

“…Since 1986, we know that repeated brief episodes of ischemia do not have cumulative deleterious effect, as shown by Reimer et al, noting that four ten-minute episodes of myocardial ischemia did not cause necrosis, while a single 40-minute episode of ischemia had this effect 14 . Among the many changes caused by ischemia and reperfusion, there is is bacterial translocation (BT), resulting from the breakdown of the epithelial barrier by inflammatory cytokines, as suggested by some authors 15,16 .…”

Atherosclerotic renal artery stenosis is associated with elevated cell cycle arrest markers related to reduced renal blood flow and postcontrast hypoxia

“…Repetitive periods of myocardial ischemia cause no harm to cardiac tissue [32]. More recently, 'remote' ischemic preconditioning using repetitive, transient tourniquet occlusion to arm blood flow has been shown to prevent contrast-induced AKI in high-risk patients and reduces the development of AKI after cardiac surgery [33,34].…”