Does reperfusion extend necrosis? A study in a single territory of myocardial ischemia--half reperfused and half not reperfused.

Ganz, William; Watanabe, Ichiro; Kanamasa, Ken; Yano, Juliana; Han, Dong-Sun; Fishbein, Michael C.

doi:10.1161/01.cir.82.3.1020

Cited by 26 publications

(6 citation statements)

References 62 publications

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“…The occurrence of contraction band necrosis during reperfusion following 30-60 minutes of ischemia in pig hearts can neither support nor disprove the concept of postischemic cell death [17]. As is similar to our findings, one histochemical study failed to prove the existence of reperfusion injury in canine hearts [8]. In this study, a tetrazolium stain was used to delineate the infarcted tissue in the absence or presence of reperfusion.…”

Section: Lack Of Ultrastructural Evidence For the Existence Of Lethalcontrasting

confidence: 50%

“…However, many of the positive studies have been questioned by negative findings [reviewed in [5][6][7]. In addition, the transmural degree of necrosis determined histochemically with tetrazolium salt did not differ in nonreperfused and short-term reperfused canine myocardium [8]. The major problem in the study of postischemic cell death is related to the accurate diagnosis of myocardial necrosis.…”

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confidence: 99%

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Ultrastructural evaluation of postischemic cell death (lethal reperfusion injury) in porcine hearts

et al. 1996

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This study investigated whether reperfusion results in an increase of ultrastructurally determined myocardial injury in pig hearts. The left anterior descending coronary artery (LAD) was distally occluded in 12 pigs for 35-45 minutes and then reperfused for 3 hours. At the end of ischemia, as well as after 3 hours of reperfusion, one transmural biopsy was removed from the center of the risk region and subdivided into four-specimens, representing the subendocardial (I), subendo-midmyocardial (II), subepi-midmyocardial (III), and subepicardial layers (IV). The degree of injury was assessed by electronmicroscopy and was scored as reversible (1), an almost equal mixture of reversible and irreversible (2), and totally irreversible (3) damage. In addition, infarct size was determined as the ratio of infarcted (tetrazolium stain) to ischemic (dye technique) myocardium. Infarct sizes ranged from 29.3% to 93% (mean 61.2%). The scores of injury of the four tissue layers before and after reperfusion did not differ significantly: layer I, 2.4 +/- 0.8/2.3 +/- 0.9; layer II, 2.2 +/- 0.9/2.0 +/- 0.9; layer III, 1.8 +/- 0.9/2.0 +/- 0.9; and layer IV, 1.6 +/- 0.9/1.3 +/- 0.6. The means of the four layers were almost identical at the end of ischemia (2.1 +/- 0.8) and after 3 hours of reperfusion (2.0 +/- 0.6). A linear regression analysis with 95% confidence limits of the score values before and after reperfusion indicated that maximally 25% of a mean final infarct size of about 50% may be due to lethal reperfusion injury. This study suggests that cell death in regional ischemia and reperfusion occurs predominantly during ischemia and not during reperfusion.

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Section: Lack Of Ultrastructural Evidence For the Existence Of Lethalcontrasting

confidence: 50%

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confidence: 99%

Ultrastructural evaluation of postischemic cell death (lethal reperfusion injury) in porcine hearts

et al. 1996

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“…However, it is possible that restoration of blood flow to previously ischemic but reversibly injured myocardium could provoke further cellular damage (34)(35)(36). Precise causes of this so-called 'reperfusion injury' have not been established, and the mechanisms involved remain controversial (37,38).…”

Section: Myocardial Protectionmentioning

confidence: 99%

Coronary vasoregulation in health and disease

Kingma

Rouleau

2007

Canadian Journal of Cardiology

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E arly interests of clinical researchers at the Quebec HeartInstitute focused on various aspects of cardiac physiology, biochemistry (ie, metabolism) and pathology. In the late 1970s, the Quebec Heart Institute recruited Dr Jacques Rouleau, a cardiologist whose primary research interests focused on biophysical mechanisms that regulate the distribution of blood flow across the ventricular wall. The later addition to this laboratory of Dr John Kingma, whose research focused on mechanisms involved in myocardial protection following ischemia-reperfusion injury, created a basic scienceclinical research collaboration that continues today.The principal function of the heart is to supply the different organs in the body with blood containing essential nutrients and oxygen required for their proper functioning. In addition, the heart is essential for the transport of metabolic waste products, the accumulation of which would influence organ function. Mechanical work necessary to pump blood is performed by the myocardium. Proper functioning of the myocardium depends on blood flow in the coronary circulation, which comprises large epicardial conductance vessels originating from the coronary ostia. These large vessels branch into smaller vessels that supply the capillary network responsible for the transport of oxygen and nutrients to the myocytes. Comprehension of mechanisms responsible for regulation of the coronary circulation requires the interpretation of information from several disciplines, including cardiology, physiology, biochemistry and physics; this list is far from exclusive because new information regarding interactions of molecular and mechanical signals is consistently being added to the equation. The present review summarizes several achievements resulting from this research collaboration over the past two decades. REGULATION OF THE DISTRIBUTION OF MYOCARDIAL BLOOD FLOWControl of the coronary circulation involves a host of interactions among mechanical factors, such as arterial pressure, blood flow, ventricular contraction and myocardial wall tension. Suffice it to say that coronary blood flow is never constant but rather adaptive in relation to the metabolic and oxygen requirements of the myocardium; approximately 70% of oxygen transported is extracted from blood flowing in arterial vessels. This intrinsic capacity of arterial vessels to adjust in calibre and maintain constant perfusion over a range of arterial pressures is referred to as 'coronary autoregulation' (Figure 1). Principal mechanisms involved in the control of coronary blood flow include metabolic mediator(s) between myocytes and vascular cells, myogenic tone (induced by stretch) and neurogenic stimulation. However, studies on flow control mechanisms in the coronary circulation are limited because function of intramyocardial resistance vessels cannot be investigated with the currently available techniques. Exercise-induced increases in myocardial oxygen demand are accommodated by increases in coronary blood flow, the latter being controlled by ...

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“…Morphological studies also yielded inconsistent results. Some investigators could not demonstrate the extension of necrosis by reperfusion by electron microscopy (9) and attributed cell death predominantly to ischemia and not reperfusion (16). On the other hand, others published findings consistent with the occurrence of necrosis during reperfusion (5,19,26).…”

Section: Discussionmentioning

confidence: 99%

The effect of a low molecular weight inhibitor of lipid peroxidation on ultrastructural alterations to ischemia-reperfusion in the isolated rat heart

Nagy¹,

Myklebust²,

Valen³

et al. 2001

Acta Physiologica Hungarica

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The effects of H290/51, a novel indenoindole derivative inhibitor of lipid peroxidation, on ultrastructural changes during cardiac ischemia-reperfusion injury were investigated. Langendorff-perfused rat hearts were exposed to 30 minutes of global ischemia followed by 20 minutes of reperfusion: Group A: Control hearts with standard buffer perfusion with vehicle added. Group B: H290/51 (10(-6) mol/l) added to buffer throughout stabilisation and reperfusion. In an additional Group C, where hearts were given H290/51, but not subjected to ischemia, the ultrastructure was preserved till the end of reperfusion. Absolute volumes and calculated volume fractions (Vv) of tissue and subcellular components were assessed with quantitative stereologic morphometry. After ischemia the increase in volume of extracellular interstitium was inhibited by H290/51 (247 +/- 80 vs. 159 +/- 50 microl, mean +/- SD, groups A and B, respectively, p<0.05). The Vv (interstitium/myocard) was higher in control hearts (0.318 +/- 0.062 vs. 0.206 +/- 0.067, p<0.05). Vv (cell edema/myocyte) was higher in the control group (0.144 +/- 0.07 vs. 0.083 +/- 0.033, p<0.05). Vv (myocyte/myocard) was higher in group B after ischemia than in the control group (0.622 +/- 0.071 vs. 0.707 +/- 0.052, p<0.05). The decreased Vv (capillary/myocard) after ischemia was inhibited by H290/51. After reperfusion there was no difference between groups. Treatment with H290/51 reduced edema and ensured better preserved sarcolemmal membrane structure during ischemia. The effect was no longer present after reperfusion.

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Does reperfusion extend necrosis? A study in a single territory of myocardial ischemia--half reperfused and half not reperfused.

Cited by 26 publications

References 62 publications

Ultrastructural evaluation of postischemic cell death (lethal reperfusion injury) in porcine hearts

Ultrastructural evaluation of postischemic cell death (lethal reperfusion injury) in porcine hearts

Coronary vasoregulation in health and disease

The effect of a low molecular weight inhibitor of lipid peroxidation on ultrastructural alterations to ischemia-reperfusion in the isolated rat heart

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