Experimental Studies on the Healing of Cardiac Necrosis

Róna, G; Kahn, David

doi:10.1111/j.1749-6632.1969.tb16726.x

Cited by 22 publications

(25 citation statements)

References 18 publications

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“…Rona et al, 24 using doses of isoproterenol considerably greater than those used here (85 mg/kg), reported a rapid appearance of grossly apparent necrosis within 8 hours of treatment, peak development by 48 hours, and regression and disappearance of necrotic muscle by 72 hours. The significance of the present study lies in the ability to detect necrosis even earlier and with considerably greater sensitivity.…”

Section: Radioautographic Analysismentioning

confidence: 53%

“…Maximal myocyte necrosis and myocardial fibrosis are both confined to the subendocardium and midwall. 24 - 25 No significant scarring developed in the subepicardium, and necrotic myocytes were not observed in this region of the heart. Second, the appearance of necrosis and fibrosis are closely related in time.…”

Section: Radioautographic Analysismentioning

confidence: 90%

“…Our study confirms earlier reports that myocyte permeability develops within a very short period after isoproterenol administration. 24 - 29 The level of labeling rises to a maximum between 12-24 hours after treatment and then declines to control levels by 72 hours. The rapid rise and fall of myocyte labeling suggests that necrosis was produced during a single short-lived period.…”

Section: Radioautographic Analysismentioning

confidence: 99%

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Isoproterenol-induced myocardial fibrosis in relation to myocyte necrosis.

Benjamin

Jalil

Tan

et al. 1989

Circulation Research

313

174

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Treatment of rats with the ^-adrenergic agonist isoproterenol results in cardiac hypertrophy, myocyte necrosis, and interstitial cell fibrosis. Our objectives in this study have been to examine whether hypertrophy and fibrosis occur in a compensatory and reparative response to myocyte loss or whether either process may be occurring independently of myocyte loss and thus be a reactive response to adrenergic hormone stimulation. We have examined this question by evaluating each of these responses in rats treated with different doses and forms of isoproterenol administration. Myocyte necrosis was evaluated using in vivo labeling with monoclonal antimyosin for identification of myocytes with permeable sarcolemma, which was indicative of irreversible injury. Myocardial fibrosis was evaluated by morphometric point counting of Gomori-stained tissue sections and by assessment of the stimulation of fibroblast proliferation by determination of increased levels of DNA synthesis. Stimulation of fibroblast DNA synthesis was determined from DNA specific radioactivities and radioautography after pulse labeling with [ 3 H]thymidine. The evidence provided by this study suggests that the degree and timing of myocardial hypertrophy does not follow the course of myocyte loss and, thus, appears to be either a response to altered cardiac loading or a reactive response to /3-adrenergic hormone stimulation rather than a compensation for myocyte loss. Myocardial fibrosis, on the other hand, appears to be more closely related to myocyte necrosis with respect to collagen accumulation in the same areas of the heart, its dose-response relation to the amount of isoproterenol administered, and the timing of increased DNA synthesis, or fibroblast proliferation, after myocyte loss.

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Section: Radioautographic Analysismentioning

confidence: 53%

Section: Radioautographic Analysismentioning

confidence: 90%

Section: Radioautographic Analysismentioning

confidence: 99%

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Isoproterenol-induced myocardial fibrosis in relation to myocyte necrosis.

Benjamin

Jalil

Tan

et al. 1989

Circulation Research

313

174

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“…The reentry of arterial blood during the early phase of this process has the potential to influence the speed of healing and/or the quality of scar that is formed (Rona and Kahn, 1969;Shetlar et al, 1979;Roberts et al, 1983). Early reperfusion of necrotic myocardium may predispose it to ventricular rupture (Lewis et al, 1969;Bates et al, 1977;Rasmussen et al, 1979) or may negatively influence scar formation by washing out a factor, such as lactate, which stimulates collagen synthesis (Comstock and Udenfriend, 1970), or an extracellular enzyme, such as lysyl oxidase, necessary for collagen fiber crosslinking (Prockop et al, 1979a(Prockop et al, , 1979b.…”

mentioning

confidence: 99%

Effects of reperfusion after coronary artery occlusion on post-infarction scar tissue.

Connelly¹,

Vogel²,

Wiegner³

et al. 1985

Circulation Research

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SUMMARY. Early reperfusion after a coronary occlusion may reduce myocardial infarct size, but late reperfusion into necrotic myocardium may alter post-infarction healing. In rabbits, we compared 1-or 3-week-old scars resulting from permanent coronary occlusion to those resulting from a 1-or 3-hour occlusion followed by reperfusion. Reperfusion at 1 hour post-occlusion did not affect scar mechanical properties assessed at 1 week post-infarction, but at 3 weeks postinfarction, these scars had a tensile strength significantly lower than those not reperfused (78 ± 11 vs. 158 ± 15 g/mm 2 , P < 0.001). They also were composed of a mixture of fibrous tissue (58 ± 8%) and myocytes (43 ± 8%) with a hydroxyproline content of 23 ± 2.5 mg/g dry weight. The nonreperfused scars had a higher proportion of fibrous tissue (73 ± 3%) by histological evaluation and a 35% higher hydroxyproline content (31 ± 2 mg/g dry weight, P < 0.001) than the scars reperfused after 1 hour. In contrast, 3-week-old scars resulting from late' reperfusion at 3 hours post-occlusion were similar to nonreperfused scars in fibrous tissue composition and hydroxyproline content. Nonetheless, the tensile strength of these scars reperfused 3 hours post-occlusion was significantly less than that of the nonreperfused scars (72 ± 5 vs. 158 ± 15 g/mm 2 , P < 0.001). The lower tensile strength was associated with a lower collagen cross-link density in this reperfused group of scars. At physiological stress levels (approximately 3 g/mm 2 ), all groups of reperfused and nonreperfused scars had similar mechanical properties in terms of natural strain, stiffness, creep, and stress relaxation. Thus, although the reperfused scars ruptured more easily at high stresses, when assessed at physiological stresses their mechanical properties were not significantly different from those of nonreperfused scars. (Circ Res 57: 562-577, 1985)

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“…Myocardial infarction or acute myocardial infarction, commonly known as heart attack is due to the interruption of blood supply to the heart, causing anoxia and death of heart cells [2]. Isoproterenol (ISO), a synthetic catecholamine and nonselective b-adrenoceptor agonist, at high doses, has been reported to produce weakening of endogenous antioxidant system, contractile dysfunction, cardiotoxicity, and cardiac damage (infarct-like lesions) due to positive chronotropic and inotropic effects [3].…”

Section: Introductionmentioning

confidence: 99%