The histological lateral border of acute canine myocardial infarction. A function of microcirculation.

Factor, Stephen M.; Okun, Ellen M.; Kirk, Edward S.

doi:10.1161/01.res.48.5.640

Cited by 64 publications

(31 citation statements)

References 31 publications

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“…2), which localized IGFBP-2 to islands of proximal viable tissue within the necrotic proximal zone. The histological origins of these islands as peninsulas of homogenous proximal viable tissue, separated by the plane of section, has been well described by Factor et al (1978Factor et al ( , 1981. Their presence, located within the necrotic proximal zone and showing high levels of labelled IGF-I binding to IGFBPs as well as to receptors, explains the results shown in Fig.…”

Section: Igf-ii Igf-ii Message Was Below the Threshold Of Detection Osupporting

confidence: 65%

Changes in IGFs in cardiac tissue following myocardial infarction

Matthews

Devlin²,

Conaglen³

et al. 1999

Journal of Endocrinology

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Section: Igf-ii Igf-ii Message Was Below the Threshold Of Detection Osupporting

confidence: 65%

Changes in IGFs in cardiac tissue following myocardial infarction

Matthews

Devlin²,

Conaglen³

et al. 1999

Journal of Endocrinology

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“…For example, it is possible that the functional border zone consists of an intermingling of peninsulas of normal and ischemic myocardium, supplied in turn by two capillary beds discrete and unconnected, one from the nonoccluded artery and one from the occluded artery. 20 After inotropic stimulation, the capillaries supplied by the nonoccluded artery could result in hyperemic flow, whereas flow in the occluded artery would remain markedly decreased. This would create a normal mean flow in the region of the functional border zone, although function would be reduced due to the admixture of ischemic fibers.…”

Section: Discussionmentioning

confidence: 99%

The effect of inotropic stimulation on normal and ischemic myocardium after coronary occlusion.

Buda¹,

Zotz²,

Gallagher³

1987

Circulation

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During acute myocardial ischemia, there exists a zone of myocardial dysfunction that surrounds the central ischemic area that has been termed the functional border zone. We hypothesized that this nonischemic but dysfunctional myocardium may respond to an inotropic challenge. To . We conclude that (1) nonischemic myocardium adjacent to ischemic tissue responds to inotropic challenge, (2) dobutamine produces a significant decrease in the size of the functional border zone, and (3) dynamic changes in wall thickening after inotropic intervention are greater in the functional border zone of the lateral free wall than at the septal border of the ischemic area.

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“…The blood supplies of both the region at risk and normal zones were defined using two Microfil solutions, one red and one white (Canton Bio-medical Products).1I' 12 Microfil is a silicone rubber compound that has a low viscosity, fills the capillary microcirculation, and gels in situ. The dogs were reanesthetized before being killed and a second thoracotomy was performed.…”

Section: Definition Of Blood Flows To Region At Riskmentioning

confidence: 99%

“…Their history of angina ranged from 6 months to 12 years (average 44 months). All patients had angiographically demonstrable coronary artery disease, and had at least 70% narrowing of luminal diameter in at least one major coronary artery.…”

Section: Patientsmentioning

confidence: 99%

Acute myocardial infarct extension into a previously preserved subendocardial region at risk in dogs and patients.

Forman¹,

Cho²,

Factor³

et al. 1983

Circulation

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SUMMARY In this study we quantitated the region of preserved myocardium between a subendocardial myocardial infarct (SEMI) and the endocardium in dogs and determined whether this preserved zone was within the region at risk and whether infarct extension could occur in this region. We also evaluated whether a similar subendocardial region exists in patients with SEMI. A 40-minute temporary occlusion of the left anterior descending coronary artery (LAD) in eight dogs resulted in a 35 ± 5% transmural infarct with 8 + 1% subendocardial preservation as assessed by point-counting of the histologic specimens. In vivo perfusion of coronary vessels with Microfil showed that this preserved subendocardial zone was within the region at risk. The preserved subendocardial zone had significantly fewer cell layers in the dogs ventilated with room air than in dogs ventilated with 100% oxygen (8 ± 4 vs 19 ± 4, p < 0.001), which suggests that diffusion from the ventricular cavity was the mechanism of cell preservation. In contrast, the inspired oxygen concentration did not influence the size of the SEMI. Reocclusion of the LAD for 24 hours in an additional eight dogs, 1 week after a SEMI had been created by a 40-minute temporary occlusion, resulted in both subendocardial and subepicardial extension involving 5 ± 1% and 29 ± 9%, respectively, of the transmural myocardium at the infarct center. Subendocardial infarct extension of a similar dimension to that in dogs ventilated on 100% oxygen was observed in postmortem material from eight patients with infarct extension. The preserved layers of subendocardium presumably receive sufficient nutrients from the ventricular cavity to maintain the viability of this region during temporary, but not permanent, reduction of blood supply from the coronary arteries. magnitude and direction of infarct extension when a new infarct was superimposed on a healing SEMI. Finally, we examined postmortem specimens from patients who died with healed SEMI and acute infarct extension to determine whether a similar vulnerable region of subendocardial preservation exists in humans. Methods Studies in DogsA SEMI was produced in 12 dogs, eight ventilated with 100% oxygen and four with room air; the dogs were killed after 24 hours. In an additional eight dogs ventilated with 100% oxygen, a similar SEMI was created, infarct extension induced on the seventh day and the dogs were killed on the eighth day. These times were chosen in the infarct extension experiment so that the two infarcts could be readily distinguished histologically in the same specimen. Ventricular fibrillation and death occurred shortly after release of the temporary coronary occlusion in seven additional dogs ventilated with 100% oxygen and three additional dogs ventilated with room air. These dogs were not included in the subsequent analysis.

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The histological lateral border of acute canine myocardial infarction. A function of microcirculation.

Abstract: Van Orden DE, Farley DB (1973) The

Cited by 64 publications

References 31 publications

Changes in IGFs in cardiac tissue following myocardial infarction

Changes in IGFs in cardiac tissue following myocardial infarction

The effect of inotropic stimulation on normal and ischemic myocardium after coronary occlusion.

Acute myocardial infarct extension into a previously preserved subendocardial region at risk in dogs and patients.

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