Effects of time on volume and distribution of coronary collateral flow

Ml, Marcus; Kerber, R. E.; Ehrhardt, James C.; Abboud, François M.

doi:10.1152/ajplegacy.1976.230.2.279

Cited by 49 publications

(15 citation statements)

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“…Schaper and Pasyk (29) have shown that collateral flow measured 10 sec after coronary occlusion does not change in the ensuing hour, and changes only slightly up to 4 h after occlusion. Although one group has reported an increase in collateral flow within 1 h following coronary occlusion (22), the vast majority of evidence agrees with that of Schaper and Pasyk (29) and indicates that there is no significant change in collateral perfusion for sever al hours (2, 6, 8. 27).…”

Section: Regional Blood Flowsupporting

confidence: 70%

Effect of Inosine on Ventricular Regional Perfusion and Infarct Size after Coronary Occlusion

Devous¹,

Jones²

1979

Cardiology

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In 16 dogs inosine was infused at 0.5 mmol/min i.v. for 5 min beginning 15 min after coronary occlusion. Tracer microspheres were used to estimate flow in subepicardium and subendocardium of nonischemic, central ischemic, and borderline ischemic muscle. Estimates of flow before occlusion, 5 min after occlusion, during inosine infusion, 30 min after infusion and 60 min after infusion were obtained. Coronary occlusion reduced flow in the central ischemic regions by 75-95%. The reduction in flow was greatest in subendocardium. In the borderline regions subendocardial flow was reduced by 30% while subepicardial flow was unaffected. The major effects of inosine were seen in nonischemic and borderline ischemic regions. Flow in borderline subendocardium returned to its pre-occlusion value, and flow in nonischemic myocardium increased by approximately 60-80%. However, only in the ischemic regions was the increase in flow sustained for the entire 60 min. In 20 dogs infarct size was determined using nitro blue tetrazolium stain. In 10 controls infarct size was 20.1%, while in 10 inosine-treated dogs infarct size was 15.2% of left ventricular weight (p < 0.01). Thus, following coronary occlusion inosine infusion was associated with an increase in perfusion of ischemic myocardium and a reduction in infarct size.

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Section: Regional Blood Flowsupporting

confidence: 70%

Effect of Inosine on Ventricular Regional Perfusion and Infarct Size after Coronary Occlusion

Devous¹,

Jones²

1979

Cardiology

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“…This prospective study is based on the fact that collateral vessels do not open imme diately in response to the occurrence of myo cardial ischemia [6][7][8], Indeed, in the present study, when exercise was started with a fixed work load which was the maxi mal attainable level for each patient, the extent of ST depression at 3 min of exercise was greater than that at the end of exercise. Since the rate-pressure product indicative of myocardial oxygen requirement was smaller at 3 min compared with the value at the end of exercise, it is reasonably speculated that the collateral blood flow does not reach its maximal value before the collateral vessels are completely dilated, being mediated by ischemia-related chemical substances such as adenosine in the interstitial tissue of the myocardium [10], As shown in figure 1, the improvement in ST segment depression dur ing exercise with a fixed work load clearly indicates that the increase in collateral flow contributed to the alleviation of myocardial ischemia.…”

Section: Discussionmentioning

confidence: 85%

“…It has been demonstrated in animal ex periments [6][7][8] that the collateral blood flow increases gradually following acute cor onary occlusion. In the present study, a de layed response of collateral vessels to myo cardial ischemia has also been shown in hu mans.…”

Section: Discussionmentioning

confidence: 99%

“…First, the extent of narrowing of the ischemia-related coro nary artery is decreased by the alleviation of coronary artery spasm, thereby resulting in an increase in myocardial oxygen supply [4,5], Second, the gradual recruitment of the collateral circulation may account for this phenomenon. The collateral function is aug mented progressively in response to myocar dial ischemia resulting from myocardial oxy gen imbalance [6][7][8]. In the present study, patients having a subtotal coronary occlu sion but still with good collateral flow were excluded from the analysis because in these patients not only changes in collateral flow, but also dynamic changes in the extent of coronary stenosis may contribute to the at tenuation of myocardial ischemia during ex ercise.…”

Section: Introductionmentioning

confidence: 99%

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Improvement of ST Segment Depression by Gradual Recruitment of Collateral Circulation

Tanaka

Fujita²,

Hirai³

et al. 1990

Cardiology

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The purpose of the present study was to document that the coronary collateral vessels do not open immediately upon the occurrence of myocardial ischemia. A multistage bicycle exercise was performed to determine a maximal tolerable work load until the onset of angina and significant ST segment depression in 10 patients with well-developed collateral circulation. On a different day, exercise with the maximal tolerable work load was repeated for a comparable exercise duration. In 2 of the 10 patients, anginal pain was gradually alleviated despite the continuation of exercise with fixed work load. The extent of ST segment depression at 3 min of exercise with fixed work load was 0.20 ± 0.10 (SD) mV, significantly (p < 0.05) greater than 0.16 ± 0.08 mV at the end of exercise with fixed work load. In contrast, the rate-pressure product was smaller at 3 min than at the end of exercise with fixed work load (20,900 ± 5,500 vs. 22,700 ± 5,700 mm Hg · beats/min; p < 0.05). In 5 patients without well-developed collateral circulation, the extent of ST depression changed in parallel with changes in rate-pressure product during exercise with fixed work load. Thus, it is concluded that the delayed collateral opening plays a critical role in the pathogenesis of myocardial ischemia in patients with a totally occluded coronary artery.

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“…It has been shown that, in dogs, occlusion of the coronary artery does not reduce Qm to nil, but rather, that myocardial blood flow generally falls to 10%-30% of the pre-occlusion flow [10][11][12]. In animals and humans, vascular channels that link large coronary arteries to one another, known as coronary collaterals, provide flow to the occluded area.…”

Section: Native Collaterals (Q1)mentioning

confidence: 99%

New collateral flow increasing early after coronary occlusion prevented myocardial necrosis in dogs

et al. 1995

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Increases in regional myocardial blood flow (Qm) developing soon after myocardial infarction may minimize myocardial necrosis. To test this hypothesis, Qm in the area surrounding an acutely occluded coronary artery was determined successively over 4 weeks in 11 dogs. Non-radioactive colored microspheres were injected into the left atrium 5 s (Qm at this time is referred to as Q1), 3 h (Q2), 12 h (Q3), and 4 weeks (Q4) after occlusion of the coronary artery. After termination of the experiment, the heart was removed, and Qm and three indices of myocardial necrosis i.e., myocardial creatine kinase activity (CK), infarct size determined by triphenyl tetrazolium chloride stain (TTC), and myocardial fibrosis visualized by Azan-Mallory stain, were determined. Each Qm was expressed as a percentage of normal: Qm (% of normal) = [Q/Qc] ischemic area/[Q'/Qc']non-ischemic area x 100, where Qc indicates Qm determined before coronary occlusion. In the ischemic area of the left ventricle, Q1, Q2, Q3, and Q4 were 25 +/- 3%, 30 +/- 3%, 31 +/- 3%, and 42 +/- 3% of normal, respectively, in the inner layer, and 31 +/- 3%, 52 +/- 4%, 52 +/- 4%, and 77 +/- 6% of normal, respectively, in the outer layers. During the 4-week period, the increase of Qm in the outer layer was greater than that in the inner layer. The inner layer showed a small increase of flow from Q3 to Q4 (9 +/- 2%), but in the outer layer there were greater flow increases from Q1 to Q2 (21 +/- 3%) and from Q3 to Q4 (24 +/- 6%).(ABSTRACT TRUNCATED AT 250 WORDS)

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Effects of time on volume and distribution of coronary collateral flow

Cited by 49 publications

References 0 publications

Effect of Inosine on Ventricular Regional Perfusion and Infarct Size after Coronary Occlusion

Effect of Inosine on Ventricular Regional Perfusion and Infarct Size after Coronary Occlusion

Improvement of ST Segment Depression by Gradual Recruitment of Collateral Circulation

New collateral flow increasing early after coronary occlusion prevented myocardial necrosis in dogs

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