A canine model for a standardized induction of collaterals is presented with a fixed external constrictor that is not designed to induce an occlusion of the coronary artery and at least over the timespan of 6 weeks does not impair perfusion under resting conditions in the myocardium-at-risk. The coronary constriction was standardized by a reduction of the postocclusive reactive hyperemia of 50%. Flow measurements were performed by flowmeter and by radioactive microspheres acutely and after an interval of 6 weeks of constriction. The results showed an increase of the collateral flow from 21.2 +/- 11.8 ml/100 g/min-1 to 42.8 +/- 16.2 ml/100 g/min-1 (p less than 0.05). The regional perfusion exhibited a transmyocardial gradient in favour of the subepicardial layers with 49.3 +/- 25 ml/100 g/min-1 as compared to 33.1 +/- 17.3 ml/100 g/min-1 (p less than 0.05) of the endocardial layers. Reactive hyperemia, as determined by flowmeter, was decreased by 21% after 6 weeks on account of slow progression of the coronary constriction due to intimal reactions, whereas reactive hyperemia, as determined by the microsphere method, increased by 9% due to additional collateral channels.

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Influence of hyaluronidase on infarct size following experimental coronary occlusion of short (90') or long (24 hrs) duration.

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Animals↗

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Experimental occlusion of two small coronary arteries in the same heart. A new validation method for infarct size manipulation.

A method for the evaluation of interventions aimed at manipulation of infarct size is described. This method has 2 advantages over other methods: 1. Two small-to-medium sized coronary branches of the same heart are occluded and reperfused in sequence. Thereby a "control-infarct" can be compared with a "test-infarct", both within the same heart. 2. The amount of infarcted tissue in both areas is quantitated by using the p-NBT method. A condition of the method is that the areas of perfusion of both arteries are equal. Infarct size is always expressed as a percentage of the perfusion area of the occluded artery. Validation experiments with simultaneous occlusion and reperfusion of both arteries resulted in infarcts of equal size. Validation experiments with regard to the p-NBT method showed that reperfusion accelerates the washout of dehydrogenases from infarcted tissue which allows early and precise diagnosis of infarcts after relatively short occlusion- and reperfusion periods.

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PubMedDate not supplied

The influence of reperfusin on infarct size after experimental coronary artery occlusion.

Reperfusion following various intervals of coronary occlusion has produced conflicting results: increase in infarct size, especially with hemorrhage into the tissue, was reported as well as salvage of ischemic myocardium. To examine the problem and for the validation of our own method for infarct size measurement, which depends to a certain degree on reperfusion, we occluded two coronary arteries of the same heart in each of 12 open-chest dogs. One artery was reperfused, the other not. Comparable conditions for both occlusions were warranted by selection of small-to-medium sized arteries of equal size and by maintaining of constant MVO2. Reperfused and non-reperfused myocardium did not differ with regard to infarct size, neither after a three-hour nor after a six-hour occlusion. Reperfusion always led to hemorrhagic infarction when performed after six-hour occlusion, while nonreperfused infarctions showed no hemorrhage. Hemorrhage infarcts were not larger as compared to the non-hemorrhagic infarct in the same heart.

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PubMedDate not supplied

The effect of beta-adrenergic blockade on infarct size following experimental coronary occlusion.

The effect of Pindolol on myocardial infarct size was studied in 10 open chest dogs. In each animal a sequential occlusion and reperfusion of 2 medium-sized branches of the left coronary artery was performed in the same heart. After occlusion and reperfusion of the control artery the initial dose of Pindolol (0.25 mg/kg body weight) was administered. Thereafter the test artery was occluded, followed by a maintenance dose of Pindolol (0.3 mg/kg body weight). The drug caused a significant decrease in LVP and LV-dp/dt but no change in heart rate. MVO2 also decreased significantly. Regional myocardial blood flow was measured with the tracer microsphere method. Collateral flow in the perfusion area of the control artery was 11.2 +/- 5.9% and in the area of the test artery 10.0 +/- 4.4% of normal. No change in the endo/epi ratio as a result of treatment was observed. The area of infarction (p-nitroblue tetrazolium-reaction) was divided by the area of perfusion (angiography). Infarct size, expressed as the percentage of the perfusion area, was 48.2 +/- 22.2% in the region of the control artery and 43.0 +/- 23.9% in the region of the test artery. The difference was statistically not significant.

Adrenergic beta-Antagonists↗

PubMedDate not supplied

Myocardial protection by collateral vessels during experimental coronary ligation: a prospective study in a canine two-infarction model.

Previous work of this laboratory has shown that collateral flow can be increased over six weeks by a subcritical external constriction of the circumflex artery causing a 50 +/- 10% reduction of postocclusive reactive hyperemia. To investigate collateral function in acute myocardial infarction, the model was used to ligate two distant coronary branches on the ventricle simultaneously in order to compare in 8 dogs infarct size and perfusion area of the ligated vessels in control and collateralized sections. The acute collateral flow measured 7.2 +/- 2.5 ml/100 g/min-1 and increased to 17.3 +/- 6.7 (p less than 0.001) over 6 weeks. Separate analysis revealed a predominant increase of collateral flow in the epicardial layers 23.1 +/- 7.5 (p less than 0.01) versus 6.9 +/- 2.8 (p less than 0.01) in the subendocardium. Infarct size in the control area was 52.0 +/- 14.7% of the perfusion area, in the collateralized zone 19.0 +/- 14.2% (p less than 0.001). Infarct size expressed as per cent of perfusion area and collateral flow in the area at risk expressed as per cent of flow of normal sections correlated: (r = 0.76; p less than 0.05). Therefore, infarct size after a 6 hour coronary occlusion can be considered a function of the collateral flow over normal perfusion ratio. Localized induction of collaterals in this model caused a significant reduction of infarct size in relation to the perfusion area at risk.

Animals↗

PubMedDate not supplied

Experimental myocardial infarction in a closed-chest canine model. Observations of temporal and spatial evolution over 24 hours.

Myocardial infarction was induced in 7 mongrel dogs by transfemoral intraluminal occlusion of the left anterior descending coronary artery. Perfusion area at risk was determined by post-mortem coronarography and infarct size by macrohistological staining with para-nitrophenoltetrazolium. Regional flow was determined by injection of radioactive microspheres 0.2 hours, 12 hours, and 24 hours post occlusion. Infarct size as determined by planimetry of post-mortem angiograms and macrohistological stains at identical magnification revealed 74.5 +/- 12.1% infarcted tissue of the perfusion area at risk. The flow of the necrotic tissue was below 13 Ml/100 g min without exception, indicating a threshold perfusion for maintenance of myocardial viability. Accordingly, a flow of less than or equal to 10 ml/100 g min identified 93% of the entire infarcted myocardium, resulting in 71 +/0 20% as compared to the perfusion area at risk. Based on the good agreement of macrohistological and flow data, the evolution of myocardial injury was determined by flow measurements. The results indicated a different progression of the borders of critical flow in the subendocardial and subepicardial layers, whereas in the subendocardium 85% of the tissue at risk was identified by the critical flow at 0.2 hours and 97% at 12 hours, the subepicardial flow changed at a different pace: only 53% showed subcritical perfusion at 0.2 hours, 61% at 12 hours with a final increase of 39% from 12 to 24 hours.

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