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Biomedical subjects

B Wüsten

Publications and source records attributed to B Wüsten.

33 records · Page 2Linked to original sources
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Local dilatory reserve in chronic experimental coronary occlusion without infarction. Quantitation of collateral development.

The local dilatory reserve of the canine coronary vasculature was studied with the particle distribution technique. Normal ventricles and hearts with slowly progressive narrowing of both the left circumflex coronary artery and the right coronary artery were studied. In spite of chronic occlusion of 2 coronary arteries myocardial infarction did not occur in the majority of animals because of collateral development. Coronary reserve was determined by producing graded to maximal coronary vasodilation. In normal hearts flow increased homogeneously over the entire left ventricle. In hearts with chronic coronary occlusion coronary vasodilation produced non-homogeneous increases in flow: collateral dependent myocardium received less blood flow than myocardium supplied by normal coronary arteries. Early after coronary occlusion the total coronary reserve was less than normal and the dilatory reserve of collateral dependent vessels was markedly diminished. Late (6 months) after coronary occlusion the total coronary reserve was still below normal but the dilatory reserve of collateral dependent vessels had improved. A new quantitative index of collateral function is defined as the level of coronary flow (delivered through normal coronary arteries) at which collateral flow deviates from homogeneous perfusion. Collateral function, when so defined, increases by a factor of almost 6 times between 4 weeks (early after coronary occlusion) and 6 months (late after occlusion) after the implantation of occluding devices.

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Cardiac function in the chronically volume-overloaded canine heart.

In the chronically volume-overloaded canine heart due to AV-block evaluations of cardiac function were performed during the development of hypertrophy and at stable hypertrophy. In an early stage (1 and 2 weeks of AV-block) when no or only a slight increase of cardiac muscle occurred, contractility measured from dP/dtmax at comparable load is elevated, while later (10 weeks of AV-block) when stable hypertrophy is present, contractility becomes again normal, In the hypertrophied heart a non-depressed cardiac performance and contractility and functional reserve was established from insitu experiments and from evaluations in the isolated heart.

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Influence of tachycardia on regional myocardial flow in chronic experimental coronary occlusion.

The influences of tachycardia on regional myocardial flow was studied in normal dogs and in dogs with chronic coronary artery occlusions. Coronary vasodilation was induced by coronary occlusion and subsequent release, i.e. by reactive hyperemia. Local myocardial blood flow was determined with the tracer microspheres technique. In normal hearts atrial pacing produced a slight but significant increase in coronary resistance in the subendocardial layers of the left ventricle. The coronary resistance of the subepicardium remained unaffected. In the right ventricle atrial pacing had no influence on the resistance to flow. In hearts with multiple coronary occlusions tachycardia-induced changes of coronary resistance were more pronounced. In the collateral dependent subendocardium coronary resistance increased from 0.4-2.2 resistance units when the heart rate was raised to 200 beats/min. Perfusion of the right ventricular myocardium became also rate-dependent when the right coronary artery was chronically occluded. We conclude that regional perfusion dependes upon the relationship between the effective perfusion pressure, which is reduced in chronic coronary occlusion, and the integral of effective tissue pressure, which is increased with tachycardia. The results cannot be explained by assuming excessive O2-demand but rather by a rate-induced lowered O2-supply.

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Development of collaterals. Application of external subcritical fixed constrictors in a canine model.

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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Dilatory capacity of the coronary circulation and its correlation to the arterial vasculature in the canine left ventricle.

The functional capacity of flow limiting myocardial conductance vessels was evaluated in canine hearts. In an isolated heart preparation transmural coronary flow distribution during maximal vasodilation was measured in the unloaded diastolic arrested left ventricle with tracer microspheres. The ratio of subendocardial versus subepicardial (ENDO/EPI) flow in the left ventricular free wall was 1.6. Measurements in 8 different wall layers showed a successive increase in maximal coronary flow from the subepicardium towards the deeper layers. A decreased subendocardial vascular resistance due to a better vascularization is forwarded as a mechanism to compensate for the extravascular compression during cardiac contraction. This statement contradicts the commonly accepted hypothesis that a diminished vascular tone with a reduction of the dilatory reserve in the subendocardium accounts for a homogeneous flow distribution in the normal beating heart. An augmentation of subendocardial supplying vessel capacity could be established from the angiographic determination of the coronary arterial volume of intramural small arteries and arterioles. From a strict parallelity in maximal coronary flow and coronary arterial volume within the wall, it becomes probable that these vascular structures are the flow-limiting factors which determine regional coronary flow reserve in the absence of extravascular compressive forces.

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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.

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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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