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.

Animals↗

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Hypertrophy due to chronic volume overloading in the dog heart. A morphometric study.

Cardiac hypertrophy due to chronic volume overloading was produced in dogs by experimental complete AV-block. Ten weeks after operation a quantitative electron microscopic study was carried out for determination of the volume density of contractile material and mitochondria. The results were compared with a two-week group and normal dogs. The ratio of the volume density of contractile material and mitochondria is nearly constant during the course of developing hypertrophy.

Animals↗

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The relationship between the perfusion deficit, infarct size and time after experimental coronary artery occlusion.

It is well known that coronary occlusions of short duration do not produce infarcts in the dog heart, but permanent occlusions always do. The aim of this paper was to investigate with quantitative direct measurements the determinants of infarct size within these two extremes. We measured left ventricular MV2, coronary and collateral blood flow and infarct size after occlusion times varying between 45 minutes and 24 hours. MVO2 was kept low in one group by establishing low heart rates with a synthetic opiate. In another group, MV2 was kept elevated by giving synthetic catecholamines (dobutamine) that stimulated contractility and heart rate. Under the described experimental conditions LV-coronary blood flow reflected the true demand for blood and oxygen. The ratio of collateral blood flow over coronary blood flow (both measured with tracer microspheres) was therefore a good approximation of the supply-demand ratio (SD). Since collateral flow was inhomogeneously distributed across the left ventricular wall, the SD-ratio showed similar variations. As the collateral blood flow increased with elapsed time after coronary occlusion, the SD-ratio improved. Since high LV-O2-demand increased coronary flow but exerted practically no influence on collateral flow, this situation influenced the SD-ratio in a negative way. Decreased O2-demand had the opposite effect. The SD-ratio is thus a valid expression of the relative and absolute blood flow deficit as influenced by the local and general O2-demand. We found significant and characteristic correlations between the SD-ratio and infarct which was only influenced by time. A blood flow deficit of 90% (i.e., collateral flow = 10% of required flow) produced a 50%-infarct (relative to the risk-region) with a 45-min occlusion but a 90%-infarct with occlusion times of 3 hrs and longer. If the perfusion deficit is only 0.5 (collateral flow = 50% of required flow), no infarct is detectable at occlusion times shorter than 3 hrs. Small perfusion deficits of only 20% below required flow caused infarctions at 24 hrs and longer. In the group where the SD-ratio was closer to unity because of a low overall LV-O2-consumption (bradycardia), infarcts at t = 24 hrs were significantly smaller than in the group with a high LV-MVO2.

Animals↗

PubMedDate not supplied

Experimental coronary artery occlusion. II. Spatial and temporal evolution of infarcts in the dog heart.

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Animals↗

PubMedDate not supplied

Measurement of radioactive tracer microsphere blood flow with NaI (T1)-and Ge-well type detectors.

An intrinsic Ge-well type detector was applied for the detection of gamma rays from labeled tracer microspheres. The high energy resolution and the large peak-to-Compton ratio of this spectrometer ensures the application of all available differently labeled tracer microspheres in one experiment. The superior energy resolution of the Ge-detector was documented with the separated photopeak regions of 103-Ru and 85-Sr-labeled tracer microspheres, which result in a single photopeak when an NaI(T1) detector is used. The Ge-well type detector was compared with an NaI(T1) spectrometer by counting samples of cardiac muscle in either spectrometer systems. Regression analysis between both spectrometer systems demonstrate identical flow values in these samples for 5 differently labeled tracer microspheres which were administered in 5 dogs. The high sensitivity of the Ge-well-type detector together with a suitable technique for sampling of myocardial tissue accomplishes a high spatial resolution of myocardial perfusion for all available differently labeled tracer microspheres.

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.

Animals↗

PubMedDate not supplied

Quantitative ultrastructure of the myocardium in chronic aortic valve disease.

Light and electron microscopic morphometry was carried out in tissue samples which were obtained from the left ventricular free wall in 29 patients with chronic aortic valve disease during open-heart surgery. 6 patients had aortic stenosis, 9 had aortic insufficiency and 14 had a mixed aortic valve lesion. Hemodynamics were studied before operation. Patients with mixed aortic valve disease had a higher left ventricular mass, a lower ejection fraction and mean circumferential fiber shortening rate than patients with aortic stenosis. Peak systolic wall stress was comparable between groups. The intracellular content of contractile material was lower and the sarcoplasmic volume was higher in mixed aortic valve disease than in aortic stenosis. Mitochondrial volume and interstitial fibrosis were not different between groups. Patients with aortic insufficiency showed no significant difference of parameters as compared to both other groups. We conclude that an intracellular deficiency of myofibrils causes lack of contractility in advanced hypertrophy due to mixed aortic valve disease.

Aortic Valve Insufficiency↗