Latex agglutination test for tuberculosis.
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Female↗
Biomedical subjects
F C White
Publications and source records attributed to F C White.
Coronary artery reperfusion: effects of occlusion duration on reactive hyperemia responses.
In 24 unanesthetized dogs, we monitored reactive hyperemia responses in the coronary vascular bed after different durations of coronary occlusion and during coronary artery reperfusion. After two hours of occlusion, no significant changes in functional capacity occurred, evidenced by unchanged peak reactive hyperemia, reactive hyperemia flow and repayment of flow debt responses. With occlusions of six hours or more, these responses were impaired upon reperfusion, and remained diminished for up to five days. In those animals reperfused after two and six hours of coronary occlusion, myocardial infarcts were significantly smaller than those seen in animals reperfused after 24 to 72 hours of occlusion (4%, 14%, 20% and 21%, respectively). Thus, the effectiveness of any reperfusion procedure depends on its early institution when the coronary vascular bed has minimal change in functional capacity and the size of the infarct can still be reduced.
Animals↗
Effect of coronary collateral development on ventricular fibrillation threshold.
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Animals↗
Coronary collateral reserve during exercise induced ischemia in swine.
We determined coronary collateral vasodilator reserve during exercise-induced ischemia in 17 mini-swine. We induced coronary collateral development in the left circumflex bed by placing an ameroid occluder on that artery. Four weeks later we studied the animals at rest and during exercise (EX) eliciting heart rates (HR) of 240 and 265 beats/min. We measured myocardial blood flow with microspheres and myocardial function by wall thickness sonomicrometry gauges. At matched exercise HRs we treated the animals with nifedipine (10 micrograms/kg IV) (EXN 10), nifedipine (100 micrograms/kg IV), (EXN 100), and adenosine infusion (1.2 mg/min/kg) EXAD. EXN 10 did not significantly alter hemodynamics compared to EX but EXN 100 and EXAD both decreased blood pressure significantly (p less than 0.05). Ischemic endocardial/nonischemic endocardial flow ratios and collateral resistance served as indices of vasodilator reserve. In the ischemic zone exercise reduced vasodilator reserve to 24 +/- 3% in the endocardium and 64 +/- 7% in the epicardium. Neither EXN 10 nor EXAD improved exercise-induced ischemia measured either as flow or function. However EXN 100 improved function during exercise-induced ischemia without improving coronary collateral flow. We conclude there is no additional coronary flow reserve during exercise-induced ischemia in the collateral dependent bed of the pig a few days after occlusion that can be recruited. Large doses of nifedipine improve function by direct action on the myocardium or by reducing afterload. The lack of development and deep myocardial distribution of the coronary collateral vessels in the pig may be an important factor of why these nifedipine responses differ from those reported in species which have primarily large epicardial coronary collaterals.
Adenosine↗
Coronary collateral circulation in the pig: correlation of collateral flow with coronary bed size.
Coronary bed sizes were measured in pigs. The left anterior descending bed occupies about 31% of the heart, the right coronary bed about 38% of the heart and the left circumflex bed about 31% of the heart is (including atria). The right coronary artery supplies about 81% of the right ventricle and 23% of the left ventricle with its blood supply. The remaining portion of the right ventricle is supplied by the LAD. The collateral circulation was measured in each of the 3 coronary beds using tracer microspheres. Measurements, are in ml/min/100 g. Transmural collateral flow in the LC is 5.6, the LAD 1.0, the RC in LV 3.7 and the RC in RV 4.3. Our experiments showed that the coronary bed sizes were relatively uniform in pigs, but that collateral flow was significantly different between the beds.
Animals↗
Myocardial blood flow distribution in miniature pigs during exercise.
Total and regional myocardial blood flow was measured in miniature pigs at rest and during two levels of treadmill exercise, including maximal exercise. Exercise increased the myocardial blood flow in a linear manner with heart rate (r = 0.87). At rest the endocardial/epicardial blood flow ratio was significantly greater than unity with flow favoring the endocardium. Exercise failed to appreciably alter the distribution of coronary blood flow. Thus the myocardium was capable of further dilatation and perfusion of blood without compromising endocardial flow even during the most severe level of exercise when maximal heart rates were attained.
Animals↗
Myocardial characteristics of thyroxine stimulated hypertrophy. A structural and functional study.
The effects of thyroxine-stimulated hypertrophy (TSH) were studied in the porcine left ventricular myocardium. Hypertrophy was produced in six adult pigs by administration of triiodothyronine (1 mg/kg; i.v.) for eight days. Six pigs served as controls. The degree of hypertrophy, determined by left ventricular-to-body weight ratio, was 47%. With hypertrophy there was a significant increase in heart rate, blood pressure and myocardial blood flows. Minimal coronary resistance measured during adenosine infusion was lower in the TSH group compared with the control group. Anatomic studies revealed a balanced proliferative response of mitochondria, myofibrils and the t-tubular system during TSH. Analysis of the microvasculature indicated that the capillary and arteriolar beds both experienced growth which paralleled myocyte growth during TSH. These results suggest that thyroxine administration promotes angiogenesis in the microvascular bed which provides a partial anatomic rationale for the lowered minimal coronary resistance.
Animals↗
Effect of acute exercise stress in cardiac hypertrophy: I. correlation of regional blood flow and qualitative ultrastructural changes.
Ultrastructural myocardial cell changes were determined in eight miniswine after the development of pressure-overload hypertrophy induced by supra-valvular aortic constriction. Four miniswine served as control animals. Regional myocardial blood flows were measured at rest and during exercise stress with radioactive microspheres after two days and one month of aortic constriction. Exercise stress, causing the heart rate to increase to 85 percent of its maximum, was imposed twice weekly for 7 minutes on four pressure-overloaded animals and the four control animals to elicit differences between the control and experimental groups that might not occur at rest. After one month of pressure overload the swine were killed and myocardial samples were processed for electron microscopy. Ultrastructural changes similar to those in hypertrophied hearts were present throughout the left ventricular walls of the pressure-overloaded animals. Other changes consistent with ischemic injury were present in the subendocardial regions of pressure-overloaded animals subjected to exercise stress. These changes included disorganization of myofibrils, disintegration and broadening of Z-bands, swelling and aggregation of mitochondria, electron-dense deposits in mitochondria, decreased cristal density and vacuolization of mitochondria, intracellular edema, margination and clumping of nuclear chromatin, and a decrease of glycogen granules. Regional ischemia in the subendocardium of these animals was confirmed by functional studies which showed decreased regional myocardial blood flow to the subendocardium during exercise and S-T segment elevation for the first 2-10 days after inducing pressure overload. The ischemia, as shown by flow studies, during exercise stress persisted in the compensatory stage of hypertrophy although S-T segments returned to normal. Thus, the combined effect of pressure overload and exercise stress can produce focal subendocardial ischemia in the compensated, hypertrophied heart.
Animals↗