Recent advances in studies on cardiac structure and metabolism最新文献

Histopathological studies were carried out on right ventricular myocardium in 104 patients with tetralogy of Fallot (T/F). Detailed analysis of the correlation between morphological and clinical data was performed. Right ventricular hypertrophy in T/F was found to initiate immediately after birth, and the diameter of right ventricular muscle fiber (D) increased with age (r = 0.74). There was a correlation between D and the hemoglobin level. There was, however, no correlation between D arterial oxygen saturation (SaO2), and pulmonary trunk/aorta diameter (PA/Ao) ratio. Histopathological alterations were related directly to D and to the age of the patient, and were unrelated to hemoglobin, SaO2, and PA/Ao ratio. Irreversible histopathological alterations were first observed when the D exceeded 15 micron, when most patients were four years old or more. From these findings, it is considered that the optimal age for corrective surgery to prevent irreversible alteration of the right ventricular muscle fibers in patients with T/F is less than three years.

Insulin increases the contractile force of myocardium with hyperpolarization and a faster rate of fall of the action-potential plateau. This phenomenon is augmented inthe reduced-K+ or ouabain solution. It is suggested that the insulin-induced positive inotropism can be explained by facilitation of inward movement of Ca2+, which possibly is associated with an increase in outward movement of K+.

Fibrillation-like beating of cardiac muscle cells in culture was induced by altering the concentrations of various ions. Fine structural changes of cell membrane and intercellular alteration of cardiac muscle cells appeared to be more prominent in cells with fibrilliation-like beating than in others. From the results of the present study, it may be concluded that fibrillation-like beating may occur in the presence of altered concentrations of certain ions, accompanied by fine structural changes in the cells.

To obtain further information on the mechanism by which catecholamines produce myocardial ischemia, the effects of propranolol on metabolic and mechanical responses to adrenaline or noradrenaline were investigated in coronary-constricted dogs. Propranolol suppressed the myocardial ischemia produced by noradrenaline and adrenaline in dogs with moderate coronary constriction.

Mongrel dogs were subjected to cardiopulmonary bypass with hemodilution and to normothermic anoxic arrest for 30 minutes, to study the subepicardial and the subendocardial myocardial ultructure and the DPTI/TTI ratio. "No-reflow phenomenon" was demonstrated in the myocardium after cardiopulmonary bypass, associated with normothermic anoxic arrest. No-reflow phenomenon was a contributing factor to subendocardial ischemia in the normotrophied ventricle after open-heart surgery. Severe hemodilution with hemoglobin less than 5.0 g% resulted in irreversible damage in both myocardial layers.

Changes in metabolic activity of removed heart valve allografts have been measured. The fresh heart valves were sterilized and stored in antibiotic solution before implantation in patients. Viability was determined before insertion and after removal from patients by two methods: 1) tissue culture, and 2) autoradiography, using tritiated thymidine. The length of storage in the Hank's antibiotic or nutrient-antibiotic medium before insertion did not seem to influence the final metabolic activity nor the structural integrity of the allografts when they were removed. Results from the present study show that the most severe degenerative changes occur in valves stored in Hank's solution and then implanted in the mitral position. The viability percentage declined progressively during the time that a valve treated in this manner was functioning in a patient.

Previous studies from this laboratory have demonstrated the usefulness of myocardial gas tensions as measured by mass spectrometry for the quantitative assessment of regional myocardial ischemia (Khuri et al., 1975a). Progressive increases in myocardial carbon dioxide tensions were noted when progressive reduction in coronary blood flow was created by means of a variable constrictor. The present study was designed to determine if changes in myocardial oxygen and carbon dioxide tension were greater in deep, compared to more superficial, myocardial layers. In eight anesthetized dogs, progressive reduction in circumflex coronary flow was associated with a progressive reduction in myocardial oxygen tension and a progressive increase in myocardial carbon dioxide tension and intramyocardial ST-segment voltage. Evidence of a transmural gradient in the severity of ischemia was present at all degrees of flow reduction. These results confirm the findings of previous metabolic studies, which demonstrated gradients in lactate and high-energy phosphates. Myocardial carbon dioxide tension, which can be monitored continuously by mass spectrometry, would appear to provide a useful means of quantitatively assessing changes in regional myocardial metabolism.

X-ray microanalytical techniques using wavelength dispersive (WDS) and energy dispersive spectrometry (EDS) indicate that Ca2+ is present in intramitochondrial granules which occur in myocardial cells following irreversible ischemic injury. Preliminary results using tissue prepared for routine electron microscopy suggest that the degree of calcium binding that occurs in the mitochondria increases with increased duration of ischemia. Free ions are leached out of the tissue during processing; hence, the role of ion redistribution in producing myocardial necrosis cannot be elicited from a study of this nature. However, with continued progress in the development of techniques of tissue preparation x-ray spectrometry may provide a means of assessing quantitative ion alterations that occur during ischemia.

With a polysaccharide microsphere suspension (Sephadex), coronary flow of isolated perfused rat hearts was reduced by approximately 70%. During this Sephadex-induced ischemia, the energy charge and creatine phosphate content of the myocardial tissue dropped significantly, while total nucleoside and lactate release from the heart increased. During hypoxia (30% O2), changes in high-energy phosphate content and lactate and nucleoside release were similar to the changes induced by ischemia. During hypoxia, coronary flow rate was increased by 47%. Thus, Sephadex-induced reduction of coronary flow could be a useful model in studies of metabolic change during ischemia.

In in situ canine hearts, chlorpromazine induced a time (preceding cycle length)-dependent decrease in conduction velocity within the ventricle. Thus, QRS duration of nonpremature beats was lengthened at rapid pacing rates while QRS duration of atrial premature beats was lengthened at short coupling intervals. These slow conductions were not due to reduced take-off potential of ventricular action potentials but to drug-induced slow recovery of the rapid Na+ system. The phenomenon may be responsible for reported QRS prolongation and fatal ventricular arrhythmias encountered in patients receiving phenothiazines.