ISSN:0002-9629    

出版商:OVID    

年代:1969

数据来源: OVID

摘要:

The performance of the hypertrophied and failing myocardium has been analyzed in the isolated heart muscle from experimental animals, intact ventricle of experimental animals, and now the intact ventricle of conscious man. It is apparent there are characteristic intrinsic depressions of contractility in the hypertrophied heart in which circulatory compensation is maintained. These depressions are found in the overtly failing heart to a greater degree. The basic abnormality appears to be a decrease in the intensity of the active state of the contractile elements within the myocardial fibers. This decrease in the intensity of active state is not associated with any changes in the duration of active state and does not appear to be associated with any changes in the resting tension characteristics of the muscle. The basic decrease in intensity of active state in hypertrophied and failing heart muscle finds expression in the decrease in the maximum intrinsic velocity of shortening (Vmax) and in decreased rate of ventricular pressure rise (dP/dt). This basic decrease in intrinsic contractile element performance is compensated for by a number of mechanisms in order to maintain circulatory performance despite decreased function of cardiac muscle. When the ventricle is chronically stressed by an abnormal load, there is a rapid response to increase the total muscle mass. This increase in muscle mass operating in conjunction with the Frank-Starling mechanism, and an increased sympathetic stimulation, maintains overall circulatory compensation despite depression of the intrinsic contractile state of each unit of myocardium. As the intrinsic contractile state of each unit of myocardium becomes more severely depressed, there is a more extensive fall in the maximum velocity of shortening, a further decrease in maximal isometric force, a decrease in the rate of force development, and also the sympathetic nerve support of cardiac contractility becomes impaired. At some point, circulatory compensation can no longer be maintained despite maximal utilization of the compensatory mechanisms provided by the Frank-Starling mechanism and the increases in muscle mass; overt congestive heart failure then ensues with a fall in cardiac output.

ISSN:0002-9629    

出版商:OVID    

年代:1969

数据来源: OVID

摘要:

A review of the ultrastructure of normal heart muscle and the ultrastructural basis of cardiac contraction has been presented to provide a better understanding of fine structural cellular pathology of the heart, and to refer derangements of cardiac function to specific structural loci. Alterations in the fine structure of myocardial cells and cellular organelles have been noted in cardiac dilatation and hypertrophy, coronary insufficiency, and alcoholic cardiomyopathy. Cardiac dilatation has been examined in terms of alterations in sarcomere length (the Frank-Starling mechanism), fibril slippage, and the relation of these factors to disordered ventricular function. Similarly, cardiac hypertrophy, coronary insufficiency, and alcoholic cardiomyopathy have been described in terms of alterations of cellular organelles, such as the sarcotubular system, mitochondria, myofilaments, and the interealated disc. The possible relation of these ultrastructural modifications of cardiac dysfunction has been examined. Moreover, the effects of such factors as tissue sampling sites and preparative techniques upon fine structural patterns of both intact (normal) and injured cells and their relation to the ultrastructural examination and interpretation of the failing heart have been discussed.

ISSN:0002-9629    

出版商:OVID    

年代:1969

数据来源: OVID

摘要:

In many forms of heart failure a depression of myocardial performance has been identified. Ultimately this implies that a biochemical limitation of cardiac function may be the cause of the heart failure state. This limitation could involve the areas of energy metabolism, protein synthesis, or excitation-contraction coupling. Mitochondrial function and the uptake of substrates and oxygen by the failing heart cannot be implicated as causal factors in heart failure. Similarly, myocardial energy stores are adequate for normal function, and the efficiency of energy utilization is not decreased in the failing myocardium. The production of acute cardiac overload in the experimental animal causes an augmentation of protein synthesis involving increased rates of RNA production and amino acid incorporation into protein. However, the greatest portion of this activity take place in noncontractile cells. While a diminution of these processes is associated with the heart failure state, it is certainly not clear what stimulus evokes the diminution of these processes or whether they are causally related to the onset of heart failure. Finally, there is evidence that alterations of contractile state in the myocardium may be mediated by alterations in the process of excitation-contraction coupling which involves the release and reuptake of calcium ion from the sarcoplasmic reticulum. While many factors operating together may ultimately explain the onset of heart failure, a desect in excitation-contraction coupling remains the most likely single possibility.

ISSN:0002-9629    

出版商:OVID    

年代:1969

数据来源: OVID

摘要:

The acute effects of cholera exotoxin on selected absorptive and secretory functions of the small intestine of the dog were studied before and during fluid production induced by cholera exotoxin. To minimize systemic fluid and electrolyte depletions and to permit serial observations, short Thirty-Vella loops of either jejunum or ileum were employed. The unidirectional sodium flux from lumen to blood was unchanged during exotoxin-induced fluid production. Sodium flux from blood to lumen, however, was markedly increased. Glucose absorption was unaltered. These observations in the dog indicate a preservation of the lumen to plasma flux of sodium and the absorption of glucose with an increased plasma to lumen flux of sodium associated with secretion of water and other electrolytes during cholera exotoxin fluid production. It is suggested that one of the principal actions of cholera exotoxin is to stimulate the movement of fluid and electrolytes into the intestinal lumen.

ISSN:0002-9629    

出版商:OVID    

年代:1969

数据来源: OVID

摘要:

The present study was designed to determine whether dopamine could be of value in phenobarbital or salicylate intoxication. Accordingly, large doses of either drug were given to dogs and the effects of dopamine on the renal clearances of these drugs were measured. It was found that dopamine increased blood pressure, urine flow and renal clearance of phenobarbital in dogs made hypotensive by the barbiturate. Thus, dopamine might have a role in the treatment of severe barbiturate intoxication. Dopamine also increased the clearance of salicylate in dogs given bicarbonate. Since hypotension was not produced by the salicylate, dopamine has less potential applications in salicylate than in barbiturate intoxication.

ISSN:0002-9629    

出版商:OVID    

年代:1969

数据来源: OVID

摘要:

The persistent question of the induction of hypertension in chronic lead intoxication lead to this study. Rats of a strain characterized by the ease of inducing renal disease and hypertension were chosen. Blood pressures were measured in double-blind fashion in animals receiving lead by gastric intubation during 138 days. Evidence of lead intoxication includes anemia, reticulocytosis, siderocytosis, abnormal bone marrow and renal histology, and elevated concentrations of lead in blood and bone (p < .001). During nearly six months of observation, hypertension and renal function impairment did not develop. The failure to induce hypertension in susceptible animals proven to be lead intoxicated warrants the search for those factors influencing lead availability and toxicity.

ISSN:0002-9629    

出版商:OVID    

年代:1969

数据来源: OVID

ISSN:0002-9629    

出版商:OVID    

年代:1969

数据来源: OVID

ISSN:0002-9629    

出版商:OVID    

年代:1969

数据来源: OVID