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Biomedical subjects

R R Taylor

Publications and source records attributed to R R Taylor.

At least 127 records · Page 7Linked to original sources
PubMed1976

Influence of myocardial mechanical activity and coronary blood flow on myocardial digoxin uptake.

The myocardial content of digoxin 60 min after intravenous administration in open-chest dogs correlated with heart rate controlled in individual dogs between 64 and 215 beats/min. In other dogs, increasing right ventricular mechanical work by constriction of the pulmonary artery resulted in greater right ventricular digoxin uptake. Increase in myocardial blood flow per se could not explain these findings since, in further dogs, increasing regional myocardial blood flow by adenosine infusion did not much affect digoxin uptake. Active uptake of cardiac glycosides is probably influenced by myocardial mechanical and metabolic activity.

Animals↗
PubMed1975

Series elasticity in the intact heart. Evidence for the application of the Hill model for muscle to the intact left ventricle.

Several recent studies have shown that the contractile state of the intact heart may be described by the instantaneous relationships between contractile element velocity, length and stress. However, there is little direct evidence that the intact heart can be described by a model containing at least a contractile element and a series elastic component (SEC). In isolated muscle the series elastic component can be analyzed by determining the length changes following quick releases to known loads during contraction. The characteristics of the effective SEC of the intact left ventricle (LV) were determined by a quick release method in 8 dogs in which the left ventricle contracted isovolumically against a balloon inserted via the mitral annulus. During active contraction, sequential withdrawals of 0.5 to 7.0 ml of fluid were performed rapidly (5-18 msec) by an electrically-timed, springloaded syringe. From these releases the calculated maximum extension of the SEC averaged 4.03 +/- 0.27% of LV circumference at LV pressures averaging 79/6 mmHg (systolic/end-diastolic; range 66-107/0-15 mmHg.) The reductions of the left ventricular midwall circumference were plotted against the corresponding changes in mean wall stress. The load extension curve determined in this manner was unchanged by varying the time of release and by norepinephrine infusion. These data support a model for the intact LV that contains an undamped SEC, the characteristics of which resemble those of isolated cardiac muscle.

Animals↗
PubMed1975

Familial hypertrophic cariomyopathy and lentiginosis.

Members of three generations of a family studied, manifest profuse lentiginosis and hypertrophic cardiomyopathy. The autosomal dominant inheritance of this syndrome is established. Lentiginosis should alert the physician to possible underlying heart disease.

Adolescent↗
PubMed1975

Augmentation of myocardial digoxin concentration in hemorrhagic shock.

The effect of the shock state on myocardial digoxin uptake and plasma digoxin levels was examined in unanesthetized dogs following hemorrhage. Five minutes after intravenous administration of tritiated digoxin the myocardial digoxin content in animals with shock was greater than in normal animals in both left ventricle (LV) (165 plus or minus 15 (SD) ng/g vs 130 plus or minus 26 ng/g, P smaller than 0.02 and right ventricle (RV) (142 plus or minus 13 ng/g vs 111 plus or minus 22 ng/g. P smaller than 0.02) as was the plasma digoxin concentration (61.6 plus or minus 11.8 ng/ml vs 44.3 plus or minus 4.6 ng/ml, P smaller than 0.02). After one hour, in another group of dogs, the difference in myocardial concentration of digoxin between test and normal groups was even greater (LV: 213 plus or minus 26 ng/g vs 133 plus or minus 13 ng/g, P smaller than 0.001; RV: 171 plus or minus 9 ng/g vs 111 plus or minus 8 ng/g. P smaller than 0.001) despite lower plasma digoxin concentration in the test group (12.9 plus or minus 2.9 ng/ml vs 17.3 plus or minus 2.5 ng/ml, P smaller than 0.05). Diminished peripheral blood flow, peripheral digoxin delivery and uptake were probably responsible for the early difference in plasma digoxin levels. Resultant greater plasma concentrations of digoxin presented to the myocardium in the early phase, coupled with relative preservation of myocardial blood flow, may explain the greater myocardial uptake in animals with shock although myocardial mechanical factors may also be implicated. Augmented uptake of digoxin by the myocardium in canine hemorrhagic shock may be relevant to the altered susceptibility to glycoside action in clinical shock syndromes.

Animals↗
PubMed1974

Digitalis-induced increase in aortic regurgitation and the contrasting effect of glucagon in the sedated dog.

The hemodynamic and phasic ascending aortic flow changes induced by acetylstrophanthidin and glucagon were studied in closed-chest sedated dogs with aortic regurgitation. While the positive inotropic effect of both agents was reflected in an increase in peak rate of rise of left ventricular pressure, acetylstrophanthidin increased aortic regurgitation, while glucagon decreased it. With the former, left ventricular end-diastolic pressure rose from 20+/-6 to 27+/-6 mm Hg (P < 0.005), but fell from 18+/-4 to 11+/-3 mm Hg (P < 0.001) with glucagon. Acetylstrophanthidin increased systemic vascular resistance, aortic diastolic pressure, and diastolic regurgitant flow rate, and, heart rate and the duration of regurgitation per beat and per minute being unchanged, regurgitant flow per beat increased 32+/-15% (P < 0.001). Glucagon decreased regurgitant flow per beat 27+/-14% (P < 0.001) because of abbreviation of diastole associated with tachycardia, and because of reduction in regurgitant flow rate. Despite tachycardia, the duration of regurgitation per minute was unchanged, and the small fall in regurgitant blood flow per minute was not significant, but this pertained in the face of 47% increase in effective cardiac output (P < 0.001). In contrast, acetylstrophanthidin increased regurgitant flow per minute 28+/-14% (P < 0.001) without change in effective cardiac output. The increase in cardiac contractility, tachycardia, and systemic vasodilatation induced by glucagon preferentially enhanced forward blood flow, which led to reduction in left ventricular volume overload, while it increased cardiac output. Contrarily, acetylstrophanthidin increased aortic regurgitation and, despite its inotropic effect, increased left ventricular volume overload without an increase in cardiac output.

Animals↗