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Biomedical subjects

W E Shell

Publications and source records attributed to W E Shell.

At least 37 records · Page 2Linked to original sources
PubMed1981

Differences in beta-adrenoceptor binding in anterior and inferior myocardial wall microsomes of normal canine left ventricle.

Myocardial beta-adrenoceptor binding was investigated, with (-)3H dihydroalprenolol as radioligand, in microsomes derived from anterior (ALV) and inferior (ILV) myocardial wall sections of the canine left ventricle. Characterisation of specific binding sites revealed a hierarchy of myocardial beta-adrenoceptor binding with greater binding occurring to the anterior than the inferior wall of the left ventricle, under identical experimental conditions. Equilibrium analysis by Scatchard plots suggested a significant (P less than 0.01) difference in the number of receptors (Bmax ALV = 70 fmol . mg-1 protein vs Bmax ILV = 37 fmol . mg-1 protein) with no alteration in the binding affinity of the receptors (KDALV = 10.1 nmol . litre-1 vs KDILV = 6.7 nmol . litre-1). Such differences in the extent of binding of beta-adrenoreceptors in cardiac muscle may be of physiological and pathological significance and may account for the heterogeneity of regional autonomic responses in the heart.

Adrenergic beta-Antagonists↗
PubMed1979

Sensitivity and specificity of MB creatine kinase activity determined with column chromatography.

Several analytic techniques are used to estimate the activity of creatine kinase (CK) isoenzymes. These techniques are undergoing continual refinement because the MB CK molecule appears to be nearly cardiospecific. An improved column chromatographic assay is presented with a lower limit of analytic detection of 0.8 mlU/ml. The assay was applied to normal subjects and to patients with myocardial infarction and with complex disease states. Results of the column chromatography were compared with those of agarose and cellulose acetate electrophoresis. There was MB CK activity in all normal sera (no. = 19, mean +/- standard deviation = 2.4 +/- 7). After acute myocardial infarction the MB CK activity increased by 650 percent (no. = 86, mean +/- standard error of the mean = 158.2 +/- 12.6 mlU/ml). The sensitivity for myocardial infarction was 100 percent. The specificity, evaluated in multiple clinical states, approached 100 percent. The column assay was compared with both agarose and cellulose acetate electrophoresis, and poor correlations with these semiquantitative systems were demonstrated. Finally, peak MB CK activity was closely correlated with kinetic analyses used to estimate infarct size (r = 0.94). Thus, column chromatography is a sensitive and specific method of estimating MB creatine kinase activity and is more precise than current electrophoretic methods.

Acute Disease↗
PubMed1978

Quantification of myocardial injury during coronary artery bypass graft.

Serial intraoperative myocardial-specific creatine-kinase (MB-CK) samples were obtained in 32 patients undergoing coronary artery bypass graft (CABG). Based upon their postoperative ECG and technetium pyrophosphate SCAN results, each patient was classified as either Group A (MI), B (normal), or C (equivocal). Peak MB-CK was reported for each group. The mean value for Group A (75 +/- 17 IU/L) is higher than for Group B (18 +/- 1 IU/L) or Group C (30 +/- IU/L). The concept of measuring and a formula for calculation of intraoperative myocardial injury are presented. The mean value for Group A (MI, 10,709 +/- 5885) is higher than either groups B (normal) or C (equivocal) by a test of proportionality (P < 0.001). Likewise, Group C (898 +/- 159) is higher than B (466 +/- 71) (P < 0.05). This index, while in need of further validation, corresponds closely to the clinical status of the 32 patients studied and should provide a means more refined than mortality or incidence of MI upon which to judge efficacy of any proposed means of operative myocardial preservation.

Aged↗
PubMed1977

Augmentation of serum CPK activity by digitalis in patients with acute myocardial infarction.

The effect of acetyl strophanthanin on the rate of creatine phosphokinase (CPK) efflux was evaluated in 59 predominantly class I and II patients randomly allocated between treated and control. Therapy (0.5 mg) was begun 11-15 hours after the onset of symptoms and repeated four hours later (0.25 mg). Accumulated CPK activity (ACA) was determined from serial serum CPK changes sampled every two hours and compared to predicted CPK activity (PCA) determined from the first seven hours of CPK changes. In the control group, ACA was not significantly different from PCA. Digitalis consistently resulted in an augmentation of CPK efflux into serum which was temporally related to drug administration and resulted in a corresponding increase in ACA (P less than 0.001). Thus acetyl strophanthanin appears to increase apparent CPK activity in serum in class I and II patients.

Acute Disease↗
PubMed1976

Biochemical markers of ischemic injury.

Enzymatic estimation of infarct size entails assumptions requiring analysis and modification during evolution of the method. Myocardial creatine phosphokinase (CPK) depletion reflects infarct size under many experimental conditions, and release of CPK into the circulation has been correlated with histologically demonstrable necrosis. Use of a one compartment model relating serum CPK changes to myocardial CPK depletion is a simplification requiring estimates of CPK disappearance rate (kd) as one parameter. Conformity of kd to first order kinetics and its lack of variance despite marked hemodynamic perturbations, myocardial infarction per se, or successive daily determinations have been documented. In patients with myocardial infarction, enzymatic estimates of infarct size correlate with morbidity and mortality, functional cardiac impairment, severity of clinical manifestations, frequency of ventricular dysrhythmia, and morphologically estimated infarct size. Improved estimates result from MB CPK analyses which avoid difficulties due to noncardiac CPK in the circulation and from individualization of values of kd. The discriminant power of enzymatic estimates as an index of prognosis has been demonstrated by discriminant function analysis. Prediction of infarct size enzymatically requires additional assumptions and conventionally employs an empirical algorithm rather than a physiological, deterministic model. Although predictions can probably be improved by incorporation of parameters reflecting processes governing CPK release and disappearance, the need for a prolonged interval during which observations are required prior to prediction limit the applicability of this approach to evaluation of therapeutic interventions whose effects are likely to be maximum when early implementation is possible.

Animals↗
PubMed1976

Coronary vascular responses to nitroglycerin following aorta-coronary saphenous vein grafting in dogs.

Phasic coronary arterial flow responses to nitroglycerin were evaluated in 15 open-chest greyhounds before and after aorta-coronary saphenous vein grafting. Coronary flow was measured with electromagnetic probes proximal and distal to the vein graft site. Simultaneous measurements of branchiocephalic flow, aortic and left atrial pressure, left ventricular pressure, and dp/dt were made. Grafts were placed during normothermic hemodilution cardiopulmonary bypass and induced ventricular fibrillation. Before grafting, intravenous nitroglycerin (0.6 mg.) elicited an abrupt rise in diastolic coronary flow which decreased as aortic pressure fell and systolic coronary flow increased. However, after grafting, nitroglycerin elicited no change in diastolic coronary flow, whereas systolic coronary flow increased and aortic pressure fell. In 6 control dogs treated similarly except for aorta-coronary grafting, coronary flow responses to nitroglycerin were unchanged. These acute experiments suggest that, in dogs with aorta-coronary saphenous vein grafts, the coronary dilating effect of nitroglycerin is virutally abolished.

Animals↗