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Biomedical subjects

A H From

Publications and source records attributed to A H From.

At least 73 records · Page 4Linked to original sources
PubMed1980

Q-wave abnormalities in chronic obstructive pulmonary disease and myocardial infarction.

ECGs taken from patients with chronic obstructive pulmonary disease (COPD) frequently mimic myocardial infarction (MI), and may, therefore, cause diagnostic difficulties for the physician. In many previous studies, criteria to differentiate electrocardiographically between COPD and MI were either untested in large numbers of cases or too complicated for routine use. This study was undertaken to find simple new criteria, using scalar measurements which are easily obtainable in clinical practice. To assure the stability and repeatability of our results, the accuracy of these criteria was tested in a large series of cases. Three-hundred and ninety-six (396) cases of COPD and eight-hundred and seventy-eight (878) cases of MI comprised the material for this study. The COPD cases were grouped into two: a training set of 266 cases and a test set of 130 cases. There were three MI subgroups: AMI-344 cases, PDMI-449 cases, and LMI-85 cases. By applying the proposed ECG criteria specifically on the "COPD--MI mimics," we were able to reduce the number of potentially mis-diagnosed COPD cases (based purely on Q-wave abnormality) from 158 cases (40% of all COPD cases) to 71 cases (18%).

Computers↗
PubMed1980

Alternating bundle branch block.

Mechanisms postulated for alternating bundle branch block are incomplete- and cycle-length-dependent-block in both the right and left bundle branches. A patient with severe longstanding cardiac conduction disease who developed alternating bundle branch block during treatment for advanced ischemic heart disease and malignant ventricular arrhythmia is presented. In this patient alternation was induced by atrial premature beats as well as spontaneous and pacemaker induced premature ventricular beats. Right bundle branch block which followed a premature atrial beat resulted from the longer refractory period of the right bundle. The maintenance of right bundle branch block at long cycle lengths was presumed to be due to continuous retrograde reentry. This was terminated when a pause following a premature beat allowed functional recovery of the right bundle branch. This patient died suddenly at home with a functioning pacemaker, demonstrating the high risk of death from ventricular dysrhythmia in the post myocardial infarction patient with a new conduction defect.

Aged↗
PubMed1979

Digitalis genin activity: side-group carbonyl oxygen position is a major determinant.

The Na+,k+-adenosine triphosphatase-inhibiting activity of digitalis genins and their analogs is a function of side-group carbonyl (C = O) oxygen position. For each 2.2 angstroms that this oxygen is displaced from its position in digitoxigenin, activity drops by one order of magnitude. This quantitative relation resolves previously proposed models which have attempted to describe the molecular basis of genin activity. A multidisciplinary (crystallographic, conformational energy, synthetic, biological) approach to structure-activity relations is described.

Animals↗
PubMed1979

Cardenolide analogues. 4. (20R)- and (20S)-Cardanolides: on the roles of the 20(22)-ene and 14beta-hydroxyl in genin activity.

(20R)-20,22-Dihydrodigitoxigenin (3a) and (20S)-20,22-dihydrodigitoxigenin (3b) were isolated from (20R,S)-20,22-dihydrodigitoxigenin (3) by three fractional crystallizations each from ethyl acetate. The two diastereomers have distinct NMR spectra and similar (Na+,K+)ATPase inhibitory activities (I50 = 1.1-1.4 X 10(-5) M)--about 1/100 as active as digitoxigenin (1). Their activity compared with other cardenolide analogues suggests a passive geometric role for the 20(22) double bond in eliciting (Na+,K+)ATPase inhibition, keeping the lactone carbonyl in the proper orientation. (20S)-3 beta,14 beta-Dihydroxy-22-methylene-5 beta,14 beta-cardanolide (7a) was then synthesized from 3a, and (20R)-3 beta,14 beta-dihydroxy-22-methylene-5 beta,14 beta-cardanolide (7b) from 3b. They were found to be equivalently active in inhibiting (Na+,K+)ATPase, with I50 values of 7.0 x 10(-5) M. Although it has been usually believed that the 14 beta-hydroxyl of cardenolides increases binding to the receptor, 2b (the 14-ene derivative of 7b) was more than twice as active (I50 = 3.0 X 10(-5)) than either 7a or 7b.

Animals↗
PubMed1979

Assessment of left ventricular function in aortic insufficiency using echocardiography, gated scintigraphy and contrast angiography.

Echocardiography, gated scintigraphy and contrast angiography were used to measure left ventricular ejection fractions in 20 patients with varying degrees of aortic insufficiency. There was good correlation between the radionuclide and the angiographic ejection fractions. Echocardiographic ejection fraction correlated less well with the angiographic ejection fraction. The radionuclide left ventricular ejection fraction may prove valuable in the noninvasive serial evaluation of left ventricular function in patients with chronic aortic insufficiency.

Adult↗
PubMed1979

Polymyxin B sulfate modification of bacterial endotoxin: effects on the development of endotoxin shock in dogs.

The effects of endotoxin (lipopolysaccharide [LPS]) on the pathogenesis of canine endotoxin shock were compared with those of LPS which had interacted with polymyxin B sulfate prior to administration. Both LPS and polymyxin B-modified LPS caused comparable early decreases in aortic blood pressure, leukocyte and platelet numbers, and serum complement levels. However, in dogs receiving polymyxin B-modified LPS the late hypotensive phase was significantly ameliorated and lethality was significantly decreased. These data indicate that polymyxin B-modified LPS, though significantly less lethal than unmodified LPS, was capable of major interactions with several components of the humoral defense system, and support the concept that such interactions are not determinative in the pathogenesis of canine endotoxin shock.

Animals↗
PubMed1977

Cardenolide analogues. 2. 22-Methylenecard-14-enolides.

22-Methylene-3beta-hydroxy-5beta,20(S)-card-14-enolide (11) and 22-methylene-3beta-hydroxy-5beta,20(R)-card-14-enolide (12) were synthesized from digitoxin (1). Attempts to prepare the 14beta-hydroxy-22-methylene analogues were unsuccessful. The 20(R) isomer (12) was found in Na+, K+-ATPase inhibition studies to be twice as active as 14-dehydrogitoxigenin (17). The 20(S) isomer (11) was significantly less active than 17. The hydrolysis of steroid 3beta-tert-butyldimethysilyl ethers was also found to be much more difficult than with nonsteroids.

Adenosine Triphosphatases↗
PubMed1977

Hypereosinophilic syndrome with biventricular involvement.

In a 45-year-old man with hypereosinophilic syndrome, cardiac disease, mainly endocardial thickening and extensive mural thrombosis of both ventricles, was confirmed at autopsy. Early in the course of the disease, right ventricular endocardial biopsy had demonstrated the basic process. Restriction in filling and contraction of the right ventricle were demonstrated by functional studies. By echocardiographic study, progressive reduction in size of the right ventricular cavity and premature opening of the pulmonary valve were demonstrated, while this method was less adequate in identifying the process in the left ventricle.

Autopsy↗
PubMed1976

Cardenolide analogues. 1. A 17beta-unsaturated aldehyde.

A 17beta-unsaturated aldehyde analogue [3beta,14beta-dihydroxy-5beta-pregn-17beta-trans-20-en-22-al (7)] of the cardenolides was synthesized and studied. In earlier studies by Rappoport, unsaturated aldehydes were found to be highly active electrophiles, more active, for example, than unsaturated nitriles or methyl esters. The synthesis followed in part a scheme previously reported by Thomas for the syntheses of the 17beta-unsaturated nitrile 9 and the 17beta-unsaturated methyl and ethyl esters 8 and 10. Both 9 and 8 are more Na+,K+-ATPase inhibiting and slightly less inotropic than digitoxigenin (1b). However, the unsaturated aldehyde 7 was less Na+,K+-ATPase inhibiting (I50 - 9.9 +/- 0.7 X 10(-7) M) and less inotropic (100% increase in contractile force at 8.5 +/- 1.0 X 10(-6) M) than 1b (I50 - 4.6 +/- 1.6 X 10(-7) M; 100% increase at 3.0 +/- 1.0 X 10(-7) M).

Adenosine Triphosphatases↗
PubMed1976

Role of platelets in the pathogenesis of canine endotoxin shock.

Endotoxin-platelet interactions are thought to be of major importance in the response of dogs and other species to bacterial endotoxin; the mechanisms postulated are: (i) the release of vasoactive substances, (ii) the formation of occlusive platelet aggregates, and (iii) induction of intravascular coagulation. The role of platelets in canine endotoxin shock was examined in animals with thrombocytopenia induced by estrogen pretreatment (less than 10,000 platelets/mm3) and in controls. After intravenously administered endotoxin, the hemodynamic responses, mortality, and gross necropsy findings were similar in both groups. These data indicate that endotoxin-platelet interactions are not determinative in the pathogenesis of canine endotoxin shock.

Animals↗
PubMed1975

Significane of intravascular coagulation in canine endotoxin shock.

The contribution of disseminated fibrin clot formation to the pathogenesis of canine endotoxin shock was explored in control dogs and in those defibrinated with a purified fraction of Malayan pit viper venom. The hemodynamic and humoral responses after the administration of an intravenous challenge dose of Escherichia coli endotoxin were comparable as was mortality. It is concluded that, although the role of the coagulation sequence in canine endotoxin shock is unclear, it does not appear to be determinative.

Animals↗
PubMed1975

Ethacrynic acid induced inotropism.

Ethacrynic acid (ECA), a sulfhydryl group inhibiting diuretic was examined for positive inotropic effects. These were found to be present in isolated guinea pig left atria studied in 0.9 and 1.8 mM Ca bathing solutions and were partially dependent upon adrenergic mechanisms (presumably secondary to norepinephrine release from sympathetic nerve endings) and partly independent of such mechanisms as demonstrated by propranolol induced beta-blockade and reserpine-induced catecholamine depletion. The mechanism of the non-beta adrenergic inotropism is unclear but may relate to the ability of ECA to inhibit the sarcolemmal Na-K-Mg-dependent ATPase. ECA-induced premature contractile failure occurred in all atria as well as a late increase in diastolic tension, the latter being comparable to that described for toxic doses of cardiac glycosides in similar preparations.

Animals↗