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Biomedical subjects

J J Kane

Publications and source records attributed to J J Kane.

At least 55 records · Page 3Linked to original sources
PubMed1975

Electrophysiology of atropine.

The effect of atropine on the refractory periods of the human atrium, A-V node, and His-Purkinje system was studied. The A-V node in man appears more sensitive to atropine than the atria as evidenced by a reduction in the effective and functional refractory periods of the A-V node without alteration of atrial conduction. Although atropine does not directly alter the refractory periods of the His-Purkinje system, atropine-induced facilitation of A-V nodal conduction results in block of premature atrial impulses in the His-Purkinje system, demonstrating an indirect effect of atropine on His-Purkinje conduction. Rarely, atropine may precipitate re-entrant atrial tachycardia (one patient) through facilitation of A-V nodal conduction.

Adult↗
PubMed1975

Electrophysiological significance of rapid atrial pacing as a test of atrioventricular conduction.

Although rapid atrial pacing is frequently used as a test of atrioventricular conduction, no studies have compared this method with other conduction parameters. The purpose of this study was to compare the results of rapid atrial pacing with refractory period measurements utilizing the extrastimulus technique. Determination of the refractory periods of the atrium, A-V node, and His-Purkinje system were accomplished in 41 patients undergoing diagnostic cardiac catheterization, and the results compared with rapid atrial pacing to the point at which A-V Wenckebach occurred (WP). The results showed significant correlation (P less than 0.01) between the WP and functional refractory period (FRP) of the A-V node (r=0.89, FRP=865-2.6 WP), and significant correlation between the WP and the effective refractory period (ERP) of the total A-V conducting system(r=0.81, ERP=729-2.6 WP). The relationship between WP and the refractory periods also allowed prediction of the occurrence of physiological His-Purkinje block during introduction of premature atrial contractions and the site of the effective refractory period of the total A-V conducting system. This study establishes a close relationship between these methods and confirms the usefulness of rapid atrial pacing as a reliable test of A-V conduction in man.

Atrial Function↗
PubMed1975

In-hospital mortality after acute myocardial infarction.

In order to determine if the risk factors contributing to mortality from acute myocardial infarction (MI) during the period of coronary care unit (CCU) observation are different from those in patients dying in the hospital after CCU discharge, the hospital records of 172 acute MI patients seen over an 18-month period were reviewed. Of the 32 deaths from acute MI, 25 per cent occurred suddenly outside the CCU. The risk factors identified in the 32 deaths were (1) anterior MI (2) Previous MI, (3) cardiac failure, (4) significant ventricular arrhythmia, (5) intraventricular conduction defects, and (6) murmur suggestive of papillary muscle dysfunction. These same risk factors were found to be far more frequent in the patients dying suddenly outside the CCU.

Adult↗
PubMed1975

Tritiated digoxin: studies in renal disease in human subjects.

Digoxin is excreted primarily in the urine as the unchanged glycoside: 60-80% can be recovered from the urine in 7 days after a single intravenous dose in the human subject. Definition of the role of the kidney in digoxin excretion, turnover and metabolism was studied in 57 patients with renal disease, transplant candidates and/or donors and recipients of renal transplants. A single dose of 3H digoxin was given to the subjects, frequent serum samples were obtained and all urine and stools were saved for 7 days. All specimens were extracted with chloroform and digoxin, and its metabolites were separated by column chromatography. Results reveal that the serum T1/2 and the dominant T1/2 of digoxin are prolonged in renal disease in direct proportion to the reduction in creatinine clearance (r = 0.833). The blood urea nitrogen (BUN) is also related to digoxin clearance (r = 0.742). The higher the BUN, the less digoxin excreted in the urine. Anephric patients excrete more digoxin in stool, but this does not compensate for the lack of renal excretion. Transplanted kidneys excrete digoxin in proportion to renal functional capacity, as do patients who have experienced unilateral nephrectomy. Peritoneal or hemodialysis is not effective in removing digoxin from the human subject and may lead to digitalis intoxication if K+ is allowed to fall to critical levels. Digoxin excretion is not volume related, as patients with nephritogenic diabetes insipidus excrete the drug normally with urine volumes of 12 liters a day. Digoxin doses in renal insufficiency should be dictated by knowledge of renal functional ability of the kidneys and after "normal" loading doses, and maintenance doses should be 1/4 to 1/2 those usually administered.

Adult↗
PubMed1975

Impairment of mitochondrial function following reperfusion of acutely ischemic myocardium.

This study examines indices of respiratory function in mitochondria prepared from transiently ischemic myocardium that had been reperfused in order to evaluate the validity of performing early surgical revascularization procedures. Experiments were performed in pigs with temporary ligation (15-80 min) of an anterior descending coronary artery followed by a 2-hr reperfusion period. Mitochondria preparations were studied simultaneously from normal and reperfused mitochondria in malate and glutamate substrates using the polarographic method. Results revealed a marked decrease of oxygen consumption of mitochondria from reperfused myocardium with relative preservation of oxidative phosphorylation (near normal ADP/O ratio). These results are compatible with a block in electron transport, a theory which was further supported by the data obtained using dinitrophenol as an uncoupler. Additional studies suggested the block was located at site I in the electron transport chain since mitochondrial oxygen consumption, including ATP-linked oxygen consumption, was enhanced by the use of succinate in combination with glutamate. The abnormal mitochondrial function observed is probably due to ischemia persisting despite reperfusion.

Acute Disease↗