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Biomedical subjects

R F Gilmour

Publications and source records attributed to R F Gilmour.

82 records · Page 5Linked to original sources
PubMed1981

Effects of carnitine and atractyloside on canine cardiac electrical activity.

It has been proposed that electrophysiological changes following coronary artery occlusion result from inhibition of the adenine nucleotide translocase and that these changes can be reduced by carnitine infusion or reproduced by infusion of K+-atractyloside. In the present study, we recorded bipolar electrograms during serial 3- to 5-min occlusions of the left anterior descending coronary artery in open-chest, anesthetized dogs. DL-Carnitine (100-200 mg/kg iv) prior to coronary artery occlusion did not significantly alter ischemia-induced electrogram changes. L-Carnitine (100 mg/min ia) distal to the site of occlusion during coronary artery occlusion partially reversed ischemia-induced electrogram changes, but these effects resembled those produced by intra-arterial infusion of NaCl. During normal perfusion, intra-arterial infusion of K+-atractyloside (750 mumol/10 min) or equimolar KCl produced similar reversible flattening of perfused zone electrograms. Sodium atractyloside (750 mumol/10 min ia) did not produce electrogram changes. We conclude that 1) carnitine does not attenuate ischemia-induced electrogram changes in this model and 2) K+-atractyloside-induced electrogram changes are primarily due to K+.

Animals↗
PubMed1981

Effect of aprindine on transmembrane currents and contractile force in frog atria.

The effects of aprindine on transmembrane currents in frog (Rana Ridibunda) atrial trabeculae were studied using a voltage clamp technique. Aprindine (1 x 10(-6) g/ml) reduced maximum inward sodium current by 38.6 +/- 7.2% (mean +/- S.E.M., n = 6), but had no effect on the slow inward current or outward current. A higher dose of aprindine (2.8 +/- 10(-5) g/ml) suppressed both the fast inward current and the slow inward current. Outward current was decreased at membrane potentials between -80 and -45 mV and increased at membrane potentials positive to -20 mV. In addition, aprindine was tested on frog (R. Ridibunda) atrial strips in which the transmembrane action potential and contractile force were recorded. The low dose of aprindine (1 x 10(-6) g/ml) depressed action potential amplitude and dV/dt and slightly increased action potential duration, but had no effect on contractile force. The higher dose (2.8 x 10(-5) g/ml) significantly reduced developed tension and dP/dt, decreased action potential amplitude and dV/dt and increased action potential duration. Aprindine (2.8 x 10(-5) g/ml) also depressed slow channel dependent membrane oscillations induced in atrial trabeculae by injection of current pulses. These data indicate that aprindine possesses fast and slow channel blocking properties, the latter being more apparent at high concentrations of the drug, and affects outward current differentially, depending on the membrane potential.

Animals↗
PubMed1980

Studies with aprindine.

Aprindine is a very effective antiarrhythmic agent with a narrow therapeutic-toxic ratio. It has been used successfully in treating patients who have both supraventricular and ventricular tachyarrhythmias. Aprindine slows conduction in all cardiac fibers and suppresses digitalis-induced after-depolarizations. Voltage-clamp studies indicate that aprindine, in higher doses, suppresses the slow inward current in frog atria. In the dog subjected to coronary artery occlusion, aprindine may be arrhythmogenic, antiarrhythmic, or have no effect on the development of arrhythmias, depending on the temporal relationship between time of administration and time of occlusion.

Agranulocytosis↗
PubMed1980

Electrophysiological characteristics of rodent myocardium damaged by adrenaline.

Myocardial cell injury was produced in rats and guinea pigs by injecting 3.0 mg.kg-1 1-adrenaline subcutaneously. Ventricular myocardium removed from animals 24 h after the injection exhibited marked electrophysiological alterations when studied in vitro. These alterations included: (1) reduced resting membrane potential, action potential amplitude and duration, and dV/dt; (2) conduction disturbances such as delay, unidirectional block, summation and inhibition; (3) abnormal automatic activity including triggered sustained rhythmic activity and post-overdrive acceleration. Conduction disturbances were affected by stimulus intensity, duration, rate and site of pacing. Isoprenaline (10(-7) mol.litre-1) improved conduction. Automatic activity was modified by changes in entrance and exit block and depolarising or hyperpolarising current pulses. These data indicate that diverse abnormal electrophysiological alterations occur in myocardium damaged by adrenaline.

Action Potentials↗
PubMed1980

Analysis of the urethral pressure profile using a mechanical model.

Using a model of the urethra designed to ensure a predictable pressure profile along its length, we investigated optimal parameters for gas and water profilometry. In gas profilometry, the response characteristics of the machine, attributable to the highly compressible nature of gas, were shown to be the most important determinants of accuracy. Gas and water profilometry have drawbacks that make clinical results inaccurate. However, if all measuring parameters are carefully recorded and considered when a pressure profile is analyzed, system error can be decreased from 62 to 5% by using the optimal pull and flow rates determined by this study.

Hydrostatic Pressure↗
PubMed1980

Primary hydronephrosis. Assessment of diuretic renography, pelvis perfusion pressure, operative findings, and renal and ureteral histology.

Hydronephrosis generally implies ureteropelvic junction obstruction, but may be mimicked by a variety of other disorders. The authors have attempted to determine the relative diagnostic value of diuretic renography and the pelvis perfusion test in children with hydronephrosis by correlating the results with operative findings, renal and ureteral histology, and postoperative results.

Child↗
PubMed1977

Myocardial uptake of Tc-99m skeletal agents in the rat after experimental induction of microscopic foci of injury.

The cardiac uptake of Tc-99m tagged skeletal agents was studied after myocardial injury produced by subcutaneous catecholamine injection and random foot-shock stress. Rats stressed for 2 hr developed microfocal myocardial injury, without gross change, whereas those stressed for 12 hr sustained more confluent and sometimes grossly visible damage. Tc-99m MDP and Tc-99m PPi concentrations in these hearts were significantly above control (undamaged) heart levels, producing positive gamma-camera images. Subcutaneous epinephrine injections resulted in grossly visible lesions, with tracer concentrations higher than those previously reported in vasoocclusive infarcts. We postulate that the stress-induced scattered microfocal lesions may accumulate radiopharmaceutical on a per-gram basis in the same way as the larger catecholamine-induced lesions, since tracer delivery to the injured areas in each case is probably less impeded than in frankly vasoocclusive models. Such microfoci, then, could provide an explanation for some of the "false positive" myocardial scans observed clinically.

Animals↗
PubMed1977

Protective effect of ethanol against epinephrine-induced myocardial necrosis in rats.

Myocardial necrosis was produced in rats by the subcutaneous injection of a single dose of epinephrine (3 mg base/kg). The severity of the cardiac injury produced was assessed by visual inspection, determination of the release of LDH, CPK, GOT, and HBDH from isolated perfused hearts, and measurement of cardiac uptake of technetium-99m-methylene diphosphonate in vivo. Ethanol, given in doses of 0.5 to 6.0 gm/kg 15 minutes or two hours prior to epinephrine administration protected the hearts against the epinephrine-produced injury, the degree of protection increasing with dose. Investigations of possible mechanisms of action of ethanol indicated that the protective action of the latter does not appear to be due to a lowering of plasma free fatty acid levels, a reduction of cardiac contractility, a non-specific caloric effect, an interference with epinephrine-induced platelet aggregation, or ethanol-induced analgesia.

Animals↗
PubMedDate not supplied

Inhibition of epinephrine-induced myocardial necrosis in rats by administration of single doses of ethanol.

The oral administration of single doses (0.5-6.0 g/kg) of ethanol to rats, shortly before injecting them with a large dose (3.0 mg base/kg) of epinephrine subcutaneously, significantly reduced the severity of the myocardial damage produced by the epinephrine. The larger the dose of ethanol, the greater was the protective effect. The results were the same, regardless of the method used to determine the degree of cardiac injury. Experiments employing various agents to determine the mechanisms of ethanol action have tentatively suggested that a platelet de-aggregating or an osmotic effect of alcohol may be involved.

Animals↗