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Biomedical subjects

M F Murnaghan

Publications and source records attributed to M F Murnaghan.

At least 19 recordsLinked to original sources
PubMed1981

Effect of fatty acids on the ventricular arrhythmia threshold in the isolated heart of the rabbit.

1 The ventricular arrhythmia threshold (VAT) was measured in the isolated Ringer-perfused rabbit heart (Langendorff preparation) by applying a single 10 ms square-wave pulse of current to the left ventricle during the vulnerable period of the late systole under normoxic and hypoxic conditions. 2 The sodium salt of the fatty acid was bound to albumen and incorporated in the Krebs-Henseleit solution which was maintained at 37 degrees C and gassed with 95% O2 and 5% CO2 (normoxia) or 5% CO2 in air (hypoxia). 3 Saturated fatty acids failed to alter the VAT under normoxia. 4 Naturally occurring long-chained saturated and mono-unsaturated fatty acids with chain lengths varying from 14 to 20 carbons, but not the 12 carbon lauric acid, potentiated the effect of the hypoxia in lowering the VAT. 5 Short-chained 8 and 10 carbon saturated and long-chained polyunsaturated fatty acids antagonized the effect of hypoxia on the VAT. 6 In addition the polyunsaturated acids antagonized the potentiating effect of the long-chained saturated and mono-unsaturated acids on the hypoxia in lowering the VAT. 7 The fatty acids did not alter the duration or type of the induced arrhythmia.

Animals↗
PubMed1975

The effect of sympathomimetic amines on the ventricular fibrillation threshold in the rabbit isolated heart.

1 The ventricular fibrillation threshold (VFT) was measured in the isolated heart of the rabbit perfused via the aorta with McEwen's solution at 37 degrees C by applying a single 10 ms pulse of current during the vulnerable period of late systole. The arrhythmia induced was either fibrillation or a rapid tachycardia. 2 The catecholamines adrenaline, noradrenaline and isoprenaline, but not dopamine, when infused at rates which produced similar moderate effects on cardiac rate and force, significantly lowered the VFT; it was reduced slightly more by adrenaline than by the other two. Phenylephrine and methoxamine were ineffective. Only those sympathomimetic amines which lowered the VFT also shortened the vulnerable time, i.e. minimal time after the R-wave of the ECG at which the pulse had to be applied to induce the arrhythmia. 3 The lowering effect of adrenaline on the VFT was not influenced by phentolamine but was blocked by propranolol and pindolol. 4 Chloroform potentiated the lowering effect of adrenaline, but not that of isoprenaline, on the VFT. Carbachol did not alter the effect of adrenaline on the VFT. 5 The results indicate that adrenaline, noradrenaline and isoprenaline lower the VFT by a direct action on the cardiac musculature and that this effect is mediated via beta-adrenoceptors.

Amines↗
PubMed1975

The effect of anoxia on the ventricular fibrillation threshold in the rabbit isolated heart.

1. The ventricular fibrillation threshold (VFT) was measured in the isolated heart of the rabbit perfused via the aorta with McEwen's solution at 37 degrees C by applying a single 10 ms pulse of current during the vulnerable period of late systole. The arrhythmia induced was either fibrillation or a rapid tachycardia. 2. Gassing the McEwen's solution with 5% CO2 in N2 (anoxia) instead of with carbogen caused a negative inotropic and chronotropic effect and significantly lowered the VFT. Although anoxia releases noradrenaline from the heart the effect of anoxia on the VFT was not prevented by beta-adrenoceptor blockade with propranolol or pindolol or by previous treatment with reserpine. 3. Perfusion with adenosine (5 muM) which is released from the heart muscle by anoxia, or with dipyridamole (10 muM) which protects the adenosine from binding or destruction by the tissues, or with both combined failed to alter the VFT significantly. Furthermore neither adenosine nor dipyridamole significantly altered the effect of anoxia on the VFT. 4. Anoxia, adenosine and dipyridamole significantly increased the duration of the induced arrhythmia when compared with that of the controls. 5. Anoxia and adenosine significantly shortened the vulnerable time, i.e., the minimal time after the R-wave of the ECG at which the pulse had to be applied to induce the arrhythmia. 6. Perfusion with the McEwen's solution gassed with 5% CO2 in air (hypoxia) significantly lowered the VFT but the effect was not as great as with anoxia. Isoprenaline when infused lowered the VFT but this effect was not potentiated by hypoxia. 7. The results indicate that (a) anoxia lowers the VFT in the perfused isolated heart of the rabbit and that this effect is not due to adenosine or noradrenaline released by the anoxia and (b) hypoxia does not sensitize the heart to the arrhythmic effect of isoprenaline.

Adenosine↗
PubMed1968

Restoration of the chronotropic effect of tyramine on rat atria after reserpine.

1. The restoration by various sympathomimetic amines of the chronotropic response to tyramine was studied on the isolated atria of rats pretreated with reserpine. The atria were exposed to the "restorative" sympathomimetic amine for 10 min, washed over a period of 1 hr and then tested with 10 muM tyramine. The effect of noradrenaline, dopamine and norphenylephrine before and after inhibition of monoamine oxidase by 0.5 mM iproniazid were compared with their alpha-methyl and N-alkyl analogues in their ability to restore the chronotropic response to tyramine.2. Noradrenaline and adrenaline restored the chronotropic response to tyramine, the degree of restoration depending on the concentration of the restorative amine used. Noradrenaline after iproniazid and alpha-methylnoradrenaline were equipotent and were about 1,000 times more active than noradrenaline where monoamine oxidase was not inhibited. Dopamine, epinine, norphenylephrine, phenylephrine, octopamine, synephrine and isoprenaline in the absence of monoamine oxidase inhibition had no effect. Dopamine after iproniazid and alpha-methyldopamine were equipotent and were about 1/10 as active as alpha-methylnoradrenaline. Norphenylephrine after iproniazid and metaraminol were equipotent and were about 1/500 as active as alpha-methylnoradrenaline. Octopamine after iproniazid was even less active. The N-methylated analogues were about 1/10 as active as their nor-compounds but the N-isopropyl analogue, isoprenaline, was devoid of activity.3. Dopamine after iproniazid and alpha-methyldopamine were inactive if a dopamine-beta-hydroxylase inhibitor, disulphiram or sodium diethyldithiocarbamate, was present.4. It is concluded that, in atria of reserpinized rats, (a) protection from monoamine oxidase increases; (b) N-substitution decreases; and (c) hydroxyl groups at the beta-carbon and ring positions 3 and 4 increase the capabilities of a sympathomimetic amine to restore the chronotropic response to tyramine.

Animals↗