The effect of lignocaine on myocardial function, high energy phosphate stores, and oxygen consumption: A comparison with propranolol

Nayler, Winifred G.; McInnes, Iain B.; Carson, Valerie; Stone, J A; Lowe, T. E.

doi:10.1016/0002-8703(69)90041-6

Cited by 18 publications

(8 citation statements)

References 17 publications

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“…The effect of tocainide on ventricular function when severely depressed function is present at rest or when higher drug doses are used is, therefore, still unknown. Thus the effects of tocainide on cardiac performance resemble those of lignocaine, which in large doses in experimental animals produces myocardial depression (Austen and Moran, 1965;Nayler et al, 1969;Asokan et al, 1968) but in conventional doses in man is devoid of significant cardiovascular effects (Harrison et al, 1963;Grossman et al, 1969;Rahimtoola et al, 1971). Tocainide, however, has a major advantage that lignocaine does not have: it can be administered orally.…”

Section: Discussionmentioning

confidence: 99%

Effects of tocainide on left ventricular performance at rest and during acute alterations in heart rate and systemic arterial pressure. An echocardiographic study.

Ryan¹,

Karliner²

1979

Heart

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SUMMARY To determine if the new antiarrhytbmic agent tocainide depresses left ventricular function we performed a double-blind cross-over trial of tocainide and placebo in 10 patients with valvular heart disease and recorded echocardiograms (a) in the basal state, (b) during atropine-induced increases in heart rate, and (c) during acute pressure loading with phenylephrine. The drug doses were 400 mg every 8 hours for 3 days, and the mean tocainide plasma concentration in the tocainide group was 5-3 ,ug/ml.Except after atropine when there was a slightly higher mean systolic blood pressure in the tocainide group than in the placebo group (mean blood pressure difference 7 mmHg, P < 0.02) heart rates and systolic blood pressures for both groups were closely matched during these pharmacological interventions. For the placebo and tocainide groups mean heart rates increased after atropine by 27 and 26 beats/minute, respectively, and during infusion of phenylephrine (when no significant heart rate slowing occurred) mean blood pressures rose by 51 nmmHg in the placebo group (to 175 + 6 mmHg) and by 45 mmHg in the tocainide group (to 176 ± 6 mmHg). During tocainide administration mean velocity of circumferential fibre shortening (mean VCF) in the basal state averaged 1-29 4 0-06 diam/s. This increased to 1-39 ± 0-08 diam/s with atropine (NS) and then declined to 1-17 ± 0 09 diam/s during infusion of phenylephrine (P < 0 01 vs atropine). No significant differences were found when the corresponding values during placebo were compared with these values. Similar directional changes occurred in the average mean posterior wall velocity (mean VPW) during tocainide administration when the corresponding values were 0 75 + 0.05, 0-87 ± 0 07 (P < 0.05), and 0-71 ± 0 05 (P < 0 01 vs atropine) s-1, respectively. Again placebo values did not differ significantly from tocainide values.Thus, in patients with valvular heart disease tocainide in the dose employed has no significant depressant effect on left ventricular function either in the basal state or during acute alterations in heart rate or blood pressure. These data suggest that tocainide can be used safely for antiarrhythmic therapy in patients with mild to moderate left ventricular dysfunction.Recent reports of animal (Duce et al., 1973; Coltart in anaesthetised dogs have been shown to depress et al., 1974) and human studies (McDevitt et al., left ventricular function (Coltart et al., 1974Winkle et al., 1976;Woosley et al., 1977; determine whether tocainide similarly depresses Ryan et al., 1978) indicate that an oral analogue myocardial function in man we administered typical of lignocaine, tocainide, is effective in suppressing therapeutic doses of the drug to patients with ventricular arrhythmias and is a promising new anti-organic heart disease, and using ultrasound assessed arrhythmic agent. However, high doses of tocainide left ventricular function at rest and during acute alterations in heart rate and systemic arterial

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Section: Discussionmentioning

confidence: 99%

Effects of tocainide on left ventricular performance at rest and during acute alterations in heart rate and systemic arterial pressure. An echocardiographic study.

Ryan¹,

Karliner²

1979

Heart

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Section: Inotropic and Chronotropic Effects Of Glucagon In Animal Heartsmentioning

confidence: 99%

“…In early work on paced canine papillary muscles, glucagon starting at 0.25 μM exerted a positive inotropic effect [ 33 ]. This effect was attenuated by Mn 2+ , suggesting an inhibition of the currents through the LTCC ([ 33 ], compare Section 9 ). In parallel, glucagon increased the transport rate of Ca 2+ into canine cardiac microsomes [ 33 ], suggesting that glucagon via cAMP increases and the phosphorylation of phospholamban increases the pumping rate of SERCA ( Figure 1 ).…”

Section: Inotropic and Chronotropic Effects Of Glucagon In Animal Heartsmentioning

confidence: 99%

Glucagon and Its Receptors in the Mammalian Heart

Neumann

Hofmann

Dhein

et al. 2023

IJMS

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Glucagon exerts effects on the mammalian heart. These effects include alterations in the force of contraction, beating rate, and changes in the cardiac conduction system axis. The cardiac effects of glucagon vary according to species, region, age, and concomitant disease. Depending on the species and region studied, the contractile effects of glucagon can be robust, modest, or even absent. Glucagon is detected in the mammalian heart and might act with an autocrine or paracrine effect on the cardiac glucagon receptors. The glucagon levels in the blood and glucagon receptor levels in the heart can change with disease or simultaneous drug application. Glucagon might signal via the glucagon receptors but, albeit less potently, glucagon might also signal via glucagon-like-peptide-1-receptors (GLP1-receptors). Glucagon receptors signal in a species- and region-dependent fashion. Small molecules or antibodies act as antagonists to glucagon receptors, which may become an additional treatment option for diabetes mellitus. Hence, a novel review of the role of glucagon and the glucagon receptors in the mammalian heart, with an eye on the mouse and human heart, appears relevant. Mouse hearts are addressed here because they can be easily genetically modified to generate mice that may serve as models for better studying the human glucagon receptor.

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“…IDOCAINE has both direct depressant and indirect L stimulant cardiovascular effects (1,2). Although subseizure doses of lidocaine have a direct myocardial depressant effect, this effect can be counterbalanced by increased sympathetic activity.…”

mentioning

confidence: 99%

Lidocaine‐induced hemodynamic effects are enhanced by the inhibition of endothelium‐derived relaxing factor in dogs

Toyoyama

Yukioka

Hayashi

et al. 1997

Acta Anaesthesiol Scand

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The effect of lignocaine on myocardial function, high energy phosphate stores, and oxygen consumption: A comparison with propranolol

Cited by 18 publications

References 17 publications

Effects of tocainide on left ventricular performance at rest and during acute alterations in heart rate and systemic arterial pressure. An echocardiographic study.

Effects of tocainide on left ventricular performance at rest and during acute alterations in heart rate and systemic arterial pressure. An echocardiographic study.

Glucagon and Its Receptors in the Mammalian Heart

Lidocaine‐induced hemodynamic effects are enhanced by the inhibition of endothelium‐derived relaxing factor in dogs

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