Termination of digitalis‐induced ventricular tachycardias by clonidine involves central α<sub>2</sub>‐adrenoceptors in cats

Chen, Shih‐Ann; Liu, Ren-Hon; Ting, Tso-Hui; Chang, Mau‐Song; Chiang, Benjamin N.; Kuo, Jon‐Son

doi:10.1111/j.1476-5381.1991.tb12309.x

Cited by 10 publications

(9 citation statements)

References 6 publications

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“…To assess the sensitivity of blink reflex control mechanisms to pharmacological manipulation, the noradrenergic α 2 agonist clonidine (5 µg/kg) and the α 2 antagonist yohimbine (0.5 mg/kg) were administered by intraperitoneal injection 30 min prior to testing (Hilakivi 1983;Chen et al 1991). Control injections of vehicle solutions were not tested because they did not alter blink parameters in pilot studies and risked injury to intraperitoneal structures.…”

Section: Data Collectionmentioning

confidence: 99%

“…Systemically administered adrenergic agents were used in an attempt to enhance potential differences in the control and modulation of R1 and R2. Alpha-adrenergic agents were chosen because of their substantial effects on motor systems (Barbeau et al 1993;Morgan et al 1993) and the availability of an agonist and antagonist that cross the blood-brain barrier (Chen et al 1991). …”

Section: Introductionmentioning

confidence: 99%

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Blink reflex to supraorbital nerve stimulation in the cat

LeDoux¹,

Lorden

Weir

et al. 1997

Exp Brain Res

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Neurophysiological studies of the blink reflex to supraorbital nerve stimulation were conducted in eight alert, adult male cats. The cat, like other mammals, shows both short-latency (R1) and long-latency (R2) orbicularis oculi electromyographic (OOemg) components. Measures of OOemg latency, duration, integrated area, and maximum amplitude (MA) were obtained at a stimulus magnitude of 1.5xR2 threshold. The mean (+/-SE) minimal latencies for R1 and R2 were 8.26+/-0.85 and 22.97+/-1.53 ms, respectively. On average, R1 MA was larger than R2 MA. R1 and R2 area measures were similar. Three stimulus paradigms were tested. In a paired-stimulus paradigm, the interstimulus interval (ISI) was randomly varied from 100 to 1200 ms. Ratios were constructed for the OOemg area and MA by dividing the test response by the conditioning response. In this paradigm, although a significant linear relationship was observed only between ISI and R2 MA, conditioning effects were noted on both R1 and R2 area and MA test responses at several ISIs. In a habituation paradigm, both R2 and R1 showed habituation at stimulus frequencies from 0.5 to 2 Hz. In a stimulus-response paradigm, stimulus magnitude was randomly varied between threshold and 2xthreshold. In this paradigm, OOemg area and MA of both R1 and R2 were linearly related to stimulus magnitude. Neither the systemically administered centrally acting alpha2-adrenergic antagonist yohimbine nor agonist clonidine had significant effects on blink reflex parameters, habituation, or the paired-stimulus paradigm. Overall, these results suggest that there are important similarities in the control and modulation of the R1 and R2 components of the blink reflex to supraorbital nerve stimulation in cats.

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Section: Data Collectionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Blink reflex to supraorbital nerve stimulation in the cat

LeDoux¹,

Lorden

Weir

et al. 1997

Exp Brain Res

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“…Several previous reports have shown that the central nervous system (CNS) affects the genesis of different types of arrhythmias including this type (Waxman et al, 1989;Podrid et al, 1990;Chen et al, 1991;Hayashi et al, 1991a,c). Recently, we demonstrated that an a2-adrenoceptor agonist dexmedetomidine, which has a weak affinity for imidazoline receptors (Wikberg & Uhlen, 1990;Wikberg et al, 1991), inhibits adrenaline-induced arrhythmia under halothane anaesthesia through its action on the CNS (Hayashi et al, 1991b).…”

Section: Introductionmentioning

confidence: 99%

Antiarrhythmic action of rilmenidine on adrenaline‐induced arrhythmia via central imidazoline receptors in halothane‐anaesthetized dogs

Mammoto

Kamibayashi

Hayashi

et al. 1996

British J Pharmacology

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To elucidate the role of central imidazoline receptors in the genesis of adrenaline‐induced arrhythmias under halothane anaesthesia, we investigated the effects of rilmenidine, a selective agonist at imidazoline receptors, on this type of arrhythmia in dogs. Rilmenidine (1, 3, 10 μg kg−1, i.v.) did not affect basal haemodynamic parameters (heart rate and blood pressure), but dose‐dependently inhibited adrenaline‐induced arrhythmias under halothane anaesthesia. Although, rilmenidine has a weak affinity for α2‐adrenoceptors, pretreatment with idazoxan (10 μg kg−1, intracistenally i.c.), an imidazoline receptor antagonist which has also α2‐adrenoceptor blocking potency, blocked the antiarrhythmic effect of rilmenidine (10 μg kg−1, i.v.). In contrast, pretreatment with rauwolscine (20 μg kg−1, i.c.), a classical α2‐adrenoceptor antagonist with little affinity for imidazoline receptors, did not affect the effect of rilmenidine (10 μg kg−1, i.v.). Furthermore, bilateral vagotomy completely blocked the antiarrhythmic action of rilmenidine (10 μg kg−1, i.v.). It is suggested that the antiarrhythmic action of rilmenidine is due to the activation of central imidazoline receptors and that vagal tone is critical for this action of rilmenidine.

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“…Moreover, the doses of strophanthidin required to induce ventricular tachycardia were not different in the guinea pigs pretreated with or without trilinolein. There are several possibilities to account for the results: (1) the effect of trilinolein on Ca 2+ inward current may be not strong enough to prevent Ca 2+ overload; in this study, unlike the Ca 2+ antagonists, treatment with trilinolein did not increase the risk of atrioventricular block in strophanthidin administration [17]; this result suggests that the Ca 2+ antagonist activity of trilinolein is relatively weak; (2) in the report of Shen and Hong [23], 0.01 or 0.1 Ìmol/l trilinolein would result in a significant increase in cytosolic Ca 2+ in human platelets; it is possible that the effects of different doses of trilinolein on different tissues or different experimental models vary widely; (3) this laboratory and other investigators found that termination of digitalis-induced ventricular tachycardia was also related to the inhibition of digitalis-induced enhanced sympathetic activity [18,24]. Although unpublished data [Chi and Su, pers.…”

Section: Effects Of Trilinolein On Strophanthidininduced Ventricular mentioning

confidence: 99%

“…Therefore, the ventricular tachycardia was maintained for at least 20 min to reduce the possibility of spontaneous termination of ventricular tachycardia [18].…”

Section: Drug Administrationmentioning

confidence: 99%

Effect of Trilinolein on Strophanthidin-Induced Ventricular Tachycardia in Guinea Pigs

Chen

Tai

et al. 1998

Pharmacology

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Trilinolein, a triacylglycerol with linoleic acid, was found to inhibit Ca²⁺ influx in cardiomyocytes. The purpose of this study was to evaluate the effects of trilinolein on ventricular arrhythmia induced by intravenous strophanthidin in guinea pigs anesthetized with intraperitoneal urethane. After strophanthidin- induced ventricular tachycardia, treatment with trilinolein (0.1, 1, 10 and 100 µg/kg) or control (0.04% propylene glycol) did not terminate ventricular tachycardia. However, 1, 10 and 100 µg/kg trilinolein could narrow the width of the QRS complex during ventricular tachycardia. Pretreatment with trilinolein before strophanthidin administration did not prevent the occurrence of ventricular tachycardia; the doses of strophanthidin required to induce arrhythmias (ventricular extrasystole and ventricular tachycardia) were similar in guinea pigs pretreated with trilinolein or control. However, there were fewer ventricular extrasystoles in guinea pigs pretreated with trilinolein than in the control group (ANOVA, p < 0.01). Moreover, the ventricular extrasystoles were fewer in guinea pigs pretreated with higher doses of trilinolein (100 µg/kg, 103 ± 60; 10 µg/kg, 188 ± 86) than lower doses of trilinolein (1 µg/kg, 366 ± 102; 0.1 µg/kg, 436 ± 145). This study demonstrated that trilinolein was not effective in terminating or preventing strophanthidin-induced ventricular tachycardia. However, trilinolein could improve ventricular depolarization and suppress ventricular extrasystoles.

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Termination of digitalis‐induced ventricular tachycardias by clonidine involves central α₂‐adrenoceptors in cats

Cited by 10 publications

References 6 publications

Blink reflex to supraorbital nerve stimulation in the cat

Blink reflex to supraorbital nerve stimulation in the cat

Antiarrhythmic action of rilmenidine on adrenaline‐induced arrhythmia via central imidazoline receptors in halothane‐anaesthetized dogs

Effect of Trilinolein on Strophanthidin-Induced Ventricular Tachycardia in Guinea Pigs

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Termination of digitalis‐induced ventricular tachycardias by clonidine involves central α2‐adrenoceptors in cats

Cited by 10 publications

References 6 publications

Blink reflex to supraorbital nerve stimulation in the cat

Blink reflex to supraorbital nerve stimulation in the cat

Antiarrhythmic action of rilmenidine on adrenaline‐induced arrhythmia via central imidazoline receptors in halothane‐anaesthetized dogs

Effect of Trilinolein on Strophanthidin-Induced Ventricular Tachycardia in Guinea Pigs

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Termination of digitalis‐induced ventricular tachycardias by clonidine involves central α₂‐adrenoceptors in cats