The effects of i.v. prostaglandins (PGs) E2 and I2 on ouabain-induced cardiac arrhythmias were investigated in chloralose-anaesthetized cats. Bilateral vagotomy and guanethidine-pretreatment interventions were employed to elucidate the involvement of vagal and sympathetic neural influences in these effects. PGE2 (1 micrograms/kg/min i.v. infusion for 5 min) and PGI2 (4-16 microgram/kg i.v. bolus injections) effectively suppressed the ouabain-induced arrhythmias in a control group of cats. The bilateral vagotomy or guanethidine-pretreatment interventions did not significantly alter the antiarrhythmic effects of PGE2 and PGI2. It is concluded that the presence of functionally intact sympathetic and vagal nerve supply to the heart is not a prerequisite for the antiarrhythmic effects of i.v. administered PGE2 and PGI2. The possible role of direct action of these PGs on the myocardium is discussed.

Anesthesia↗

PubMedDate not supplied

Contrastive effects of prostaglandin F2 alpha on normal cardiac rhythm and ouabain-induced cardiac arrhythmias in cats: possible neural basis.

The effects of prostaglandin F2 alpha (PGF2 alpha) on normal cardiac rhythm and ouabain-induced cardiac arrhythmias were investigated in chloralose-anaesthetized cats. PGF2 alpha (1-16 micrograms/kg i.v. bolus) produced ventricular arrhythmias and few incidences of AV conduction disturbances in normal cats. Changes in heart rate and blood pressure caused by PGF2 alpha in normal cats were complex, namely a decrease, an increase, or an initial decrease followed by an increase. Bilateral vagotomy antagonized the ventricular arrhythmias, AV conduction disturbances and hemodynamic changes produced by 16 micrograms/kg i.v. PGF2 alpha. On the other hand, atropine (2 mg/kg i.v.) pretreatment blocked the AV conduction disturbances and the reduction in heart rate and blood pressure, but not the ventricular arrhythmias or the increase in heart rate and blood pressure caused by 16 micrograms/kg i.v. PGF2 alpha. The ventricular arrhythmogenic effect of PGF2 alpha was prevented by propranolol (1 mg/kg i.v.). Intervention with cardiotoxic doses of ouabain augmented the PGF2 alpha-induced AV conduction disturbances, sinus bradycardia and hypotension, and attenuated the ventricular arrhythmias. Subsequent bilateral vagotomy prevented the ouabain-potentiated PGF2 alpha-induced AV block and sinus bradycardia, attenuated the hypotension and further reduced the ventricular arrhythmias. PGF2 alpha (2-16 micrograms/kg i.v.), contrary to its arrhythmogenic effect in normal cats, mainly suppressed ouabain-induced ventricular and supraventricular arrhythmias in ouabain-intoxicated cats, but aggravated the same in few cats. PGF2 alpha (16 micrograms/kg), prior to ouabain administration, produced ventricular arrhythmias in a group of 8 cats and later, in the same group of animals, when tested on ouabain-induced arrhythmias, it mainly antagonized them. These results suggest that PGF2 alpha evokes an arrhythmogenic effect on cardiac rhythm of normal hearts and mainly an antiarrhythmic effect on ouabain-induced arrhythmias largely through the mediation of two functionally opposing excitatory and inhibitory autonomic neural reflex pathways, respectively. The afferents of these pathways are of vagal origin. The efferent pathways of the inhibitory and excitatory reflexes involve in part increased vagal activity and increased sympathetic activity to the heart, respectively. Alteration by ouabain of the arrhythmogenic nature of PGF2 alpha on normal heart to its antiarrhythmic effect on the arrhythmic heart may be due to its selective potentiating effect on the inhibitory reflex pathway.

Anesthesia↗

PubMedDate not supplied

Snake bite and its treatment.

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Adrenal Cortex Hormones↗

PubMedDate not supplied

Some aspects of pharmacological profile of sodium curcuminate.

Rapid i.v. injection of sodium curcuminate (NaC) produced transient hypotension and bradycardia in anaesthetized dogs and cats which were not blocked by bilateral vagotomy, atropine, mepyramine or propranolol. In open-chest anaesthetized cats, decrease in blood pressure and heart rate was accompanied by simultaneous transient reductions in left ventricular systolic pressure, maximal rate of rise of left ventricular pressure and a concomitant increase in left ventricular end-diastolic pressure. It was concluded that the transient hypotensive effect of NaC is due to its myocardial depressant action. NaC exhibited negative inotropic and chronotropic effect on isolated perfused rabbit heart, an antispasmodic effect on smooth muscle of dog s intestine in vivo and of vas deferens of guinea-pig in vitro but no effect on the rectus abdominis muscle of frog or its response to cholinergic stimulation.

Animals↗

PubMedDate not supplied

Poison information services.

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Humans↗

PubMedDate not supplied

Changes in circulatory biogenic amines during head-up tilt testing in neurocardiogenic syncope.

The pathogenesis of neurocardiogenic syncope is not completely understood. To examine the possible role of biogenic amines in patients with neurocardiogenic syncope, 18 consecutive patients (age 30 +/- 13 years, 15 males, 3 females) of unexplained syncope were subjected to Head-Up Tilt Testing (HUTT). Blood was sampled by an indwelling cannula at baseline, end of tilt test (or at syncope) and 1 min after returning to the supine position. Biogenic amines, epinephrine (E), norepinephrine (NE), serotonin (5-HT) and their metabolites, homovanillic acid (HVA) and 5-hydroxy indole acetic acid (5-HIAA), were measured in the serum after serial organic phase extraction by high-performance liquid chromatography (HPLC) using ultraviolet detection at a wavelength of 280 nm. Twelve patients were found to be HUTT negative while 6 patients were HUTT positive. Baseline E, NE and 5-HT levels were significantly greater in the HUTT positive patients [E 510 +/- 154 versus 302 +/- 96 pg/ml (p < 0.01), NE 253 +/- 99 versus 159 +/- 62 pg/ml (p < 0.05), 5-HT 174 +/- 32 versus 118 +/- 22 pg/ml (p < 0.01)]. E and HVA levels at the end of the test were significantly higher in HUTT positive patients [E 788 +/- 268 versus 465 +/- 119 pg/ml (p < 0.01), HVA 308 +/- 91 versus 112 +/- 12 pg/ml (p < 0.001)]. A significantly greater rise of E from the baseline was observed in HUTT positive patients (510 +/- 154 versus 112 +/- 12 pg/ml (p < 0.01)]. The increase in the levels of E and HVA both at baseline and after the tilt test, without a corresponding rise in NE levels indicates enhanced activity of the adrenomedullary axis which is not paralleled by NE release from sympathetic nerve endings in patients of neurocardiogenic syncope.

Adolescent↗