Effects of anesthetics on the incidence and duration of reperfusion arrhythmias in isolated rat heart

The present study was carried out to evaluate the effect of anesthetics on reperfusion arrhythmias. Male Wistar rats (200-300 g) were injected ip with heparin (200 IU), followed by anesthesia with thiopental (40 mg/kg), pentobarbital (30 mg/kg), urethane (1.2 g/kg), either, or halothane and sacrificed by decapitation. The isolated heart (5 to 8 per group) was perfused with Locke solution by the Langendorff method and the left coronary artery was ligated for 10 min. The incidence of reperfusion arrhythmias (100 per cent ) was similar in hearts of control and previously anesthetized rats, but the duration of the arrhythmias was significantly increased by anesthesia (5-fold with thiopental, 15-fold with pentobarbital, ether and halothane, and 30-fold with urethane). In hearts taken from unanesthetized rats and perfused with Locke solution containing anesthetics (5-7 per group), the duration of reperfusion arrhythmias decreased with thiopental (0.23 +/- 0.15 min), did not change with pentobarbital (1.14 +/- 0.26 min) and increased with urethane (16.10 +/- 5.60 min). Our results show that anesthetics alter the duration of reperfusion arrhythmias in the isolated rat heart

Effect of scorpion toxin on the enterochromaffin-like cells in normal and trypanosoma cruzi-infected rats: a morphological study

A injeçäo intravenosa de toxina escorpiônica ( Tityus serrulatus) en ratos normais e infectados pelo Trypanosoma cruzi näo causou alteraçöes morfológicas ultra-estruturais das células enterocromafins-like (ECL) do estômago, embora tenha induzido a aumento significativo da secreçäo do suco gástrico

Gastric acetylcholine and histamine content of normal and Trypanosoma cruzi - infected rats

The consequences of acute Trypanosoma cruzi infection for acetylcholine and histamine levels in gastric wall and for mast cells of the stomach were studied in rats. Intraperitoneal infection with 4,000 trypomastigotes/g of a Y strain of Trypanosoma cruzi led to a 4-fold decrease in gastric acetylcholine level and to a 57 - and 15-fold increase in histamine content in the membranous and glandular regions of the rat stomach, respectively. Infection of rats with Trypanosoma cruzi also induced a 2- and 4-fold increase in mast cell numbers in the membranous and glandular regions of the muscle layer of the gastric wall, respectively, and a ganglionic inflammatory reaction with predominance of mononuclear cells. We conclude that in acutely Trypanosoma cruzi-infected rats, the reduction of acetylcholine content is due to gastric denervation and that the histamine increase might be secondary to gastric denervation and/or to an increase in the number of mast cells of the gastric wall

Oscillations of cardiac rate induced by acetylcholine in the isolated guinea pig heart

1. The effects of acetylcholine (ACh) on cardiac rate (electrocardiogram), contractile force and coronary flow recorded simultaneously were investigated in isolated guinea pig hearts perfused with Locke solution by the method of Langendorff. 2. Bolus injections of 0.5-550 nmol ACh induced oscillations of cardiac rate. These changes were not directly related to the doses of ACh injected (X**2 test, P > 0.05). 3. The presence of 10 micronM physostigmine in the Locke solution increased the number of heart rate oscillations elicited by ACh. 4. The electrocardiogram showed that the heart rate oscillations were due to wandering pacemakers, such as slow or fast junctional rhythm, and slow or fast indioventricular rhythmy, which were intermingled with sinus rhythym, A - V block or sinus bradycardia. 5. In most experiments, the increase in ventricular rate was associated with an increase in ventricular contractile force ("Bowditch Effect") and a simultaneous reduction of coronary flow. 6. The heart rate oscillations were not prevented bu reserpine or blockade of nicotinic receptors (hexamethonium plus gallamine) but were prevented blockade of muscarinic receptors with atropine. 7. We conclude that the heart rate oscillations induced by ACh are due to several electrophysiological mechanisms (automatism and/or conduction disturbances_ related to activation of muscarinic receptors