Effects of acute administration of ethanol on experimental arrhythmia.

Many studies have shown that the relationship between alcohol consumption and most cardiovascular diseases is U-shaped, with nondrinkers and heavier drinkers having higher risks than moderate drinkers. However, the association between cardiac arrhythmias and acute alcohol consumption is not well understood. We set up several experimental arrhythmia animal models to examine the effects of acute administration of ethanol on arrhythmia. The results showed 0.4, 0.8 and 1.6 g/kg ethanol consumption obviously delayed the onset time of atrial fibrillation (AF) (P < 0.05 or P < 0.01) and increased the survival rates on acetylcholine-CaCl2-induced AF in mice. Ethanol (0.4, 0.8 and 1.6 g/kg) consumption significantly delayed the onset time of ventricular tachycardia (VT), ventricular fibrillation (VF) and cardiac arrest (CA) (P < 0.01), and 0.4 and 0.8 g/kg ethanol consumption increased the survival rates on CaCl2-induced arrhythmia in rats. Ethanol (0.4 g/kg) essentially increased the cumulative dosage of aconitine required to CA (P < 0.05), and 0.8 g/kg, 1.6 g/kg ethanol reduced the cumulative aconitine dosage to induce VT, VF and CA (P < 0.05 or P < 0.01) on aconitine-induced arrhythmia in rats. Ethanol (0.4, 0.8 and 1.6 g/kg) consumption remarkably increased the cumulative dosage of deslanoside to induce ventricualr premature contraction (P < 0.01) on deslanoside-induced arrhythmia in guinea pigs. Collectively, our results indicate that low concentrations of ethanol had anti-arrhythmic effect on experimental arrhythmia, and high concentrations of ethanol may aggravated the occurrence of experimental arrhythmia.

[Effects of heroin exposure on the expression of caspase 3 in prefrontal lobe cortex, hippocampus and nucleus accumbens].

AIM: To investigate the expression of caspase 3 in the brain regions related to addiction, learning and memory in mice prenatally exposed to heroin and to ascertain whether postnatal apoptotic mechanism participates in neurobehavioral teratogenicity induced by maternal heroin abuse. METHODS: A mouse model was established by administration of diacetylmorphine (heroin, purity 98.5%, product ID No.171206-200614) 10 mg/(kg x d) subcutaneously to pregnant BALB/c mice on embryonic day (E)E8-E18. The offspring were divided into heroin(Her) and saline(Sal) groups according to the maternal treatment. The expression of caspase 3 in prefrontal lobe cortex(PFC), hippocampus(HP) and nucleus accumbens(Acb) was detected by RT-PCR and Western blot on mouse postnatal day(P)14. RESULTS: The mRNA and protein expression of caspase 3 were significantly increased in the areas of PFC, HP and Acb in Her group compared with Sal group(P < 0.05). CONCLUSION: E8-E18 prenatal exposure to heroin can induce apoptosis through caspase 3 activation in brain regions related to addiction, learning and memory, which indicates that apoptotic mechanism may be involved in neurobehavioral teratogenicity by heroin exposure in uterus.

Effects of motilin and ursodeoxycholic acid on gastrointestinal myoelectric activity of different origins in fasted rats.

AIM: To investigate gastrointestinal migrating myoelectric complex (MMC) and the effects of porcine motilin and ursodeoxycholic acid (UDCA) on MMC of gastrointestinal tract of different origins in fasted rats. METHODS: Three bipolar silver electrodes were chronically implanted on the antrum, duodenum and jejunum. Seven days later 24 experimental rats were divided into 2 groups. One group was injected with porcine motilin via sublingual vein at a dose of 20 microg/kg, the other group was perfused into stomach with UDCA. The gastrointestinal myoelectric activity was recorded 1 h before and 2 h after the test substance infusions into the rats. RESULTS: In all fasted rats a typical pattern of MMC was observed. Among the totally 68 activity fronts recorded in fasted rats under control, 67% started in duodenum, and 33% in antrum. MMC cycle duration and duration of phase III of antral origin were longer than those of duodenal origin. Administration of 20 microg/kg porcine motilin induced a premature antral phase III of antral origin. But perfusion into stomach with UDCA resulted in shorter MMC cycle duration, longer duration of phase III of duodenal origin, which were followed with shorter cycle duration and duration of antral phase III. CONCLUSION: In fasted rats, MMC could originate from antrum and duodenum respectively. The characteristics of MMC of different origins may contribute to the large variations within subjects. The mechanisms of different origins of phase III may be different. Porcine motilin and UDCA could affect MMC of different origins of the gastrointestinal tract in fasted state, respectively.

Morphological and electrophysiological study on the inferior nodal extension and transitional cellular band in the rabbit atrioventricular junctional area.

BACKGROUND: Advances in catheter ablation procedures for the treatment of supraventricular arrhythmias have created the need to understand better the morphological and electrophysiological characteristics of the inferior nodal extension (INE) and transitional cellular band (TCB) in the atrioventricular (AV) junctional area. METHODS: Firstly, we observed the histological features of 10 rabbit AV junctional areas by serial sections under light microscopy. Then we recorded the action potentials (APs) of transitional cells (TCs) in the INE, TCBs, AV node, and ordinary right atrial myocytes from the AV junctional area of 30 rabbits using standard intracellular microeletrode techniques. RESULTS: Under light microscopy, the INE appeared to be mostly composed of transitional cells linking upward to the AV node. Four smaller TCBs originated in the orifice of the coronary sinus, the region between the septal leaflet of the tricuspid valve and the coronary sinus, the inferior wall of the left atrium, and the superior interatrial septum, respectively, all linking to the INE or the AV node. Compared with ordinary atrial myocytes, the AP of the TCs in both the INE and the TCBs had a spontaneous phase 4 depolarization (not present in ordinary atrial myocytes), with a less negative maximum diastolic potential, a smaller amplitude, a slower maximum velocity of AP upstroke, and a longer action potential duration at 50% repolarization (APD50) and at 30% repolarization (APD30). The AP characteristics of these TCs were similar to those of the AV node, except that the velocities of the phase 4 spontaneous depolarization were slower and their action potential durations at 90% repolarization (APD90) were shorter. Moreover, APD50 and APD30 of the TCs of the TCBs were shorter than in the case of TCs of the AV node. CONCLUSIONS: The TCs of the INE and TCBs are similar to slow response automatic cells. They provide a substrate for slow pathway conduction. In addition, repolarization heterogeneity exists in the AV junctional area.

Effects of neurotrophins on gastrointestinal myoelectric activities of rats.

AIM: To observe the effects of mouse nerve growth factor (NGF), rat recombinant brain derived neurotrophic factor (rm-BDNF) and recombinant human neurotrophin-3 (rh-NT-3) on the gastrointestinal motility and the migrating myoelectric complex (MMC) in rat. METHODS: A randomized, double-blinded, placebo-controlled experiment was performed. 5-7 days after we chronically implanted four or five bipolar silver electrodes on the stomach, duodenum, jejunum and colon, 21 experimental rats were coded and divided into 3 groups and injected NGF, rm-BDNF, rh-NT-3 or placebo respectively via tail vein at a dose of 20 microg x kg(-1). The gastrointestinal myoelectrical activity was recorded 2 hours before and after the test substance infusions in these consciously fasting rats. RESULTS: The neurotrophins-induced pattern of activity was characterized by enhanced spiking activity of different amplitudes at all recording sites, especially in the colon. In the gastric antrum and intestine, only rh-NT-3 had increased effects on the demographic characteristics of electrical activities (P<0.05), but did not affect the intervals of MMCs. In the colon, all the three kinds of neurotrophins could significantly increase the frequency, amplitude and duration levels of spike bursts, and also rh-NT-3 could prolong the intervals of MMC in the transverse colon (25+/-11 min vs 19+/-6 min, P<0.05). In the distal colon rh-NT-3 could evoke phase III-like activity and disrupt the MMC pattern, which was replaced by a continuously long spike bursts (LSB) and irregular spike activity (ISA) for 48+/-6 min. CONCLUSION: Exogenous neurotrophic factors can stimulate gut myoelectric activities in rats.