Effect of nicotine administration on physical and psychological signs of withdrawal syndrome induced by single or repeated doses of morphine in rat

Background and purpose: Morphine addiction and morphine withdrawal syndrome are of main problems in human societies. In the present study, effect of nicotine on the strength of physical and psychological dependency, produced by single and repeated doses of morphine, was investigated

Material and method: Male wistar rats were dependent to morphine with single and repeated dose protocols. In the single dose protocol, rats received only one dose of morphine and 24h later were given Naloxone. In the repeated dose protocol, rats received incremental doses of morphine for 7 days and 24h after the last dose [8th day] were given Naloxone. In the single dose protocol, rats were given one dose of nicotine 30 min before Naloxone. However in the repeated doses they received nicotine 15 min before morphine for 4 days from 4th day to 7th day. 5 min after Naloxone each rat?s behavior was captured for 30 min. then physical and psychological signs of withdrawal syndrome were recorded

Results: Results showed that injection of repeated and even single dose of morphine can produce dependency. Nicotine consumption attenuated strength of withdrawal syndrome signs, specially increasing weight excrement and total withdrawal score in single dose protocol and weight excrement increasing, weight decreasing, place aversion, and total withdrawal score in repeated dose treatment

Conclusion: Based on our data, even a single dose of morphine can produce dependency in rats. Conversely, Nicotine consumption attenuates strength of withdrawal syndrome signs

effect of repeated diazepam administration on myocardial function in the ischemia-reperfused isolated rat heart

To evaluate whether repeated diazepam administration affects the heart in ischemia- reperfusion. This study was performed at the Medical Biology Research Center, Kermanshah, Iran, from March to September 2008. Four groups of rats were subjected to a daily injection of diazepam [group 1 [0.5 mg/kg for 21 days], group II [2.5 mg/kg for 5 days], and group III [5 mg/kg for 5 days] intraperitoneally], and saline solution [21 days] in the control groups. Isolated, perfused hearts were subjected to 40 minutes global ischemia, and 45 minutes reperfusion. The left ventricular developed pressure [LVDP], heart rate, and coronary flow were measured. Rate pressure product [RPP] was calculated. In reperfusion, released lactate dehydrogenase [LDH] enzyme in effluent was measured. It was observed that the recovery of the RPP and LVDP in reperfusion significantly decreased in the test group III [n=9] in comparison to the control [n=8]. During the reperfusion period, the released LDH significantly increased in test group II [n=8] and group III in comparison with the control. The results show that repeated administration of diazepam [5 mg/kg for 5 days] reduced the cardiac performance in reperfusion, and significantly exacerbated the ischemia-reperfusion injury. It is probably mediated by the changing of cardiac susceptibility in ischemia due to repeated administration of diazepam

Vitamin E derivative alpha-tocotrienol failed to show neuroprotective effects after embolic stroke in rats

Previous studies have demonstrated that pretreatment with alpha-tocotrienol [a-TCT] can reduce ischemic damage in mice following middle cerebral artery [MCA] occlusion. It is also reported to decrease stroke dependent brain tissue damage in 12-Lox-deficient mice and spontaneously hypertensive rats. In the present study, the neuroprotective effects of a-TCT and rosiglitazone [RGZ] at 3 hr after cerebral ischemia were investigated. Stroke was induced by embolizing a preformed clot into the MCA. Rats were assigned to vehicle, a-TCT [1 or 10 mg/kg], RGZ and sham-operation. Compared to the control group, only RGZ decreased infarct volume [P<0.05], neurological deficits [P<0.05] and sensory impairments [P<0.01] but low and high doses of a-TCT did not show any significant neuroprotective effect. Our data showed that a-TCT was not neuroprotective at 3 hr after the embolic model of stroke. Further studies should be undertaken to clarify the neuroprotective effects of a-TCT after stroke