Thermal stress causes oxidative stress and physiological changes in female rabbits.

The present study investigated the effects of heat stress on oxidative stress status and physiological changes using female New Zealand White rabbits. 24 sexually mature female rabbits weighing 1953.1-2375.4 g were divided into 4 groups of 6 animals each and subjected to ambient temperature (T0: 19-26 °C), 27-28 °C for T1, 31-32 °C for T2 and 35-36 °C for T3 using electrical heaters from 8:00 a.m. to 4:00 p.m. daily for 30 days. Feed intake and body weight gain were recorded daily. Behavioral alterations of anxiety, dizziness, aggression, withdrawal, impaired feed intake were observed. At the end of experimental period animals were sacrificed, blood samples and vital organs such as liver, kidney, heart, ovaries, uterus collected for appropriate analysis. Results revealed that animals of T2 and T3 had an 11% decrease in the final body weights and 62% body weight gain but increase in feed conversion ratio by 64.81%, 24.19% water intake, 3.64% in rectal and 2.42% in skin temperature compared to the control. Dizziness, withdrawal to a corner of the cage and reduced feed intake were observed. The live weight of lungs and kidneys increased by 37.71% and 33.78% while that of ovaries and uterus decreased in the same animals of T2 and T3. Animals from T2 and T3 showed significant decrease (p < 0.05) by 23.64% in hemoglobin concentration, 12.73% in red blood cells, 11.93% in packed cell volume, 12.02% in total protein while mean corpuscular volume, white blood cells, lymphocytes, creatinine, urea and aspartate transaminase increased respectively by 10.73%, 42.37%, 15.53%, 28.98%, 53.2% and 23.31% compared to the control. The kidney level of malondialdehyde was significantly increased in T2 and T3 animals by 74.29%, whereas protein, catalase, superoxide dismutase and glutathione peroxidase activity were significantly lower (p < 0.05) compared with control. It was concluded that long-term exposure of female rabbits to elevated ambient temperatures induces heat stress and accompanying oxidative stress that consequently impairs physiological function.

Effects of antiarrhythmic drugs (verapamil, propranolol and lignocaine) on the electrocardiogram and haematology in adrenaline-induced arrhythmias in dogs anaesthetized with halothane.

Twenty adult (1-3 year old) mongrel dogs of either sex were used to study the effects of antiarrhythmic drugs in adrenaline-induced arrhythmias. The dogs were divided randomly into four groups of five dogs each (n = 5), anaesthetized with halothane and pretreated intravenously (i.v.) with verapamil 0.1 mg kg-1, propranolol 0.06 mg kg-1, or lignocaine 4 mg kg-1 while the controls received sterile physiological saline. Adrenaline (4 micrograms kg-1) was administered i.v. 10 min after drug pretreatments. Lead II of the ECG was recorded and blood collected for haematology. Ventricular fibrillations preceded by ventricular tachycardia occurred in the control dogs and three died within one minute of adrenaline administration. The predominant arrhythmias were ventricular premature beats, ventricular tachycardia, and second degree heart block. A significant increase (P < 0.05) in T wave amplitude was observed in the control group from 0.16 +/- 0.05 mV to 0.43 +/- 0.09 mV while only minimal increases were noted in the drug pretreated groups and there were no deaths. Data obtained from this study suggest that verapamil when administered early compares well with propranolol in the control of adrenaline-induced ventricular arrhythmias in the dog. Lignocaine when administered early prior to the induction of the arrhythmias protected against death but not arrhythmias. Drug pretreatments did not have any clinically significant effects on electrocardiographic parameters.