Effects of the administration of a catalase inhibitor into the fourth cerebral ventricle on cardiovascular responses in spontaneously hypertensive rats exposed to sidestream cigarette smoke

OBJECTIVE: Previous studies have demonstrated a relationship between brain oxidative stress and cardiovascular regulation. We evaluated the effects of central catalase inhibition on cardiovascular responses in spontaneously hypertensive rats exposed to sidestream cigarette smoke. METHODS: Male Wistar Kyoto (WKY) rats and spontaneously hypertensive rats (SH) (16 weeks old) were implanted with a stainless steel guide cannula leading into the fourth cerebral ventricle (4th V). The femoral artery and vein were cannulated for arterial pressure and heart rate measurement and drug infusion, respectively. The rats were exposed to sidestream cigarette smoke for 180 minutes/day, 5 days/week for 3 weeks (CO: 100-300 ppm). The baroreflex was tested using a pressor dose of phenylephrine (8 μg/kg, bolus) and a depressor dose of sodium nitroprusside (50 μg/kg, bolus). Cardiovascular responses were evaluated before and 5, 15, 30 and 60 minutes after injection of a catalase inhibitor (3-amino-1,2,4-triazole, 0.001 g/100 μL) into the 4th V. RESULTS: Vehicle administration into the 4th V did not affect the cardiovascular response, whereas administration of the central catalase inhibitor increased the basal HR and attenuated the bradycardic peak (p<0.05) to a greater extent in WKY rats exposed to sidestream cigarette smoke than in WKY rats exposed to fresh air. However, in spontaneously hypertensive rats, the effect of the catalase inhibitor treatment was stronger in the fresh air condition (p<0.05). CONCLUSION: Administration of a catalase inhibitor into the 4th V combined with exposure to sidestream cigarette smoke has a stronger effect in WKY rats than in SH rats. .

ATZ (3-amino-1,2,4-triazole) injected into the fourth cerebral ventricle influences the Bezold-Jarisch reflex in conscious rats

OBJECTIVES: Many studies have investigated the importance of oxidative stress on the cardiovascular system. In this study we evaluated the effects of central catalase inhibition on cardiopulmonary reflex in conscious Wistar rats. METHODS: Male Wistar rats were implanted with a stainless steel guide cannula in the fourth cerebral ventricle. The femoral artery and vein were cannulated for mean arterial pressure and heart rate measurement and for drug infusion, respectively. After basal mean arterial pressure and heart rate recordings, the cardiopulmonary reflex was tested with a dose of phenylbiguanide (PBG, 8 μg/kg, bolus). Cardiopulmonary reflex was evaluated before and μl15 minutes after 1.0 μl 3-amino-1,2,4-triazole (ATZ, 0.01g/100μl)0.01 g/100 μl) injection into the fourth cerebral ventricle. Vehicle treatment did not change cardiopulmonary reflex responses. RESULTS: Central ATZ significantly increased hypotensive responses without influencing the bradycardic reflex. CONCLUSION: ATZ injected into the fourth cerebral ventricle increases sympathetic inhibition but does not change the parasympathetic component of the cardiopulmonary reflex in conscious Wistar rats.

Brain biogenic amine levels after methanol administration: possible mechanism of action on central monoaminergic neurons in discrete areas of brain in Wistar rat.

Alterations in the steady state level of rat brain biogenic amines - dopamine, nor-epinephrine, epinephrine, serotonin and 5-hydroxy indole acetic acid, in response to intraperitoneal administration of methanol (3g/kg b.w.) were studied in discrete areas of the rat brain. The monoamine changes induced by methanol were quite different from those induced by ethanol consumption. They were also region-specific; hypothalamus being more vulnerable for methanol-induced monoamine changes. The effects produced by methanol were correlated with the blood and brain level of methanol at the given time, suggesting that the effects were dependent upon the local concentration of methanol in different brain regions. Acidosis induced by ammonium chloride and sodium formate administration did not alter the monoamine levels and therefore, the effects of methanol were not possibly due to acidosis. Blocking or delaying the metabolism of methanol either by 4-Methyl Pyrazole and 3-Amino 1,2,4-Triazole or by simultaneous administration of ethanol resulted in the potentiation of methanol effect. Therefore, it was concluded that methanol induced changes in brain biogenic amines were due to methanol per se and not due to metabolic end products viz. formaldehyde or formic acid.