High blood pressure is one of the symptoms of paraquat-induced toxicity in rats.

This study investigated whether paraquat (Pq)-induced lipidic peroxidation (LP) is accompanied by changes in blood pressure and heart rate (HR) in rats. Groups of adult male Wistar rats were studied 2 and 12 h after Pq (35 mg/kg, i.p.) administration. The LP was evaluated by monitoring thiobarbituric acid reactive substances (TBARS) in the kidneys, liver and lungs, and validated by including a group treated with an antioxidant, superoxide dismutase (CuZnSOD 50,000 IU/kg), in the study. The TBARS levels were significantly higher (p<0.05) in the kidneys of the rats studied 2 h after Pq than in their respective controls. Similarly, systolic and diastolic blood pressure (DBP) were higher (p<0.05), while HR was lower (p<0.05) than basal levels 2 and 12 h after Pq administration. In contrast, the group treated simultaneously with Pq and CuZnSOD exhibited lower levels of TBARS (p<0.05) in all studied organs compared to the control group, while the mean arterial pressure and HR did not differ from those seen in the control group. These findings indicate that acute Pq poisoning symptoms include high blood pressure.

Diuretic, natriuretic and kaliuretic effects of dexamethasone

1. Thrombus formation induced by electrical stimulation of the carotid artery was investigated in anesthetized rabbits and rats. Occlusive Grade III thrombi were produced consistently in 34 normal New Zealand rabbits and 58 untreated albino Wistar rats. Thrombus formation was monitored continuously in some of the animals with a magnetic flowmeter or a thermistor probe applied on the carotid. 2. The usefulness of the model for the screening of drugs was tested by treating the animals with warfarin, heparin, prostacyclin (PGI2), dihydroprostacyclin (DiHPGI2), prostaglendin E1 (PGE1), and prostaglandin D2(PGD2). 3. All of the drugs except warfarin were infused continuously into the venous circulation during the entire experimental period at a rat of 0.2 ml/min. 4. Warfarin (10 mg/Kg), administered by gavage 24 h before experimental, prevented thrombus formation, as did heparin iv (> 34 U/Kg). 5. Of the four platelet antiaggregatory prostaglandins tested, PGI2 was the most potent inhibitor of thrombus formation and DiHPGI2 the least active, as evaluated by visual inspection of stimulated arterial segments which were excised 30 min (rabbits) or 15 min (rats) after the stimulation was stopped. PGI2 was less active in rats than in rabbits (Threshold Protective Dose ratio ca. 4:1). PGE1 and PGD2 showed intermediate activity in both animal models