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In vitro toxicity of n-hexane and 2,5-hexanedione using isolated perfused rabbit heart is reported. The hearts were perfused using Langendorf's procedure and modified Anderson's coronary perfusion apparatus. The force of cardiac contraction was significantly reduced following 1 h perfusion with 9.6 mg/l concentration of n-hexane and with 0.35% v/v concentration of 2,5-hexanedione.

In-vitro toxicity of acetone using isolated rabbit heart is reported. The hearts were perfused using Langendorf's procedure and modified Anderson's coronary perfusion apparatus. Heart rate and force of contraction were recorded mechanically and the coronary flow was measured manually. The force of contraction was significantly reduced; heart rate and coronary flow were significantly increased with acetone concentrations of 0.5% and 1.0% V/V.

Recently, we have shown that chronic administration of N-Nitro-L-Arginine Methyl Ester (L-NAME, an inhibitor of nitric oxide synthase) precipitates stroke in stroke-prone spontaneously hypertensive rats (SHRSP). Angiotensin receptor antagonist (L-158,809) was shown to delay the onset of such stroke. In the present study, five groups of 4-week-old SHRSP were used. Three groups of SHRSP were made diabetic using streptozotocin (100 mg/kg i.p.). SHRSP from groups I (non-diabetic) and III (diabetic) chronically received L-NAME(0.5 g/L) and L-158,809 (20 mg/L) in saline to drink. Diabetic SHRSP (group C) received only saline to drink. SHRSP groups I and III developed stroke in 10+/-2 and 11+/-2 days. Average stroke-free period in groups II and IV was 18+/-2 and 29+/-2 days, respectively. Protective effect of streptozotocin-induced diabetes disappeared when SHRSP drinking L-NAME and L-158,809, also received subcutaneous injections of insulin. Present data suggest that experimental diabetes delays the onset of L-NAME-induced stroke in SHRSP and this protection is seen in the absence of renin-angiotensin system.

Methylene chloride, a widely used industrial solvent, has been shown to be mutagenic by in vitro tests. The aim of this study was to determine in vivo mutagenicity. Groups of 20 Swiss-Webster (S/W) male mice were injected subcutaneously three times/week with 5 ml/kg of 5% vol/vol or 10% vol/vol solution of methylene chloride in corn oil for 4 weeks, followed by 1 week of no treatment. Other groups of 20 S/W male mice were exposed to airflow of 10 L/min carrying 100, 150, or 200 ppm of methylene chloride daily for 2 hr/day, 5 days/week for 6 weeks. Each study contained appropriate negative controls. Mating was started 1 week later for the injection group and 2 days later for the inhalation group. Each male mouse was mated with a S/W virgin adult female. The mating was allowed to continue for 2 weeks. Presence of a vaginal plug was taken as a sign of successful mating and was designated as day 0 of gestation. On day 17, the females were killed, and the fetuses were removed and processed. Male mice were killed, and the testes were removed, preserved in 10% formalin, and processed. No significant difference in any of the mutagenicity parameters was found between control and treated groups. No microscopic lesions were found in testes of the treated males.

Twenty-eight polymeric materials used in the manufacture of transit equipment were evaluated for relative inhalation toxicity. 10 g of each were pyrolysed at 450, 550, 650, 750, and 850°C and the pyrolysis products were allowed to enter a 225 L cylindrical plexiglass chamber containing a cir cular, chambered unit rotating at 3 rpm. The system was semi-closed with con stant fresh air intake and recirculation of pyrolysis products. From initial py rolysis experiments without rats, using gas chromatographic analysis at 2, 4, 6, 8, 12, 16, 20, and 30 minutes, toxicity experiments were carried out at three temperatures for all the polymeric materials. For each toxicity study, four S/D rats, two males and two females, weighing 150 ± 15 g were used. 10 g of test material were used and chamber air analysed for toxic gases at 2, 4, 6, 8, 12, 16, 20, and 30 minutes of the exposure period. Amber fog lights enabled obser vation of time to incapacitation (Ti). The number of animals dying in the cham ber, or within the following week was noted and dead animals autopsied. All the samples were ranked according to (Ti) at different temperatures, and an at tempt made to determine the rank order correlation between (Ti) and carbon monoxide or carbon dioxide.