Abstract

Young rabbits, eight at a time, were exposed to 203 and 208 h (groups I and II) and 283 and 298 h (groups III and IV) of hypoxia (O2 at 70 to 80 mmHg), at atmospheric pressure. The animals were injected ip with 25 mg X kg-1 on the first day, and with 50 mg X kg-1 on the second day and every 48 h thereafter of guanethidine (G) or 6-hydroxydopamine (6-OHDA) (O), or an equivalent volume of saline (H = hypoxic controls, or N = normoxic controls). This regime of treatment abolished, in normoxic and hypoxic animals alike, the effect of sympathetic nerve stimulation on the pupil at voltages which produced maximum dilatation in control animals. Injection of atenolol reduced heart rate by 32% in control animals, but had no effect in the guanethidine treated animals, and a very small effect in the 6-OHDA treated group. The animals in each group were litter mates of those in the other groups. In the first series the dry weight of the hypoxic right ventricles increased, relative to the normoxic controls, by 38.8% (H), 40.5% (G) and 40.9% (O). There was no left ventricular hypertrophy in the hypoxic animals, but there was a small, but not statistically significant, rise in the haematocrit (Hct). In the second series the right ventricular hypertrophy was greater (+98% (H), +89% (G) and +102% (O]. There was also a significant left ventricular hypertrophy (+38% (H), +40.3% (G) and +41% (O] and a highly significant increase in haematocrit in all the hypoxic groups. The right atria were only slightly hypertrophied in the first series, but greatly hypertrophied in the second series (+103%, H), an effect attenuated by the treatment (+34%, G, and +39%, O). When each treated hypoxic animal was compared with its untreated hypoxic littermate (n = 12), the mean treated/untreated ratio for the right ventricular dry weight was 0.991 +/- 0.022 for the guanethidine group (n = 11) and 1.023 +/- 0.043 for the 6-hydroxydopamine (n = 11). Such identity of the extent of the hypertrophy in all the hypoxic groups, irrespective of the duration of hypoxia, implies that the hypertrophy was not conditional upon sympathetic activity.

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