The roles of, and interactions between, steroids and naloxone, an opioid antagonist, in the reversal of experimental hypotensive shock were studied in normal and adrenalectomized rats. In normal rats treated with dexamethasone or deoxycorticosterone or 17-hydroxyprogesterone the hypotension and shock caused by 1% bodyweight and 2% bodyweight haemorrhage could be substantially reversed by naloxone in a dose-related manner. In contrast, the reversal of hypotension by naloxone was markedly less in adrenalectomized rats. It is concluded that there is a co-ordinate release of pressor catecholamines and depressor enkephalins from adrenal glands in hypovolaemic shock. Eventually, the use of naloxone would be of much less value in the treatment of hypotension or shock in patients with Addison's disease.
The effects of chronic thyroxine treatment on cat soleus muscle contractions were studied. Maximum twitch tension, contraction time, half relaxation time and tension-time integral of maximal twitches of the soleus muscles of thyroxine treated cats were significantly decreased. Consequently, there was a decrease in tension and degree of fusion of incomplete tetanic contractions of the soleus muscle. The maximum tetanic tension was not statistically significantly changed, suggesting that the effects may be due to a decrease in the duration of the active state of the muscle. Isoprenaline given intravenously during incomplete tetanic contractions of the soleus muscle caused a statistically significant depression of tension in the control group but not in the thyroxine treated group. This further suggests reduction in the duration of the active state of soleus muscles of thyroxine treated cats. Propranolol injected chronically with thyroxine reversed or prevented the depression of tension caused by thyroxine treatment, suggesting the involvement of beta-adrenoceptors in these effects. The decrease in tension and degree of fusion during incomplete tetanic contractions of the thyroxine treated soleus could be responsible, at least partly, for the muscle weakness and tremor of thyrotoxicosis. Cyclic AMP may possibly be the mediator of these effects.
1. The effects of thyroxine treatment on soleus and extensor digitorum longus (EDL) muscle contractions and their cyclic adenosine 3',5'-monophosphate (cyclic AMP) levels were examined in anaesthetized cats. 2. Thyroxine treatment decreased the tension of incomplete tetanic contractions of the soleus as well as the EDL muscles. The effect on tension of these muscles was not associated with an increase in the cyclic AMP level of the muscle as is the case with a beta 2-adrenoceptor agonist effect. 3. The results do not support the involvement of cyclic AMP in the tension depressant effect of thyroxine on contractions of skeletal muscle. 4. It is suggested that the muscle weakness and tremor observed in thyrotoxicosis and during administration of beta 2-adrenoceptor agonists are mediated by different mechanisms.
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