PubMed · 13618476
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H C NEWMAN. 1958. Halothane and rebreathing.. https://doi.org/10.1093/bja%2F30.12.555
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RATIONALE: Although positive modulators of gamma-aminobutyric acid(A) (GABA(A)) receptors generally produce similar behavioral effects, regardless of which modulatory site on the GABA(A) receptor complex mediates these effects, some differences have been observed between the effects of neuroactive steroids and those of other positive GABA(A) modulators. OBJECTIVE: The current study was designed to compare the behavioral effects of a neuroactive steroid to those of other positive GABA(A) modulators. METHODS: Rats responded under a multiple schedule of repeated acquisition and performance of response chains, with responding maintained under a second-order fixed-ratio 2 schedule of food presentation. RESULTS: Pregnanolone, flunitrazepam, pentobarbital and ketamine, an antagonist at NMDA receptors, dose-dependently decreased response rates and increased the percentage of errors in both components of the multiple schedule. Although the rate-decreasing and error-increasing effects of pregnanolone, pentobarbital and ketamine were quantitatively similar to each other, flunitrazepam was less effective in decreasing response rates and more effective in increasing errors than the other three drugs. A dose of 3.2 mg/kg pregnanolone potentiated the effects of flunitrazepam and pentobarbital, producing 2- to 3-fold shifts to the left in the dose-effect curves. In contrast, pregnanolone did not alter the ketamine dose-effect curves. CONCLUSIONS: The disruptive effects of the neuroactive steroid pregnanolone are qualitatively similar to those of other positive GABA(A) modulators as well as ketamine; however, the potentiation of the effects of flunitrazepam and pentobarbital, and not ketamine, emphasizes the importance of GABA(A) receptors in the behavioral effects of pregnanolone.
AIM AND METHODS: Haemorrhage is characterized by two distinct responses, sympathoexcitation that evokes tachycardia and supports blood pressure, followed by sympathoinhibition contributing to bradycardia and hypotension. It has been shown that anaesthetics alter the response to haemorrhage and we hypothesized that rat strain may also influence the response. We investigated the effect of simulated haemorrhage on heart rate (HR) responses in three strains of conscious rats, and the effect of three common anaesthetics, by comparing HR responses under anaesthesia to the conscious response. Haemorrhage was simulated by constricting the inferior vena cava. We demonstrate differential effects of anaesthetics, including both maintenance and elimination of HR responses to haemorrhage depending on anaesthetic. RESULTS: We also show that both phases of the HR response differ in different conscious rat strains, and we have demonstrated a transient increase in HR during the decompensatory phase of haemorrhage, a novel 'second HR peak' with advanced hypotension. CONCLUSION: Both rat strain and anaesthetic influence HR responses to haemorrhage, and some anaesthetics appear less suitable than others for studies of haemodynamic responses in rats. There was evidence of an additional compensatory mechanism that operates at advanced levels of hypotension in the rat.
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