PubMed · 9411390
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C Bell. 1997. Sedation for procedures.. https://pubmed.ncbi.nlm.nih.gov/9411390/
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Anesthetics operate by different mechanisms and are often used to perform urodynamics in animals. The objective of this study was to compare the effects of ketamine/xylazine and urethane anesthetics on filling, voiding, and leak point pressure (LPP) in female rats. Nineteen rats underwent awake cystometry 2 days after suprapubic bladder catheter implantation. Bladders were filled with saline (5 ml/hr), while bladder pressure was measured. Half the rats were then anesthetized with urethane i.p. and half were anesthetized with ketamine and xylazine i.p. (K/X). All rats then underwent cystometry and LPP testing under anesthesia. Spontaneous nonvoiding contractions were analyzed and capacity was determined by voiding or leakage. Capacity was significantly higher in awake rats (0.55 +/- 0.06 ml) than with either K/X (0.21 +/- 0.06 ml) or urethane (0.30 +/- 0.05 ml). The pressure just prior to voiding in awake cystometry (15.6 +/- 1.7 cm H2O) was not significantly different from that with either anesthetic (K/X: 10.1 +/- 1.0 cm H2O; urethane: 13.3 +/- 2.0 cm H2O). Spontaneous nonvoiding contractions occurred in 4 rats with urethane and 3 rats with K/X. The volume at which the first contraction occurred was significantly lower with K/X (0.05 +/- 0.02 ml) than urethane (0.19 +/- 0.04 ml). There was no significant difference in the frequency of spontaneous nonvoiding contractions between K/X (4.58 +/- 0.30/min) and urethane (5.16 +/- 2.66/min), nor was there a difference in LPP between anesthetics (K/X: 40.4 +/- 2.4 cm H2O; urethane: 36.2 +/- 3.9 cm H2O). The results suggest that urethane is preferable to K/X for anesthetized cystometry studies since it more closely simulates normal physiological responses.
In this study C. we systematically examined the effects of ketamine and propofol at various doses (5-20 mg/kg) on blood pressure, heart rate and renal sympathetic nerve activity in chronically instrumented Wistar rats. We also assessed the effects of these anesthetics on the baroreflex control of heart rate and renal sympathetic nerve activity. Ketamine (10 mg/kg) increased blood pressure by 30.0+/-4.5%, heart rate by 17.7-3.3% and renal sympathetic nerve activity by 38.8+/-14.6%, while propofol (10 mg/kg) decreased blood pressure by 18.9+/-3.5%, heart rate by 5.5+/-2.5% and renal sympathetic nerve activity by 7.5+/-2.1%. These variables showed dose-dependent responses to both agents. Both ketamine and propofol decreased the range and maximum gain of the logistic function curve obtained by relating mean blood pressure to heart rate and blood pressure to renal sympathetic nerve activity. In conclusion, ketamine and propofol had different effects on autonomic cardiovascular function, but attenuated the baroreflex sensitivity of heart rate and renal sympathetic nerve activity in a dose-dependent manner. These results suggest the possibility that baroreflex sensitivity may reflect the depth of anethesia.
The interaction of glutamatergic and dopamine neurotransmission is thought to have relevance to both the pathophysiology and pharmacotherapy of schizophrenia. For example, subanesthetic doses of the N-methyl-D-aspartate receptor (NMDA-R) antagonist ketamine induce schizophrenia-like behavioral effects in humans and both behavioral and brain metabolic activation in rodents. Blockade of NMDA-R results in dopamine release, and antipsychotic drugs that block dopamine neurotransmission decrease NMDA-R antagonist-induced behavioral activation. The involvement of dopamine receptors in brain metabolic activation induced by ketamine is, however, unknown. The present study used D(1A) knockout mice to determine the role of dopamine D(1A) receptors in the effects of subanesthetic doses of ketamine on both behavioral responses and on alterations in regional [14C]2-deoxyglucose (2-DG) uptake. There was less ketamine-induced behavioral activation in D(1A) knockout mice than in wild-type mice. In wild-type mice, ketamine (30 mg/kg) induced dramatic increases in 2-DG uptake in limbic cortical regions, hippocampal formation, nucleus accumbens, basolateral amygdala, and caudal parts of the substantia nigra pars reticulata. D(1A) knockout mice exhibited blunted metabolic activation in response to ketamine in a neuroanatomically specific manner. The selective D(1) antagonist, SCH23390 (0.3 mg/kg), inhibited both ketamine-induced brain metabolic activation and behavioral responses in the wild-type mice, with a similar neuroanatomical specificity observed in the D(1A) knockout mice. Thus, the neuroanatomically selective role that D(1A) receptors play in ketamine-induced behavior and regional brain metabolic activation in mice provides a useful model for further studies of how the D(1A) receptor function may be altered in schizophrenia.