PubMed · 4926350
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R K Waterhouse. 1971. Urology.. https://pubmed.ncbi.nlm.nih.gov/4926350/
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Some anesthetic gases interfere with the determination of blood O2 values. We evaluated, for its potential for such interference, a gas mixture containing (v/v) approximately 70% ethane, 20% sulfur hexafluoride, and 10% cyclopropane, as is currently used in trace amounts to determine ventilation-perfusion (v/Q) ratios. Normal human blood samples were first tonometered with control gas mixtures containing (v/v): (1) 20.9% O2, 0.04% CO2; (2) 16.0% O2, 4.0% CO2; and (3) 9.9% O2, 7.8% CO2. A large quantity (20.9%) of the v/Q mixture was blended experimentally into the control mixture and the tonometry repeated. The entire experiment was then repeated substituting pure N2 for the v/Q mixture as a dilution control. O2 values were determined by three methods: (1) a polarographic electrode, ABL-300 (ABL); (2) a spectrophotometric method, Co-Oximeter (COOX); and (3) a galvanic cell, Lex-O2-Con (LEX). The v/Q gas mixture lowered significantly all measured LEX values by 2.5-3.6 saturation percent (sat%), but showed no effect, dilution or otherwise, on the O2 values determined by the COOX and ABL methods. The N2 dilution lowered the LEX values by an average of only 0.9 sat%; the ABL and the COOX were approximately 0.6 sat% lower. We therefore suggest that, if any of these O2 measurement methods are used in the presence of the v/Q mixture, baseline O2 values should be determined both before and after injection of the mixture into the bloodstream, prior to performing other experimental manipulations. The difference between the two values, if any, can then be used to interpret subsequent results.
Pharmacodynamics of general anesthetic agents generally exhibit biphasic concentration-effect relationships (i.e., an activation phase at low concentrations and inhibition at higher concentrations). These relationships are usually characterized with biphasic models constructed from various combinations and modifications of the nonlinear sigmoid E(MAX) model. We tested and quantified the parameter estimability of the simplest additive biphasic pharmacodynamic models by a Monte Carlo method. The estimated model parameters were used to calculate descriptors of the concentration-effect data. Parameters and descriptors were compared with their true values. When the IC50/EC50 ratio was low (<10), E(MAX), EC50, and IC50 were poorly estimated (high coefficient of variation and pronounced bias). However, the fit to the data was excellent, and the data descriptors calculated from the estimated model parameters demonstrated high precision and accuracy. Baseline effect (E0) was estimated with good precision and accuracy. As the IC50/EC50 ratio was increased, the estimability of model parameters and data descriptors improved, with the data descriptors continuing to be more estimable than model parameters. Thus, model parameters become estimable when there is sufficient separation between EC50 and IC50 to produce a plateauing of peak effect (activation), which can be observed directly from the data signature. Data descriptors are not subject to this limitation and thus may serve as better metrics for summarizing concentration-effect relationships.
BACKGROUND AND PURPOSE: A well-demarcated infarct was observed after 4 hours of rat middle cerebral artery (MCA) occlusion with xylazine/ketamine but not pentobarbital or isoflurane anesthesia. This study examined whether this reflected vascular changes and, because xylazine induces hyperglycemia, whether glucose could cause similar vascular effects in cerebral ischemia. METHODS: To examine the effects of anesthetics, rats were anesthetized for thread occlusion of the MCA with either xylazine/ketamine, pentobarbital, or isoflurane. To evaluate the effects of glycemia, acute hyperglycemia was induced by glucose injection. In both experiments, cerebral plasma volume (CPV) was determined using 3H-inulin after 4 hours of permanent occlusion, and cerebral blood flow was measured using [14C]iodoantipyrine following 2 hours of reperfusion after 2 or 4 hours of occlusion. The presence of cerebral hemorrhage after reperfusion was checked macroscopically and infarct volume with 2,3,5-triphenyltetrazolium staining. RESULTS: The ischemic CPV was about 50% of the contralateral values with xylazine/ketamine but not with the other anesthetics. On reperfusion, ischemic cerebral blood flow with xylazine/ketamine anesthesia was approximately half that with pentobarbital. Use of xylazine/ketamine also resulted in more frequent hemorrhagic infarcts and a larger infarct volume. Induced hyperglycemia resulted in a CPV decrease in the ischemic compared with nonischemic tissue (4.0 +/- 0.5 versus 7.4 +/- 0.2 microL/g; P < .001). Hyperglycemia also caused poor reperfusion and increased the occurrence of hemorrhagic infarction (hyperglycemia, 15 of 20; normoglycemia, 1 of 11; P < .01). CONCLUSIONS: Hyperglycemia induces marked cerebrovascular changes, both during ischemia and during reperfusion, that may exacerbate tissue damage. Change in CPV during ischemia may be a useful clinical indicator in predicting poor hemodynamic recovery and occurrence of hemorrhagic infarction after reperfusion therapy.