PubMed · 4801909
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S A Koch. 1973. Ulcerative keratitis.. https://doi.org/10.1016/s0091-0279(73)50056-x
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OBJECTIVE: The purpose of this trial was to clarify the effects of intravenous ketamine at anaesthetic and sub-anaesthetic dosages on gastrointestinal motility. DESIGN: 20 beagles (group 1: 3 mg/ketamine/kg/h, n = 10; group 2: 30 mg ketamine/kg/h, n = 10), were investigated. Gastric emptying (nuclide gastric emptying studies, liquid and semi-solid test meal), intestinal transit time (Hydrogen breath test with lactulose) and intestinal motor function (perfusion manometry with 8 measuring ports) were determined. As a control condition, the tests were performed on all dogs in the two groups during infusion of physiological saline solution. RESULTS: No significant differences in the motility patterns were present between 3 mg ketamine/kg/h and the control condition. For group 2, a moderately significant (p < 0.05) increase in the interdigestive motility index was observed for 30 mg ketamine/kg/h. However, this did not change the transit criteria. There was no significant difference between ketamine and control condition tests with regard to cycle and phase lengths or the propagation rate of the activity front. CONCLUSIONS: We conclude that ketamine provokes no basic changes in gastrointestinal motility, at either sub-anaesthetic doses. It can therefore be used to advantage in the continuous postoperative analgesia of intensive care patients, where repeated interventions are necessary and no cardiopulmonary contraindications are present.
Autoradiographic studies have shown that low dose ketamine produces increases in regional glucose utilisation and blood flow in the hippocampus, cerebral cortex, and olfactory lobe in the rat brain, probably due to antagonism at the NMDA receptor. Functional MRI using deoxyhaemoglobin contrast can be used to study changes in regional cerebral blood flow (rCBF). Long TE gradient-echo sequences were used to study changes in rCBF produced by low dose ketamine in rats anaesthetised with nitrous oxide, supplemented with either halothane (HAL) or fentanyl/fluanisone/midazolam (FFM) combination. Images from rats in the FFM group showed a 10-14% increase in signal intensity in the hippocampus, cerebral cortex, and olfactory lobe following either a single bolus or a low dose infusion of ketamine (p < .05). These changes were significantly reduced in the HAL group (p < .005). Halothane is known to attenuate the changes in regional glucose utilisation produced by the noncompetitive NMDA antagonist dizocilpine (MK-801), and its effects on ketamine-induced changes in rCBF seen in this study may be due to a similar effect. The potential use of functional MRI in studying the effect of pharmacological interventions on rCBF is discussed.
Initial resistance of bacterial infection is mediated primarily by polymorphonuclear leucocytes (PMN). Anaesthetic agents have been reported to impair various aspects of PMN function. It is possible that the use of these agents to sedate critically ill patients may further compromise an already depressed host defence mechanism. A flow cytometric technique with fresh whole blood from 10 healthy volunteers was used. Phagocytic and respiratory burst activity of PMN incubated for 1 h with either propofol, thiopentone, midazolam or ketamine at both clinical plasma concentrations and 100 times this concentration were determined. Thiopentone at the higher concentration reduced both respiratory burst activity (mean peak channel 50.7 compared with control value of 77.6 (P < 0.0001)) and phagocytosis (mean peak channel 47.5 compared with 79.9 (P < 0.0001)). Ketamine at 100 times the clinical plasma concentration also reduced respiratory burst and phagocytosis, but this failed to reach statistical significance (P = 0.10 and P = 0.053, respectively). No significant depression occurred in the other groups. The results suggest that these i.v. anaesthetic agents, at clinically relevant concentrations, have minimal effects on PMN phagocytosis and oxygen free radical production. At higher concentrations thiopentone and ketamine may affect phagocytic function and thiopentone may impair intracellular cytolysis.