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Query: UMLS:C0278134 (anesthesia)
 110,339 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The baboon under general anaesthesia as a model to assess drug-induced cerebral blood flow changes (delta CBF) using single-photon emission tomography (SPET) offers great in vivo possibilities but has to comply with demands on control of anaesthesia-related influencing factors, such as PaCO2 changes. The model sought in this study and described here allows control of PaCO2, in the baboon under thiopentone anaesthesia by ventilation, and was evaluated for the functional dependence of delta CBF vs delta PaCO2, using SPET technetium-99m hexamethylpropylene amine oxime (HMPAO) and the split-dose method together with controlled ventilation. During the experiment the model was validated for normal reactivity to PaCO2 changes, and subsequently applied to investigate the mechanisms (still uncertain) of CBF increase known to follow administration of the local anaesthetic lidocaine. Six baboons received 6 mg/kg lidocaine intravenously. CBF was measured between two consecutive SPET acquisitions (split-dose method) respectively relating to HM-PAO distributions in the brain before and after the injection of lidocaine. Meanwhile the animals were maintained at constant respiratory rate and volume. The results indicate that the correlation between delta CBF and the ensuing fall in PaCO2 deviated from the baseline pattern from the model and confirmed a cerebrovascular contribution to the lidocaine-induced CBF increase. This agreed well with mean and systolic blood pressure changes and heart rate.
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PMID:Influence of intravenously administered lidocaine on cerebral blood flow in a baboon model standardized under controlled general anaesthesia using single-photon emission tomography and technetium-99m hexamethylpropylene amine oxime. 828 77

Regional cerebral blood flow (rCBF) and plasma catecholamines were measured in separate experiments during the onset of insulin-induced hypoglycemia and during recovery. The purpose of these experiments was twofold: first, to study the relationship between plasma catecholamines and rCBF to determine if increased concentrations of plasma catecholamines were responsible for the increase in rCBF observed during insulin-induced hypoglycemia, and second, to study changes in rCBF after recovery from hypoglycemia. Male Long-Evans rats were fasted overnight, surgically prepared under isoflurane anesthesia, restrained, and allowed to awake from anesthesia. In the first series of experiments, plasma catecholamines, arterial blood pressure, arterial blood gases, and electroencephalogram (EEG) were measured during the onset of hypoglycemia produced by i.v. insulin and the recovery after i.v. glucose. The EEG showed a characteristic high-amplitude, slow-wave pattern during hypoglycemia (plasma glucose, 38 +/- 2 mg/dl; n = 3). Plasma epinephrine in the normoglycemic control rats was 529 +/- 122 pg/ml (n = 5) and increased 4.5 times as plasma glucose reached 50 +/- 3 mg/dl. After the initial increase, plasma epinephrine steadily decreased toward baseline over the next 90 min as the hypoglycemia became more severe. Plasma norepinephrine significantly increased by 60% when plasma glucose was 40 +/- 2 mg/dl and remained increased during much of the recovery period. In other studies, rCBF was measured in four groups of rats, one group with normoglycemia (control), one with hypoglycemia, one at 5 min of recovery, and one at 30 min of recovery. Regional CBF increased during hypoglycemia (plasma glucose, 39 +/- 1 mg/dl; n = 6) in most regions studied and ranged from 28 to 99% above control. After 5 min of the recovery (plasma glucose, 269 +/- 15 mg/dl), rCBF returned to or decreased below baseline. In a previous study, we determined that rCBF did not increase during hypoglycemia until plasma glucose decreased to 40 mg/dl. In the present study, the peak increase in plasma epinephrine occurred when plasma glucose was 50 mg/dl. At plasma glucose concentrations which rCBF began to increase, plasma epinephrine was decreasing from its peak level. Regional CBF and plasma norepinephrine increased in parallel during the onset of hypoglycemia; however, during the recovery period, plasma norepinephrine remained increased while rCBF decreased to or below baseline. The dissociation of rCBF and plasma catecholamines casts doubt on the hypothesis that plasma catecholamines are responsible for increases in rCBF.
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PMID:Cerebral blood flow, plasma catecholamines, and electroencephalogram during hypoglycemia and recovery after glucose infusion. 829 61

This study assesses the sensitivity of the baboon model under anaesthesia to determine by single photon emission computed tomography (SPECT) and 99Tcm-hexamethylpropyleneamine oxime (HMPAO) dose responses from drugs (acetazolamide) with known regional cerebral blood flow (rCBF) effects on humans. Three dosages of acetazolamide were chosen: 250, 500 and 750 mg. The effects of these were studied by conventional SPECT 5 min after intravenous (i.v.) administration and compared to previous studies of rCBF with the baboons under anaesthesia only. An additional study concerned the effect of 500 mg acetazolamide at 15 min after administration. Haemodynamic parameters and blood gases were also monitored. No statistically significant regional effects were noted (P > 0.05). The largest increase in CBF (39%) was observed from 500 mg acetazolamide after 5 min. This was statistically significantly different from control values only at a 10% level of confidence; then followed a 27% increase above control values after 750 mg (5 min). At 15 min 500 mg yielded values lower by 10% than the high dose. No effects were observed from 250 mg acetazolamide; only pO2 showed changes which largely confirm the CBF findings. The model did not give significant results at a 5% level of confidence but large fluctuations were observed, also in the haemodynamic and blood gas values. At a 10% level a significant dose response was confirmed for acetazolamide.
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PMID:Dose response from pharmacological interventions for CBF changes in a baboon model using 99Tcm-HMPAO and SPECT. 835 17

The effect of propofol and thiopentone on cerebral (CBF), myocardial (MBF), muscular, and arterial hepatic blood flow was assessed with radiolabelled microspheres in 12 chronically instrumented dogs, six given propofol and six thiopentone. Tissue blood flows were measured in the awake animal, after 30 min of normoxic anaesthesia (room air), and after 30 min of hypoxic anaesthesia using a mixture of 10% O2 and 3% CO2 in nitrogen. The decrease in CBF from awake to normoxic anaesthesia was similar with propofol and thiopentone (propofol: 77 +/- 8 to 38 +/- 3 ml min-1 100 g-1, P < 0.01; thiopentone: 66 +/- 3 to 33 +/- 2 ml min-1 100 g-1, P < 0.01). During hypoxia, CBF rose moderately in the two groups (respectively +19% and +28%, P < 0.05). The MBF increased in propofol and thiopentone groups after 30 min of anaesthesia with air (propofol: 97 +/- 23 to 137 +/- 15 ml min-1 100 g-1; thiopentone: 82 +/- 7 to 141 +/- 10 ml min-1 100 g-1) and increased still more during hypoxia. The increase in MBF was related to an increase in heart rate and blood pressure. The quadriceps blood flow decreased during anaesthesia in normoxia and in hypoxia. The diaphragmatic blood flow increased with thiopentone under hypoxia. The hepatic arterial blood flow was unchanged. It is concluded that the effects of propofol on regional blood flows are very similar to those of thiopentone.
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PMID:Effect of propofol and thiopentone on regional blood flow in brain and peripheral tissues during normoxia and hypoxia in the dog. 845 72

The time-course of propofol concentrations in the blood and brain following rapid administration of three doses were examined using a sheep preparation and regional pharmacokinetic techniques. These were compared to the time-course of cerebral effects of propofol reported previously. There were marked differences between the time-course of propofol concentrations in arterial blood and the brain, with a close relationship between the time-course of brain concentrations and effects on depth of anaesthesia and CBF. There was evidence that the effect of propofol on cerebral blood flow altered its own rate of elution from the brain. Hysteresis between arterial propofol concentrations and cerebral effects following rapid i.v. administration therefore appears to have a pharmacokinetic basis, and conventional compartmental pharmacokinetic analysis using blood concentrations alone may fail to accurately predict the time-course of both brain propofol concentrations and depth of anaesthesia.
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PMID:Brain and blood concentrations of propofol after rapid intravenous injection in sheep, and their relationships to cerebral effects. 886 41

The pattern of capillary plasma perfusion was investigated in the rat brain during functional activation. Functional hyperemia was induced in the left whisker-barrel cortex by deflection of the right mystacial vibrissae for 2 min at frequencies of 1-7 Hz. Rats were decapitated under anesthesia 3-4 s after i.v. bolus injection of Evans blue dye. The steep increase of the arterial dye concentration ensures that divergent capillary plasma transit times result in unequal intracapillary dye concentrations. Plasma perfusion heterogeneity was determined from the coefficient of variation (CV) of Evans blue concentrations measured in numerous single capillaries of the whisker-barrel cortex. Functional hyperemia was quantified from measurements of CBF using the [14C]-iodoantipyrine technique in a second experimental group. CBF in the left whisker-barrel cortex increased with the stimulation frequency and was maximal at 5 Hz compared to the right side. Conversely, plasma perfusion heterogeneity decreased with stimulation frequency in a reciprocal way, being minimal at 5 Hz. Results indicate a decrease in the microcirculatory flow heterogeneity during functional hyperemia in the brain.
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PMID:Decreased heterogeneity of capillary plasma flow in the rat whisker-barrel cortex during functional hyperemia. 889 4

This study investigates changes of jugular bulb oxygen saturation (SjO2) measured by fiberoptic jugular bulb oximetry and changes of intracranial hemodynamics using transcranial Doppler sonography (TCD) during cardiopulmonary bypass (CPB) for coronary artery bypass graft (CABG) in 17 ASA III patients. Anesthesia was maintained with fentanyl, midazolam, and continuous infusion of etomidate. Hypothermic CPB (27 degrees C) was managed according to alpha-stat conditions. SjO2 (%) was measured by a fiberoptic catheter (Opticath F 5.5; Abbott Critical Care Systems) placed in the right jugular bulb via the right internal jugular vein. Mean blood flow velocity (Vmean, cm/s) was measured in the middle cerebral artery using a bidirectional 2-MHz TCD system (Transpect, Medasonics). Data were recorded continuously from the beginning to the end of the CPB. During cooling and hypothermia (27 degrees C); SjO2 and Vmean did not change compared with values at the start of CPB. However, with the beginning of rewarming, Vmean was increased 65% compared with stable hypothermia (27 degrees C). This increase in Vmean was associated with a 25% decrease in SjO2. Maximum desaturation occurred at a 36 degrees C jugular bulb temperature. During cooling and stable hypothermia, global oxygen balance and intracerebral perfusion seemed to be maintained. However, a major alteration in the balance of the cerebral oxygen supply and demand may occur in response to rewarming despite increases in Vmean. Findings suggest inadequate increases in CBF to meet cerebral metabolic demand. Further investigations need to validate these findings with biochemical techniques and neuropsychological tests.
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PMID:Jugular bulb oxygen saturation and middle cerebral blood flow velocity during cardiopulmonary bypass. 910 Jan 81

We studied the effects of propofol on the cerebral circulation and flow/pressure autoregulation in eight anesthetized pigs. Regional cerebral blood flow (rCBF) was measured with a cerebral venous outflow technique. Autoregulation was tested with angiotensin infusions and gradual blocks of the caval vein for hyper- and hypotensive challenges, respectively. Propofol was given in a bolus of 2.5 mg.kg-1 followed by an infusion starting at 12 mg.kg-1.h-1 and gradually reduced to 8 mg.kg-1.h-1. As expected, propofol caused a substantial reduction in cerebral metabolic rate of oxygen, which was accompanied by an increase in cerebrovascular resistance and a decrease in CBF. In the control situation, i.e., during background anesthesia (low-dose isoflurane+nitrous oxide) only, the autoregulation was well preserved, and its lower limit was found at a mean arterial blood pressure (MABP) of 48 mm Hg. Propofol did not affect autoregulation in the group as a whole: the slope of the regression line of regional cerebrovascular resistance (rCVR) versus MABP during blood pressure reduction (caval test) was not significantly changed during propofol when compared to the control, neither was the lower limit of autoregulation (MABP, 54 mm Hg). All pigs but one followed this response pattern. The nonautoregulating pig had a completely pressure-dependent rCBF during propofol anesthesia, despite a perfectly intact auto-regulation in the control situation. It is concluded that propofol in clinical dosage does not affect autoregulation in this pig model, although individual animals may display a different response pattern.
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PMID:Effects of propofol on cerebral blood flow, metabolism, and cerebral autoregulation in the anesthetized pig. 910 Jan 92

A technique is described for the chronic measurement of cerebral blood flow in conscious, unrestrained rodents, utilizing laser doppler flowmetry (LDF) removably coupled to an optical fiber permanently implanted into brain tissue by established stereotaxic procedures. Changes in relative blood flow in response to a range of pharmacological and behavioral challenges were measured in the hippocampus (HBF) and striatum (StBF) 24-72 h and up to 28-32 days after surgical implantation of the optical fiber. Intraseptal microinfusion of L-glutamate in artificial cerebrospinal fluid 48-96 h and 28-32 days after surgery increased HBF. Pentobarbital (Nembutal) and urethane anesthesia decreased HBF. On the day of euthanasia under urethane anesthesia, HBF was demonstrated to be responsive to alteration of blood CO2 via hyper/hypocapnia, and autoregulation was demonstrated in response to hypovolemic hypotension. In behavioral experiments, blood flow was found to increase with activity and locomotion, as well as during paradoxical (PS) and slow-wave sleep (SWS). The greatest increase in CBF was measured during PS. Although basal levels of blood flow were similar between regions, the increase in blood flow during PS was greater in the hippocampus. This simple procedure enables real-time measurement of qualitative changes in regional cerebral blood flow during behaviors in conscious, unrestrained animals. The observation that constancy of measurements was obtained for 1 month enables within-subject analysis in longitudinal studies and reduces the number of animals required for investigations.
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PMID:Hippocampal and striatal blood flow during behavior in rats: chronic laser Doppler flowmetry study. 910 65

The present study aimed to examine the effects of N omega-nitro-L-arginine (LNA) on the early ischemic neuronal damage (EIND). All the experiments were carried out under general anesthesia, maintaining the blood gases and the body temperature within the physiological ranges. The local CBF, the topographically corresponding cortical specific gravity, and the volume of EIND were determined in each rat, which was subjected to prolonged or temporary occlusion of middle cerebral artery (MCA) using our original miniclip. Significant cortical edema developed only in the brain area where the local CBF value was below 200 ml 100 g-1 min-1. The prolonged MCA occlusion for 1, 2, and 4 h induced a time-dependent increase in the severity of cortical edema and the volume of EIND. Removal of the clip invariably induced recirculation. Compared to that induced by 4 h prolonged ischemia, the brain damage was improved by 1 h MCA occlusion followed by 3 h recirculation, whereas it was significantly worsened by 2 h ischemia followed by 2 h recirculation. While LNA [1 mg, i.p., given two times during the experiment] only partially inhibited the activity of brain nitric oxide synthase, it remarkably ameliorated EIND of both prolonged ischemia and recirculation in this model. The above findings indicate the pathogenic role of nitric oxide in prolonged ischemia as well as recirculation.
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PMID:N omega-nitro-L-arginine attenuates early ischemic neuronal damage of prolonged focal cerebral ischemia and recirculation in rats. 917 50


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