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Biomedical subjects

E Kochs

Publications and source records attributed to E Kochs.

At least 109 records · Page 6Linked to original sources
PubMed1996

Analgesic efficacy of low-dose ketamine. Somatosensory-evoked responses in relation to subjective pain ratings.

BACKGROUND: Low-dose ketamine has been shown to exert analgesic effects. Whether ketamine-induced pain relief may be quantitated by somatosensory evoked cerebral potentials has not been established. METHODS: Thirty healthy volunteers were assigned randomly to one of three groups. Subjects of group 1 (n = 10, control) were given saline as placebo. In groups 2 (n = 10) and 3 (n = 10), intravenous ketamine (0.25 mg. kg-1 and 0.50 mg. kg-1, respectively) was administered. The following variables were recorded at baseline and for 50 min after drug administration: electroencephalographic (EEG) data, somatosensory-evoked late cortical responses (SEP) elicited by intracutaneous stimulation of the fingertip (2-3 fold pain threshold), heart rate, mean arterial blood pressure, and end-tidal PETCO2 via a tight-fitting mask. Electroencephalographic spectral power in selected frequency bands and frequency percentiles were calculated from the spontaneous EEG segment preceding each somatosensory stimulus. Somatosensory-evoked late cortical response parameters were calculated from the respective poststimulus EEG segments. After recording of each EEG response, subjects were asked to rate the individual pain sensation. RESULTS: In group 1, all variables did not change over time. Ketamine administration resulted in dose-dependent decreases in alpha-activity and increases in theta power (group 2: 190%, group 3: 440%). Electroencephalographic changes were not related to changes in pain perception. For the first 30 min after ketamine injection, a dose-dependent decrease of the long-latency N150-P250 somatosensory-evoked late cortical response component was observed (group 2: 15-20%; group 3: 25-30%). Subjective pain ratings were also different between groups, with a higher degree of pain relief in group 3 for the first 30 min. At the end of the observation period, pain relief and the N150-P250 amplitude were comparable in both ketamine groups. CONCLUSIONS: These data indicate that pain relief induced by low-dose ketamine is dose-dependent for the first 30 min after bolus injection. Changes in pain perception may be quantitated by somatosensory-evoked cortical responses. Also, EEG changes are not specific for changes in nociception, but the increase in theta power may reflect the hypnotic effect of low-dose ketamine.

Adult↗
PubMed1996

The effects of surgical stimulation on intracranial hemodynamics.

This study investigates the effects of surgical stimulation on cerebral blood flow velocity using transcranial Doppler sonography (TCD) in 1 and 2 maximum alveolar concentration (MAC) isoflurane anesthetized patients. Sixty ASA I and II patients undergoing breast surgery were studied. Anesthesia was maintained with 0.6% isoflurane (groups 1 and 2) or 1.2% isoflurane (groups 3 and 4) and nitrous oxide in oxygen (FIO2, 0.33). TCD recordings of middle cerebral artery mean blood flow velocity (Vmean, cm/s) were taken before each respective treatment and for the 15-min investigation period. In groups 1 and 3 (each n = 20), the patients were exposed to surgical stimulation (skin incision). In groups 2 and 4 (each n = 10), norepinephrine infusion (0.1 microgram.kg-1.min-1) was used to increase mean arterial blood pressure (MAP) to levels similar to those seen with surgical stimulation (groups 1 or 3). Body temperature and PETCO2 remained constant over time and did not vary between treatment groups. In groups 1 and 3, MAP increased 22 and 16% after surgical stimulation. In groups 2 and 4, MAP increased 28 and 36% after norepinephrine infusion. Vmean was increased 23 and 17% after surgical stimulation during 1 and 2 MAC isoflurane but did not change with norepinephrine infusion. These data show that cerebral blood flow velocity increases with surgical stimulation in 1 and 2 MAC isoflurane-anesthetized patients. This is not a function of changes in MAP. These data suggest that surgical stimulation increases cerebral blood flow, possibly because of arousal.

Adult↗
PubMed1995

Tumor oxygenation in a transplanted rat rhabdomyosarcoma during fractionated irradiation.

PURPOSE: To quantify the changes in tumor oxygenation in the course of a fractionated radiation treatment extending over 4 weeks. METHODS AND MATERIALS: Rhabdomyosarcomas R1H of the rat were irradiated with 60Co-gamma-rays with a total dose of 60 Gy, given in 20 fractions over 4 weeks. Oxygen partial pressure (pO2) in tumors was measured at weekly intervals using polarographic needle probes in combination with a microprocessor-controlled device (pO2-Histograph/KIMOC). The pO2 measurements were carried out in anesthetized animals under mechanical ventilation and in respiratory and hemodynamic steady state. Tumor pO2 values were correlated to the arterial oxygen pressure paO2, arterial pCO2, and pH determined with a blood gas analyzer. RESULTS: Tumor oxygenation did not change significantly during the 3 weeks of irradiation (up to 45 Gy), from a median pO2 of 23 +/- 2 mmHg in untreated controls to 19 +/- 4 mmHg after the third week. The decrease of the number of pO2 values between 0 and 5 mmHg indicated that an improved oxygenation in the tumors occurred. However, with increasing radiation dose (fourth week, 60 Gy) a significant decrease in tumor oxygenation to a median pO2 of 8 +/- 2 mmHg and a rapid increase in the frequency of pO2 values (35 +/- 4%) between 0 and 5 mmHg was found. CONCLUSION: Improved oxygenation in rhabdomyosarcomas R1H was only present in the early phase of the fractionated irradiation. Radiation does above 45 Gy led to a considerable decrease of tumor oxygenation in the later phase of irradiation.

Animals↗
PubMed1995

[Propofol-alfentanil reduced cerebrovascular CO2 reactivity in comparison with isoflurane].

The present study compared the effects of propofol/alfentanil versus isoflurane anaesthesia on cerebral vascular reactivity to changes in carbon dioxide (CO2) using transcranial Doppler sonography (TCD). METHODS. Seventeen ASA class I patients undergoing minor elective surgery were studied following IRB approval and informed consent. In group 1 (n = 10), anaesthesia was induced with thiopental 4 mg/kg and alfentanil 15 micrograms/kg. Endotracheal intubation was facilitated by vecuronium 0.1 mg/kg. Anaesthesia was maintained with 1% end-tidal isoflurane and nitrous oxide (N2O) in oxygen O2 (6 l/min; FiO2 0.3). In group 2 (n = 7), anaesthesia was induced with propofol 2 mg/kg, alfentanil 15 micrograms/kg, and vecuronium 0.1 mg/kg for endotracheal intubation and maintained by infusion of propofol, alfentanil, and N2O-O2 (6 l/min; FiO2 0.3) according to the following protocol: propofol: 10, 8, and 6 mg/kg.h for 10 min each followed by 4 mg/kg.h; alfentanil: 55 micrograms/kg.h. Monitoring included measurement of mean arterial blood pressure (MAP, mm Hg), heart rate (HR), body temperature (T), end-tidal CO2 (PetCO2, mm Hg), isoflurane concentrations, and arterial O2 saturation (SaO2, %). Mean blood flow velocity (Vmean, cm/s) was measured in the middle cerebral artery using a bidirectional 2-MHz TCD system (TranspectT, Medasonics). Mechanical ventilation was adjusted to achieve PetCO2 levels of 40-50-40-30 and 40 mm Hg. Ten minutes of equilibration were allowed at each PetCO2 level. The CO2 reactivity index was calculated as delta Vmean/delta PetCO2 (cm/s.mm Hg). RESULTS. MAP, HR, T, and SaO2 were constant over time and were not different between groups. The CO2 reactivity index over the CO2 range of 30-50 mm Hg was higher in isoflurane (2.32 +/- 1.51 delta cm/s.mm Hg) compared to propofol/alfentanil patients (1.15 +/- 0.77 delta cm/s.mm Hg) (mean +/- SD, P < 0.05). CONCLUSIONS. The data show that although CO2 reactivity is maintained during both isoflurane and propofol/alfentanil anaesthesia, the cerebral vascular response to CO2 was lower in propofol/alfentanil compared to isoflurane patients. This is likely due to propofol/alfentanil-induced cerebral vasoconstriction. These data suggest that CO2 reactivity is a function of the pre-existing cerebral vascular tone induced by the anaesthetic.

Adult↗
PubMed1995

[Enflurane blocks ion current through the nicotinic acetylcholine receptor].

AIM: The study investigates the influence of enflurane (EN) on macroscopic currents of the nicotinic acetylcholinergic receptor channel (nAChR). This ion channel is a representative member of the superfamily of ligand-gated receptor channels and is better characterized than all the other receptors in respect of structure and function. METHODS: For the experiments the patch-clamp technique was used to study the embryonic type of the nAChR expressed by cultured mouse-myotubes. Patch-clamp recordings were performed in the outside-out-mode from these preparations. To match the rapid desensitization kinetics of ligand-activated ion channels, a liquid filament switch technique was used for the application of agonists to the excised patches. This technique allows for change of solution within 300 microseconds. We used a saturating concentration of 10(-4) M acetylcholine (ACh), activating almost all available ion channels on a patch. Pulses of 10(-4) M ACh together with EN in different concentrations were applied repetitively. RESULTS: The current elicited by 10(-4) M ACh is reduced reversibly in a concentration-dependent manner by EN in clinically relevant concentrations: 1,44 x 10(-5) M EN inhibit about 10%, 1.44 x 10(-4) M 25%, 1.44 x 10(-3) M 35%, and 1.44 x 10(-2) M 75% of the ion flux (averaged results from 48 patches). EN decreases the time constant of the current decay. This acceleration of desensitisation kinetics is partly reversible if followed by application of 10(-4) M ACh. CONCLUSION: In this study we were able to show that EN reduces the currents of the ligand-gated embryonic-like nAChR in clinically relevant concentrations. Volatile anaesthetics are known to influence GABAA-, glutamate-, and glycine- activated receptors, which are members of the same family of ligand-gated receptor-channel units. Thus, the action of volatile anaesthetics on ligand-gated receptors may play a role in the mechanism of general anaesthesia. The interaction of volatile anaesthetics with nondepolarising neuromuscular blockers may also be based on this effect at the neuromuscular junction.

Acetylcholine↗
PubMed1995

Effect of renal function on neuromuscular block induced by continuous infusion of mivacurium.

We have studied the effect of renal function on the pharmacodynamics of mivacurium. Sixty patients were allocated to three groups according to creatinine clearance: group C (control), creatinine clearance > 50 ml min-1; group P (preterminal renal failure), creatinine clearance < 50 ml min-1 > 20 ml min-1; group T(terminal renal failure), creatinine clearance < 20 ml min-1. Neuromuscular transmission (train-of-four) was monitored using electromyography from the hypothenar muscle with stimulation of the ulnar nerve. After an initial bolus, mivacurium was administered continuously to maintain a T1 of 5 (4)% of baseline. The dose of mivacurium necessary to maintain 95% neuromuscular block was similar in patients with normal renal function and patients with different levels of renal impairment. Recovery from neuromuscular block after ceasing mivacurium infusion was significantly prolonged in patients with preterminal renal impairment. There was a close correlation between mivacurium pharmacodynamics and pseudocholinesterase activity, but not creatinine clearance.

Adolescent↗
PubMed1995

Surgical stimulation increases median nerve somatosensory evoked responses during isoflurane-nitrous oxide anaesthesia.

Median nerve somatosensory evoked responses (MnSSER) were recorded in 15 healthy adult patients, ASA I-II, before and during orthopaedic surgery. After induction of anaesthesia with fentanyl 0.1-0.15 mg, etomidate 0.3 mg kg-1 and vecuronium 0.1 mg kg-1, anaesthesia was maintained with 0.6% isoflurane (end-tidal) and 66% nitrous oxide in oxygen. MnSSER were recorded after establishment of steady-state anaesthesia at baseline, during preparation (n = 11) and continuously after the start of surgery. For the last measurement period, four patients were excluded from analysis because additional fentanyl was required. MnSSER were recorded at Erb's point, at C6 (neck) and at the respective contralateral primary somatosensory projection area (C3' or C4'). All MnSSER waveform components remained recordable and easily identifiable during anaesthesia. During intense surgical stimulation (e.g. periosteal stimulation) the peak-to-peak amplitude N20P25 increased significantly by more than 45% (P < 0.05), whereas latencies of all components did not change over time. These data indicate that MnSSER may be reliably monitored in the intraoperative period during steady-state isoflurane-nitrous oxide anaesthesia. In addition, concurrent changes in haemodynamic variables during nociceptive stimulation support the hypothesis that reversal of isoflurane-nitrous oxide-induced suppression of MnSSER may indicate increased nociceptive input when depth of anaesthesia is inadequate.

Adolescent↗
PubMed1995

Sevoflurane improves neurological outcome after incomplete cerebral ischaemia in rats.

We have studied the effects of sevoflurane on neurological outcome in a rat model of incomplete cerebral ischaemia. After institutional approval, 30 non-fasted male Sprague-Dawley rats (455-555 g) were anaesthetized, the trachea intubated and the lungs ventilated mechanically with isoflurane and 30% oxygen in air. Catheters were inserted into the right femoral artery, both femoral veins and into the right jugular vein for measurement of arterial pressure, drug administration and blood sampling. At completion of surgery, isoflurane was discontinued and the rats were allowed an equilibration period of 30 min according to the following regimens: group 1 (n = 10) received 70% nitrous oxide in oxygen and fentanyl (bolus 10 micrograms kg-1 i.v.; infusion 25 micrograms kg-1 h-1); group 2 (n = 10) received 1.98 vol% sevoflurane in oxygen and air (FIO2 0.3); group 3 (n = 10) received 1.98 vol% sevoflurane in oxygen and air (FIO2 0.3) and 40% glucose (6 ml kg-1 i.p.) 30 min before ischaemia. Ischaemia was produced by combined unilateral common carotid artery ligation and haemorrhagic hypotension to 35 mm Hg for 30 min. Temperature, arterial blood-gas variables and arterial pH were maintained within the physiological range. Plasma glucose concentration was measured before, during and after ischaemia. Neurological deficit was evaluated for 3 days after ischaemia. Neurological outcome was better in sevoflurane anaesthetized animals, regardless of the plasma glucose concentration, compared with nitrous oxide-fentanyl controls. This indicates that differences in plasma glucose concentrations do not account for the cerebral protection seen with sevoflurane.

Anesthetics↗
PubMed1995

Transcranial Doppler sonography indicates critical brain perfusion during hemorrhagic hypotension in dogs.

This study investigated the effects of hemorrhagic hypotension on cerebral blood flow velocity and brain electrical activity (by electroencephalogram [EEG]). Eleven mongrel dogs were anesthetized with isoflurane (1 minimum alveolar anesthetic concentration [MAC]) and catheters were placed into both femoral arteries and veins for mean arterial blood pressure (MAP) measurement, blood withdrawal, and drug administration. Brain temperature, arterial blood gases, and pH were maintained constant. EEG was recorded from temporoparietal recording sites versus a frontal reference. A pulsed transcranial Doppler (TCD) probe (2 MHz, Transpect, Medasonics) was placed on the dura via a temporal bone window to measure mean (Vmean, cm/s) and diastolic blood flow velocity (Vdiast, cm/s) in the middle cerebral artery. At the end of the surgical preparation, isoflurane was discontinued and all animals received fentanyl (bolus, 25 micrograms/kg intravenously (IV); infusion, 50 micrograms.kg-1.h-1 IV) plus 50% N2O/O2 during 30 min of equilibration. After recordings of baseline data, the dogs were hemorrhaged at a rate of 80-100 mL/min. The observation interval was 14 min. EEG spectral edge frequency (SEF 95%) and Vmean did not change when MAP was decreased from 109 +/- 10 to 63 +/- 7 mm Hg. This indicates preserved neuronal function and intact autoregulation of cerebral blood flow. Below MAP of 49 +/- 9 mm Hg, a shift of the EEG to lower frequencies was associated with decreases in Vmean and Vdiast. EEG burst suppression occurred at a MAP of 31 +/- 7 mm Hg, paralleled by a loss of the diastolic flow velocity pattern.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Effects of sufentanil on cerebral hemodynamics and intracranial pressure in patients with brain injury.

BACKGROUND: The current study investigates the effects of sufentanil on cerebral blood flow velocity and intracranial pressure (ICP) in 30 patients with intracranial hypertension after severe brain trauma (Glasgow coma scale < 6). METHODS: Mechanical ventilation (FIO2 0.25-0.4) was adjusted to maintain arterial carbon dioxide tensions of 28-30 mmHg. Continuous infusion of midazolam (200 micrograms/kg/h intravenous) and fentanyl (2 micrograms/kg/h intravenous) was used for sedation. Mean arterial blood pressure (MAP, mmHg) was adjusted using norepinephrine infusion (1-5 micrograms/min). Mean blood flow velocity (Vmean, cm/s) was measured in the middle cerebral artery using a 2-MHz transcranial Doppler sonography system. ICP (mmHg) was measured using an epidural probe. After baseline measurements, a bolus of 3 micrograms/kg sufentanil was injected, and all parameters were continuously recorded for 30 min. The patients were assigned retrospectively to the following groups according to their blood pressure responses to sufentanil: group 1, MAP decrease of less than 10 mmHg, and group 2, MAP decrease of more than 10 mmHg. RESULTS: Heart rate, arterial blood gases, and esophageal temperature did not change over time in all patients. In 18 patients, MAP did not decrease after sufentanil (group 1). In 12 patients, sufentanil decreased MAP > 10 mmHg from baseline despite norepinephrine infusion (group 2). ICP was constant in patients with maintained MAP (group 1) but was significantly increased in patients with decreased MAP. Vmean did not change with sufentanil injection regardless of changes in MAP. CONCLUSIONS: The current data show that sufentanil (3 micrograms/kg intravenous) has no significant effect on middle cerebral artery blood flow velocity and ICP in patients with brain injury, intracranial hypertension, and controlled MAP. However, transient increases in ICP without changes in middle cerebral artery blood flow velocity may occur concomitant with decreases in MAP. This suggests that increases in ICP seen with sufentanil may be due to autoregulatory decreases in cerebral vascular resistance secondary to systemic hypotension.

Anesthetics, Intravenous↗
PubMed1995

Electrophysiological monitoring and mild hypothermia.

Hypothermia affects cerebral metabolism including a variety of neurotransmitter systems. Neurophysiologic changes during hypothermia are characterized by decreases in the membrane resting potential and amplitude. The duration of the action potential is prolonged and nerve conduction velocity is decreased. Nonsynaptic responses are reduced to a lesser extent than synaptic responses. Mild hypothermia to 33.5 degrees C produces only minimal changes in the EEG with small shifts in frequencies to theta- and beta-activity. Electro-cerebral silence occurs at a temperature below 22-25 degrees C. Evoked potentials (EP) of all modalities are affected by hypothermia to a similar degrees. Amplitudes are decreased and latencies are prolonged. Cortical EP components are more profoundly affected than early, subcortical potentials. EP may be reliably recorded at temperatures > 25 degrees C. Changes in EEG and EP are not specific for hypothermia. In addition, a hysteresis between cooling and rewarming has to be taken into account for the interpretation of temperature effects on brain electrical activity. The interactive effects of anesthetics and temperature may preclude EEG and EP measure for a graded quantification of hypothermia.

Anesthesia↗
PubMed1995

Neuroprotection: fact or fantasy?

Several strategies have been proposed for protecting the brain from ischaemic and hypoxic insults, based on an understanding of the pathophysiological processes involved. They include hypervolaemic haemodilution, anaesthesia, hypothermia, normoglycaemia, calcium channel blockers, adenosine modulators, NMDA- and AMPA-receptor antagonisms and lazeroids. Some have only been shown to be effective in animals and some have clinical relevance. Only hypothermia is protective in a variety of pathological states.

Anesthesia↗
PubMed1994

[Expert systems in medicine: possible uses in anesthesia].

The euphoric assumption that powerful computers fed with sophisticated software programmes may serve as a substitute for human knowledge and decision making has been replaced by a more realistic concept of how computers may help in collecting data and their interpretation on the basis of human knowledge and experience. The computer is now used as a dedicated tool to support man in overtaking cumbersome and monotonous processes and tedious calculations. Running 24 hours a day, a specific feature of the computer is that depending on unequivocal software programmes it does neither forget or alter commands and information. Computer programmes imitating human thinking and information processing are called expert or knowledge based systems. These are especially useful when multiple possible combinations of data make a given task very complex. This review presents several systems used in different medical disciplines to describe fundamental ideas, different problem-solving methods, techniques and possible working fields including anaesthesia. It is made clear why computers have found widespread use in all administrative areas. In contrast, no system comparable in potency has been developed for use in clinical medicine in spite of 25 years of research in expert systems. This review starts with a definition of expert knowledge and the appropriate transformation of this knowledge to the computer. In addition, a general survey about the structure of expert systems and a state of the art in some current problem solving methods is given. Additional aspects and restrictions including technical, psychological and legal problems which seem to be unimportant from the outside but are essential for the development of expert systems are presented.

Anesthesia↗
PubMed1994

Surgical stimulation induces changes in brain electrical activity during isoflurane/nitrous oxide anesthesia. A topographic electroencephalographic analysis.

BACKGROUND: The aim of this study was to investigate topographic changes in electroencephalographic (EEG) power and frequency induced by abdominal surgery during anesthesia with 0.6% or 1.2% isoflurane in 66% nitrous oxide. METHODS: Forty-six patients (aged 41 +/- 13 yr) scheduled for elective abdominal surgery were studied. The trachea of each patient was intubated and the lungs ventilated. Patients were randomly assigned to one of four groups: anesthesia was maintained with 0.6% (group 1, n = 12; group 2, n = 11) or 1.2% end-tidal isoflurane (group 3, n = 12; group 4, n = 11) in 66% nitrous oxide. Data were recorded over 20 min. Groups 1 and 3 were studied without surgery (as controls). In groups 2 and 4 recording was started 6 min before skin incision. The EEG was acquired via 17 scalp electrodes placed in standard International 10-20 locations (reference Cz). Absolute and relative power densities were calculated in selected frequency bands. EEG maps of spectral power densities were coded according to a continuous color spectrum. RESULTS: During baseline recordings, alpha activity was dominant at frontal areas in groups 1 and 2. In comparison, in groups 3 and 4, delta and theta activities were dominant at frontal leads. In group 2, the start of surgery resulted in increases in delta activity and decreases in alpha activity that were most dominant frontally (delta +181% and alpha -61%, F3). The delta shift was attenuated at 1.2% isoflurane (group 4, delta +44%, F3), but decreases in alpha activity (-53%, F3) were comparable to those in group 2. The EEG response in all frequency bands was attenuated at parietotemporal recording sites at both isoflurane concentrations. CONCLUSIONS: The current data demonstrate graded EEG responses induced by abdominal surgery during anesthesia with 0.6% or 1.2% isoflurane in 66% nitrous oxide. Spatial heterogeneities in absolute spectral power densities were reflected by color changes in the EEG maps. The topographic EEG analysis indicates that these changes were most dominant at frontal areas. The increases in delta and decreases in alpha activities may be related to intraoperative "paradoxical" electrophysiologic arousal phenomena.

Adult↗
PubMed1994

[Ketamine and evoked potentials].

Ketamine-induced changes in the spontaneous and evoked electroencephalogram have been well documented in animals and humans. In contrast to the action of hypnotics, ketamine does not result in a dose-dependent suppression of neural activity. Many studies have revealed excitatory activity with induction of synchronized high-voltage slow waves in the electroencephalogram (EEG). Somatosensory evoked responses (SEP) have been found to be enhanced following induction of anaesthesia with ketamine. However, increases in amplitude were small compared with the SEP-enhancing effects of etomidate. The increase in somatosensory evoked responses may reflect dose-dependent disinhibition and/or increased excitation of cerebral neuronal activity induced by ketamine. Attenuation of late cortical somatosensory evoked responses following stimulation of thin C- and A delta-nerve fibres has been reported in volunteers given low-dose ketamine. Changes in SEP amplitude correlated to changes in subjective pain sensation. From this it was concluded that the analgesic effect of ketamine can be assessed by electrophysiological measurement methods. Recent studies suggest that the analgesic effect of the racematic ketamine mixture can probably be related to the effects of S-(+)-ketamine isomer, which has been shown to be involved in the activation of an opioidergic mechanism. Auditory evoked responses (AEP) of short latencies with origins in the brain stem have been shown to be slightly altered by ketamine. From this it was concluded that these components may not be used for assessment of the depth of anaesthesia. In contrast to the effects of hypnotics, mid-latency AEP components may be recorded during ketamine anaesthesia.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Cerebral blood flow and cerebral blood flow velocity during angiotensin-induced arterial hypertension in dogs.

Pressure-passive perfusion beyond the upper limit of cerebral blood flow (CBF) autoregulation may be deleterious in patients with intracranial pathology. Therefore, monitoring of changes in CBF would be of clinical relevance in situations where clinical evaluation of adequate cerebral perfusion is impossible. Noninvasive monitoring of cerebral blood flow velocity using transcranial Doppler sonography (TCD) may reflect relative changes in CBF. This study correlates the effects of angiotensin-induced arterial hypertension on CBF and cerebral blood flow velocity in dogs. Heart rate (HR) was recorded using standard ECG. Catheters were placed in both femoral arteries and veins for measurements of mean arterial blood pressure (MAP), blood sampling and drug administration. A left ventricular catheter was placed for injection of microspheres. Cerebral blood flow velocity was measured in the basilar artery through a cranial window using a pulsed 8 MHz transcranial Doppler ultrasound system. CBF was measured using colour-labelled microspheres. Intracranial pressure (ICP) was measured using an epidural probe. Arterial blood gases, arterial pH and body temperature were maintained constant over time. Two baseline measures of HR, MAP, CBF, cerebral blood flow velocity and ICP were made in all dogs (n = 10) using etomidate infusion (1.5 mg.kg-1 x hr-1) and 70% N2O in O2 as background anaesthesia. Following baseline measurements, a bolus of 1.25 mg angiotensin was injected i.v. and all variables were recorded five minutes after the injection. Mean arterial blood pressure was increased by 76%. Heart rate and ICP did not change. Changes in MAP were associated with increases in cortical CBF (78%), brainstem CBF (87%) and cerebellum CBF (64%).(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗