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Biomedical subjects

E Kochs

Publications and source records attributed to E Kochs.

At least 127 records · Page 7Linked to original sources
PubMed1993

[Alpha 2-agonists in anesthesia and intensive medicine].

The neurotransmitters adrenaline and noradrenaline are non-selective adrenergic agonists which interact with both subtypes of alpha- and beta-receptors. Clonidine, an alpha 2-adrenergic drug with a selectivity ratio of 200/1 for alpha 2/alpha 1 has been used in clinical practice for more than 20 years. Although alpha 2-agonists have vasoconstrictor properties, sympatholytic effects on the central nervous system predominate. As a result, the sympathetic outflow from the medullary pressor centres is decreased mediating the hypotensive effects of the alpha 2-agonists. These compounds also exhibit sedative, anxiolytic, analgesic, and haemodynamic stabilising properties. The identification of alpha 2-adrenoceptors has yielded information on their biochemical properties, signal transduction, modulation of the sympathetic nervous system and neurotransmission. The classification of alpha 2-receptors based on anatomical locations and identified as presynaptic alpha 2-receptors and postsynaptic alpha 1-receptors proved to be untenable after postsynaptic and extrasynaptic alpha 2-receptor locations had been identified. At least 3 isoreceptors which are heterologously distributed in the brain have been identified. Guanine nucleotide proteins (G proteins) couple the receptor to an effector mechanism (i.e. intracellular messenger cascade, ion channel). More selective for the alpha 2-adrenoceptor than clonidine is dexmedetomidine (1600/1 of alpha 2/alpha 1), a very potent agonist at the alpha 2-adrenoceptor. Imidazole derivatives (like clonidine and dexmedetomidine) also bind to other nonadrenergic receptors ("imidazoline receptors") which may produce some effects (i.e. vagotonia) previously ascribed to alpha 2-adrenoceptors. alpha 2-receptors exist in brain tissue and several peripheral organs and tissues including the liver, eye, kidney, pancreas and platelets. Anaesthetic interest has focussed on reductions in anaesthetic requirements since experimental and clinical studies have shown that alpha 2-agonists expert powerful analgesic and anaesthetic effects. The hypnotic response is probably mediated by activation of alpha 2-adrenoceptors in the locus coeruleus. Analgesia is induced by modulation of the nociceptive pathway at the level of the dorsal root neuron and other sites not yet unambiguously characterised. Dexmedetomidine reduces the anaesthetic requirements for halothane by more than 90%. Cerebral blood flow and intraocular pressure are reduced by alpha 2-agonists. Epidural, intrathecal, intravenous and transdermal application of clonidine resulted in pain reduction, during and following surgery and in patients with neurogenic or otherwise intractable cancer pain. Administration of alpha 2-agonists induces only minor respiratory effects. Salivary flow is reduced by alpha 2-agonists and gastric and small-bowel motility is decreased.(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenergic alpha-Agonists↗
PubMed1993

Improvement of brain electrical activity during treatment of porcine malignant hyperthermia with dantrolene.

Three months before this study, susceptibility for malignant hyperthermia (MH) had been tested in 15 pigs. In all pigs, MH was triggered by administration of 1% halothane. Brain electrical activity was examined during therapy of MH with and without administration of dantrolene. From the EEG, power densities in selected frequencies and the median frequency of the power spectrum were calculated. Therapy was started when severe respiratory changes were observed (PaCO2 > 10 kPa, mixed venous oxygen tension (PvO2) < 4 kPa). At this time, heart rate exceeded 150 beat min-1, mean arterial pressure (MAP) was less than 60 mm Hg and median frequency was less than 2 Hz. EEG was isoelectric (n = 6) or showed slow polymorphic delta-activity. For therapy, administration of all anaesthetics was terminated, 100% oxygen was delivered and ventilation was increased four-fold. Acidosis was treated by administration of sodium bicarbonate 2-4 mmol litre-1 kg-1. Animals were allocated randomly to one of two groups: group I (control, n = 7) received no dantrolene; group II (n = 8) received dantrolene 2.5 mg kg-1 i.v. All variables were measured over a period of 60 min after therapy: EEG, HR and MAP were recorded continuously and blood-gas tensions, arterial potassium and glucose concentrations and pH were measured every 150 s. In group I (no dantrolene) minor, transient improvements in EEG activity were noted, but all animals died within 15-25 min after the start of therapy. In dantrolene-treated animals, EEG total power and median frequency increased within 5 min.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

The effects of propofol on cerebral and spinal cord blood flow in rats.

The effects of low and high doses of propofol on global cerebral blood flow (CBF) and spinal cord blood flow (SCBF) as a function of mean arterial blood pressure were investigated. CBF and SCBF during propofol infusion were compared to the levels in rats anesthetized with nitrous oxide (N2O) and fentanyl. Rats in the fentanyl/N2O group (control, n = 13) received 70% N2O in O2 plus fentanyl (bolus: 10 micrograms/kg; infusion: 25 micrograms.kg-1 x h-1). Rats in the low-dose propofol group (n = 10) received 30% O2 in air and propofol infusion (0.5 mg.kg-1 x min-1). Rats in the high-dose propofol group (n = 8) received 30% O2 in air and propofol infusion (2.0 mg.kg-1 x min-1). Blood flow autoregulation was tested by manipulating the mean arterial blood pressure with phenylephrine infusion or trimethaphan infusion and blood withdrawal by measuring CBF and SCBF using radioactive microspheres. Arterial blood gases, pHa, and skull temperature were controlled. Cerebral and spinal cord vasculature showed autoregulation in all treatment groups with a pressure range of 50-140 mm Hg. Within this pressure range, when compared to fentanyl/N2O, propofol decreased cortical CBF 60% (P < 0.001), subcortical CBF 40% (P < 0.001), midbrain blood flow 30% (P < 0.001), and SCBF 20% (P < 0.05). These results indicate that propofol maintains CBF and SCBF autoregulation.

Animals↗
PubMed1993

Cerebral blood flow velocity in relation to cerebral blood flow, cerebral metabolic rate for oxygen, and electroencephalogram analysis during isoflurane anesthesia in dogs.

The purpose of this study was to correlate changes in cerebral blood flow velocity (Vmean) with cerebral blood flow (CBF) during isoflurane anesthesia in dogs. The relation between cerebral oxygen consumption (CMRO2) and electroencephalogram (EEG) analysis also was investigated. Blood flow velocity was measured in the middle cerebral artery using a pulsed transcranial Doppler (TCD). CBF was measured with radioactive microspheres. EEG was measured over both hemispheres and median EEG frequency (median frequency) was calculated after fast Fourier transformation. Baseline anesthesia was maintained with 50% nitrous oxide in oxygen and 50 micrograms.kg-1 x h-1 fentanyl. Animals of Group I (control, n = 6) were not given isoflurane. Data were recorded at baseline, and at 30, 60, and 90 min. There was no significant change in any variable over time. In Group II (n = 7), data were recorded at baseline and at 1%, 2%, and 3% end-tidal isoflurane. Mean arterial pressure was maintained at baseline levels by phenylephrine infusion. CBF increased from 70.8 +/- 10.6 mL.100g-1 x min-1 at baseline to 146.1 +/- 36.9 mL.100 g-1 x min-1 with 3% isoflurane (P < 0.01). Vmean increased from 38.3 +/- 6.7 cm/s to 65.6 +/- 9.7 cm/s (P < 0.01). The correlation between relative changes in CBF and Vmean was r = 0.94 (P < 0.01). With 1% isoflurane the EEG shifted to slow-wave, high-voltage activity, and median frequency decreased from 5.9 +/- 0.7 Hz to 1.4 +/- 0.4 Hz (P < 0.05). Median frequency was not decreased further during 2% and 3% isoflurane anesthesia.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Inhalation↗
PubMed1993

[Topographic-quantitative EEG-analysis of the paradoxical arousal reaction. EEG changes during urologic surgery using isoflurane/ N2O anesthesia].

Increases in slow-wave (delta) activity in the EEG may reflect increased depth of anaesthesia provided that hypoxia, haemodynamic instability and drug overdose have been excluded. In contrast, similar intraoperative EEG responses have been described as paradoxical arousal reactions. The aim of this study was to assess the effects of surgical stimulation on spatial EEG changes during anaesthesia with 0.6% isoflurane/66% nitrous oxide. METHODS. The present study investigated changes in EEG power and frequencies in 20 patients (mean age 36 +/- 8 years; ASA I or II) scheduled for elective urological surgery during steady-state anaesthesia with 0.6% isoflurane and 66% nitrous oxide. The following variables were measured: heart rate (HR), mean arterial blood pressure (MAP), end-tidal isoflurane (PetISO) and carbon dioxide concentrations (PetCO2), arterial oxygen saturation (SaO2%) and body temperature (degree C). Patients were randomly assigned to one of two groups: group 1 (n = 10; without surgery) and group 2 (n = 10; with surgical procedure). The EEG was recorded over 20 min. The first 5 min were taken as baseline. In group 2 surgical stimulation (skin incision with subsequent surgical preparation) was started 1-2 min after recording of baseline values. Topographical distribution of EEG output was recorded from 17 electrodes (international 10-20 system), digitized and stored on disk (CATEEM) after establishment of steady-state anaesthesia (PetISO: 0.6%; PetCO2: 35-37 mmHg). Data are given as medium (microV2/Hz) and relative changes (%) +/- SD with respect to baseline. Statistical significance was tested for F4 versus C4 for the delta- and alpha-1-frequency bands using Wilcoxon's test (P < 0.05). RESULTS. In group 1 (without surgical stimulation) all parameters did not change over time. EEG slowing with an increase in power (> 100%) was noted in 8 patients of group 2 (n = 10; during surgical stimulation). By visual inspection of the original EEG tracings paradoxical arousal patterns were seen in these patients. In group 2, delta output changed from 69.6 microV2/Hz (baseline) to 147.4 microV2/Hz at frontal leads (F4) 5-6 min after the start of surgery. Only minimal changes were observed for theta activity. At the same time, in most cases fast wave activity (alpha 1, alpha 2, beta 1 and beta 2) was decreased by more than 50% at identical cortical areas. Increases in MAP were noted continuously after start of surgery up to a maximum of 19.8% from baseline, which became significant at the 16-min level. Heart rate did not change over time. DISCUSSION. Our data demonstrate that EEG slowing may be induced by surgical stimulation during steady-state anaesthesia with 0.6% isoflurane/66% nitrous oxide in oxygen. These findings are consistent with previous reports indicating the occurrence of slow wave patterns following sensory stimulation in comatose patients. Since these events occur predominantly at frontal areas they may not be detected with single-channel parietal recordings. Our data suggest that topographical EEG monitoring may useful for assessing painful events during surgery. Using EEG monoparameters like spectral edge frequency or median the occurrence of paradoxical arousal reactions may be falsely interpreted as an increased depth of anaesthesia.

Adult↗
PubMed1992

The effects of propofol on brain electrical activity, neurologic outcome, and neuronal damage following incomplete ischemia in rats.

This study compares the effects of propofol and fentanyl/N2O on spontaneous brain electrical activity, neurologic outcome, and neuronal damage due to incomplete cerebral ischemia in rats. Thirty Sprague-Dawley rats were assigned to one of three groups: group 1 (n = 10) received 70% N2O in O2 plus fentanyl (bolus 10 micrograms.kg-1, infusion 25 micrograms.kg-1.h-1); group 2 (n = 10) received 70% N2 in O2 and propofol (infusion 0.8-1.2 mg.kg-1.min-1) adjusted to maintain EEG burst suppression during ischemia; group 3 (n = 10) was anesthetized with propofol and received 6 ml.kg-1 10% glucose intraperitoneally 15 min before the start of ischemia. Incomplete cerebral ischemia was produced by right common carotid artery occlusion combined with hemorrhagic hypotension (35 mmHg) for 30 min. Arterial blood gases, pH, and rectal temperature were kept constant in all groups. Plasma glucose was lower during ischemia in propofol-anesthetized rats compared to that in fentanyl/N2O- (P = 0.009) and glucose-loaded propofol-treated rats (P = 0.008). Neurologic outcome and brain tissue injury were significantly better in propofol-anesthetized compared to fentanyl/N2O-anesthetized rats (P less than 0.05). Elevated plasma glucose in propofol-treated rats resulted in similar neurologic outcome and histopathologic injury as seen in propofol-anesthetized rats given no glucose. Recovery of EEG theta-alpha activity after ischemia was inversely correlated to neurologic deficit (fentanyl/N2O: r = -0.71; propofol: r = -0.83; P less than 0.01). These results show that propofol improves neurologic outcome and decreases neuronal damage from incomplete cerebral ischemia when compared to fentanyl/N2O. This effect is not dependent on plasma glucose.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Ketamine decreases plasma catecholamines and improves outcome from incomplete cerebral ischemia in rats.

Central neuroexcitatory receptors (N-methyl-D-aspartate [NMDA], non-NMDA) may affect outcome from cerebral ischemia by altering sympathetic nervous system activity. We tested whether ketamine, an NMDA antagonist, and NBQX, a non-NMDA antagonist, improve outcome from incomplete cerebral ischemia in the rat and whether a change in outcome is related to changes in plasma catecholamines. There were five treatment groups: group 1 (control, n = 10) received a fentanyl infusion at a rate of 25 microgram.kg-1.h-1 and ventilation with 70% N2O in O2. Group 2 (n = 10) received the same anesthetic treatment and were given an intraperitoneal injection of 30 mg/kg NBQX 15 min prior to ischemia. Group 3 (n = 10) received a ketamine infusion of 1.0 mg.kg-1.min-1 and ventilation with room air. Group 4 (n = 10) received a ketamine infusion of 1.5 mg.kg-1.min-1. Group 5 received a ketamine infusion of 1 mg.kg-1.min-1 plus a 6 ml/kg intraperitoneal injection of 40% glucose solution 15 min before the start of ischemia. Ischemia was produced by right common carotid ligation combined with hemorrhagic hypotension to 35 mmHg for 30 min. Blood gases, pH, and skull temperature were controlled during ischemia. Plasma glucose increased during ischemia in all groups but was lower in ketamine-anesthetized rats (groups 3 and 4). Glucose-loaded ketamine-anesthetized rats (group 5) had plasma glucose concentrations similar to the control group. Plasma epinephrine and norepinephrine concentrations were significantly less in ketamine-anesthetized rats (groups 3, 4, and 5) during ischemia compared to controls (P less than 0.05). Neurologic outcome was significantly better (P less than 0.05) in all ketamine-treated rats (groups 3, 4, and 5) compared to the control group, regardless of plasma glucose concentration during ischemia. NBQX did not improve neurologic outcome. These results suggest that ketamine improves neurologic outcome from incomplete cerebral ischemia by a mechanism related to a decrease in plasma catecholamine activity.

Animals↗
PubMed1992

Cerebral and spinal cord blood flow in awake and fentanyl-N2O anesthetized rats: evidence for preservation of blood flow autoregulation during anesthesia.

Blood flow responses to alterations in mean arterial blood pressure (MABP) were measured in the cerebral cortex, subcortex, midbrain, and spinal cord of awake rats. Data were compared with those of rats anesthetized with an i.v. fentanyl infusion and inspired nitrous oxide (N2O). Regional cerebral blood flow was measured using radioactive microspheres in the following blood pressure ranges: (a) <40 mm Hg; (b) 40-60; (c) 60-80; (d) 80-100; (e) 100-120; (f) 120-140; (g) 140-160; and (h) >160. Blood pressure was increased with phenylephrine or decreased with trimethaphan combined with blood withdrawal. Cerebral blood flow was not measured when MABP was less than 60 mm Hg in awake rats. Autoregulation was seen in all brain areas between 60 and 140 mm Hg in both treatment groups. Although regional cerebral blood flow was not different between the two treatment groups, PaCO2 was 2-4 mm Hg lower in awake rats. This suggests that PaCO2-corrected cerebral blood flow may be 10-20% lower with fentanyl-N2O anesthesia.

Journal Article↗
PubMed1992

The effects of propofol on cerebral blood flow in correlation to cerebral blood flow velocity in dogs.

This study correlates the effects of propofol on cerebral blood flow (CBF) and middle cerebral artery blood flow velocity in dogs. CBF was measured using radioactive microspheres. Cerebral oxygen consumption (CMRO2) was measured with each CBF determination. Blood flow velocity was measured through a transtemporal window using a pulsed 8 MHz transcranial Doppler ultrasound system (TCD). Electroencephalogram (EEG) was continuously recorded over both cerebral hemispheres. Cardiac output (CO) was measured using an electromagnetic flow probe placed on the pulmonary artery. Baseline measures were made in all dogs (n = 11) with 0.7% isoflurane end tidal and 50% N2O in O2. There were two treatment groups. In group 1 (n = 6), propofol (0.8 mg/kg/min) was infused and a second measurement made at induction of EEG burst suppression (12 +/- 2 min). CBF and CMRO2 decreased by 70% and mean blood flow velocity decreased by 60%. Blood pressure, heart rate, and CO did not change. Propofol infusion was discontinued and all parameters were measured following recovery of EEG to baseline activity (48 +/- 9 min). CBF and blood flow velocity increased 35 and 25%, respectively, and CMRO2 increased by 32% during this period. A second propofol infusion (0.8 mg/kg/min) was started and all cerebral and systemic hemodynamic parameters were again determined at induction of EEG burst suppression (12 +/- 2 min). CBF decreased 35% and blood flow velocity decreased 25% to levels seen during the first propofol infusion. Over the entire study, changes in CBF correlated with changes in blood flow velocity (r = 0.86, p < 0.05). In group 2 (n = 5), four control measures were made at the same time intervals as in group 1. Baseline CBF and blood flow velocity were lower in group 2 compared to group 1 but these measures did not change over time. Our results show that propofol produces marked decreases in CBF in dogs and that these changes are closely correlated with CBF velocity.

Journal Article↗
PubMed1992

[The effect of sufentanil on regional and global cerebral circulation and cerebral oxygen consumption in the dog].

The intracranial hemodynamic and metabolic effects of 20 micrograms/kg sufentanil were studied in ten mongrel dogs. Anesthesia was maintained with 0.7 vol.% end-tidal isoflurane and 50% nitrous oxide in oxygen. Catheters were inserted into both femoral arteries and veins, the superior sagittal sinus, the left atrium, and the lateral cerebral ventricle for blood pressure measurement, arterial and sagittal sinus blood sampling, radioactive microsphere injections, and intracranial pressure (ICP) monitoring. Cardiac output (CO) was measured using an electromagnetic flow probe on the pulmonary artery. Following baseline measurements, sufentanil was injected and data were recorded at 5, 15, and 30 min. RESULTS. In group 1 (n = 5) blood pressure was not controlled, while in group 2 (n = 5) blood pressure was maintained at baseline level with a phenylephrine infusion. Arterial blood pressure decreased by 32% in response to sufentanil in group 1 and remained constant in group 2 according to the protocol. CO decreased by 40%-50% in both groups. Regional and global cerebral blood flow (CBF) decreased by 25%-40% with no difference between groups. The cerebral hemodynamic changes were associated with a decrease of 35%-40% in cerebral oxygen consumption. ICP did not change over time. DISCUSSION. These data are in contrast to studies in dogs, where sufentanil produced non-dose-dependent increases in CBF and ICP. Our results are more consistent with studies in humans and rats where administration of sufentanil was associated with either no change or decreases in cerebral hemodynamics, metabolism, and ICP. We conclude that in dogs with normal intracranial physiology sufentanil decreases regional and global CBF in response to a decrease in cerebral metabolic demand without significantly affecting ICP.

Analgesics, Opioid↗
PubMed1991

Concurrent increases in brain electrical activity and intracranial blood flow velocity during low-dose ketamine anaesthesia.

The purpose of the present study was to assess the effects of low-dose ketamine on spontaneous brain electrical activity (EEG) and intracranial blood flow velocity. Twenty healthy volunteers were divided into two groups: Group I (n = 10) received 0.25 mg.kg-1 ketamine iv; Group II (n = 10) received 0.5 mg.kg-1 ketamine iv. Mean arterial blood pressure (MAP), heart rate (HR), end-tidal PCO2 (PETCO2), and arterial oxygen saturation (SaO2) were measured. The EEG was recorded from temporo-occipital recording sites over both hemispheres. Blood flow velocity in the middle cerebral artery was measured using a transcranial Doppler ultrasound system. All variables were evaluated at baseline and for 60 min following ketamine. Administration of ketamine resulted in increases of MAP and HR in both groups to a similar degree. The PETCO2 and SaO2 did not change in either group over time. Ketamine caused a dose-dependent, transient shift in the EEG to synchronous high-voltage slow waves with an increase in total power (Group I: 301 +/- 38%; Group II: 104 +/- 28%). These changes were associated with dose-dependent increases in mean blood flow velocity (Group I: 35 +/- 7%; Group II: 68 +/- 10%). Our data suggest that increases in intracranial blood flow velocity are closely correlated to increases in neuronal activity and are not secondary to changes in systemic haemodynamic variables.

Adult↗
PubMed1991

[Cerebral monitoring].

Several studies have shown that most anaesthesia-related critical incidents are due to human error. There is evidence that cerebral monitoring procedures may be of value for an early detection of cerebral hypoxia or ischaemia. Monitoring of central nervous physiology includes both evaluation of systemic parameters like arterial blood pressure, arterial PO2, PCO2, and temperature, and more specific parameters for the assessment of central nervous system function and intracranial haemodynamics. It has been suggested that parameters from the processed EEG may be used as an indicator for depth of anaesthesia. Even though anaesthetic-induced EEG alterations are unspecific, depth of anaesthesia may be assessed quantitatively by combined monitoring of general parameters and processed EEG. Interpretation of the EEG signals has to take into account that critical events like hypoxia or cerebral ischaemia results in EEG patterns similar to those seen under deep anaesthesia. Sensory evoked potentials are frequently used to monitor specific neural pathways that are at risk during surgery. Different pathways may be tested using different trigger modalities (somatosensory, auditory, visual). Changes in latencies and amplitudes of primary components may indicate impaired conduction in the pathway monitored. For operations in which monitoring of evoked responses is indicated, the anaesthetic technique should have minimal impact on latencies and amplitudes. In patients, cerebral blood flow can be monitored only at discrete time intervals. In contrast, non-invasive transcranial Doppler sonography may provide continuous information on intracranial haemodynamics. Relative changes in cerebral blood flow velocity have been shown to correlate closely to changes in cerebral blood flow. Cerebral perfusion pressure can be calculated by monitoring of intracranial pressure in patients with compromised intracranial compliance.

Anesthesia↗
PubMed1991

Dexmedetomidine improves neurologic outcome from incomplete ischemia in the rat. Reversal by the alpha 2-adrenergic antagonist atipamezole.

Dexmedetomidine is an alpha 2-adrenergic agonist that decreases central sympathetic activity and reduces the anesthetic requirement for halothane. We evaluated the effect of dexmedetomidine on neurologic and histopathologic outcome from incomplete cerebral ischemia in the rat. Anesthesia was maintained with a 25-micrograms.kg-1.h-1 fentanyl infusion combined with 70% nitrous oxide. Incomplete ischemia was produced by unilateral carotid artery ligation combined with hemorrhagic hypotension to 35 mmHg for 30 min. Arterial blood gas tensions, pH, and head temperature were maintained at normal levels during the experiment. Four ischemic groups were tested: group 1 (n = 15) received an intraperitoneal (ip) saline injection (control); group 2 (n = 10) received an ip injection of 10 micrograms/kg dexmedetomidine 30 min before ischemia; group 3 (n = 10) received 100 micrograms/kg dexmedetomidine; and group 4 (n = 10) received 100 micrograms/kg dexmedetomidine plus 1 mg/kg atipamezole (an alpha 2-adrenergic antagonist). Neurologic outcome was evaluated for 3 days using a graded deficit score. Histopathology was evaluated in coronal section in caudate and hippocampal tissue segments. Dexmedetomidine (10 and 100 micrograms/kg) significantly decreased plasma catecholamines and improved neurologic and histopathologic outcome in a dose-dependent manner compared to control rats (P less than 0.05). Atipamezole abolished the decrease in catecholamines and the improvement in outcome seen with dexmedetomidine, confirming that these effects were mediated by alpha 2-adrenergic receptors. It is concluded that alpha 2-adrenoreceptor stimulation decreases sympathetic activity and decreases ischemic injury in a model of incomplete cerebral ischemia.

Adrenergic alpha-Agonists↗
PubMed1991

Captopril improves neurologic outcome from incomplete cerebral ischemia in rats.

We investigated the effects of the angiotensin-converting enzyme inhibitor captopril on neurologic outcome in a rat model of incomplete cerebral ischemia. Twenty male Sprague-Dawley rats were anesthetized with 70% nitrous oxide in oxygen and fentanyl (10 micrograms x kg-1 i.v. bolus, 25 micrograms x kg-1 x hr-1 i.v. continuous infusion). Animals in group 1 (n = 10) received no angiotensin-converting enzyme inhibitor while animals in group 2 (n = 10) were given 10 mg x kg-1 i.v. captopril 30 minutes prior to the ischemic period. Ischemia was produced by unilateral carotid artery ligation and hemorrhagic hypotension to 35 mm Hg for 30 minutes. Body temperature, arterial blood gases, and arterial pH were maintained constant. Neurologic outcome was evaluated every 24 hours for 3 days using a graded deficit score (0, normal; 18, stroke-related death). On the third day after ischemia, captopril significantly improved neurologic outcome (median deficit score = 4) compared with controls (median deficit score = 18) (p less than 0.05). These results suggest that reduced angiotensin II levels or increased tissue kinin concentrations may decrease ischemic brain injury.

Animals↗