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R F Albrecht

Publications and source records attributed to R F Albrecht.

At least 55 records · Page 3Linked to original sources
PubMed1991

Chronic hyperglycemic diabetes in the rat is associated with a selective impairment of cerebral vasodilatory responses.

Diabetes has been reported to impair vasodilatory responses in the peripheral vascular tissue. However, little is known about vasodilatory function in the diabetic brain. We therefore studied, in the N2O-sedated, paralyzed, and artificially ventilated rat, the effects of chronic hyperglycemic diabetes on the cerebral blood flow (CBF) responses to 3 acutely imposed vasodilatory stimuli: hypoglycemia (HG) (plasma glucose = 1.6-1.9 mumol ml-1), hypoxia (HX) (PaO2 = 35-38 mm Hg), or hypercarbia HC) (PaCO2 = 75-78 mm Hg). In addition, we evaluated the somatosensory evoked potential (SSEP) and plasma catecholamine changes in rats exposed to acute glycemic reductions. Diabetes was induced via streptozotocin (STZ, 60 mg kg-1 i.p.). All results in diabetic rats were compared to those obtained in age-matched nondiabetic controls. The animals were studied at 6-8 weeks (HG experiments) or 4-6 months (HG, HX, and HC experiments) post-STZ. Values for CBF were obtained for the cortex (CX), subcortex (SC), brainstem (BS), and cerebellum (CE) employing radiolabeled microspheres. Up to three CBF determinations were made in each animal. In 6-8 week diabetics vs. controls, CBF increased to a lesser value in the CX, SC, and BS (p less than 0.05). Thus, in the diabetics, going from chronic hyperglycemia to acute hypoglycemia, CBF values (in ml 100 g-1 min-1 +/- SD) increased (p less than 0.05) from 89 +/- 22 to 221 +/- 57 in the CX, from 82 +/- 21 to 160 +/- 52 in the SC, and from 79 +/- 34 to 237 +/- 125 in the BS. In controls, going from normoglycemia to acute hypoglycemia, the CBF changes (p less than 0.05) were 128 +/- 27 to 350 +/- 219 (CX), 117 +/- 11 to 358 +/- 206 (SC), and 130 +/- 29 to 452 +/- 254 (BS). CBF changes and absolute values in the CE were similar in the two groups. At 4-6 months post-STZ, a complete loss of the hypoglycemic CBF response was found in the CX, SC, and CE. In the BS, a CBF response to hypoglycemia was seen in the diabetic rats, with the CBF increasing from 114 +/- 28 (hyperglycemia) to 270 +/- 204 ml 100 g-1 min-1 (p less than 0.05), compared to a change from 147 +/- 36 (normoglycemia) to 455 +/- 299 ml 100 g-1 min-1 (p less than 0.05) in the control group.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
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

Postischemic treatment with hypothermia improves outcome from incomplete cerebral ischemia in rats.

It is known that hypothermia can improve outcome when induced during ischemia. We evaluated whether hypothermia can decrease ischemic injury if it is induced after incomplete ischemia. Rats were anesthetized with 1.4% inspired isoflurane, and ischemia was produced by right carotid ligation combined with hemorrhagic hypotension to 30 mm Hg for 30 min. Hypothermia (31 degrees C) was induced or normothermia (37 degrees C) was maintained for 1 h after completion of the ischemic challenge. Isoflurane anesthesia was maintained during this period. Five of 15 normothermic rats and 3 of 15 hypothermic rats died of stroke after ischemia. For all rats tested, hypothermic-treated animals had a significantly better neurologic outcome than normothermic rats (p less than 0.05). Histopathology showed a correlation of r = 0.67 (p less than 0.05) with neurologic outcome, and neuronal damage was significantly worse in normothermic compared with hypothermic rats (p less than 0.05). These results show that postischemic hypothermia will decrease neuronal injury and improve neurologic outcome associated with incomplete ischemia.

Animals↗
PubMed1991

Effects of ethanol on spinal cord blood flow in the rat.

This study examines the effects of low and high concentrations of ethanol on spinal cord blood flow (SCBF) in the rat. SCBF was measured in the following blood pressure ranges: (a) <60 mm Hg, (b) 60-90 mm Hg, (c) 90-120 mm Hg, (d) 120-150 mm Hg, and (e) >150 mm Hg. Rats were anesthetized with 1.4% isoflurane in air and randomly assigned to the following treatment groups: group 1 (n = 12), intraperitoneal (i.p.) saline injection; group 2 (n = 10), 1 g/kg of ethanol i.p.; and group 3 (n = 14), 4 g/kg of ethanol i.p. Blood pressure was increased by intravenous phenylephrine infusion or lowered by a combination of intravenous trimethaphan and blood withdrawal. The SCBF was measured in cervical, thoracic, and lumbar segments using radioactive microspheres. The plasma ethanol concentration was 0 mg/ml for group 1, 0.64 +/- 0.06 mg/ml (mean +/- SEM) in group 2, and 4.18 +/- 0.11 mg/ml in group 3. In control rats, the cervical SCBF was higher than the thoracic or lumbar SCBF, evaluated over the entire blood pressure range (analysis of variance, p <0.05). This difference in regional SCBF was abolished by ethanol. Ethanol produced a significant decrease in cervical and lumbar SCBF (p <0.05) but not thoracic SCBF (p = 0.07). This decrease in SCBF was most pronounced at high blood pressures. These results suggest that ethanol produces vasoconstriction in the spinal cord that is countered by autoregulatory vasodilation at low blood pressures.

Journal Article↗
PubMed1991

Intracarotid saline infusion improves outcome from incomplete ischemia in rats.

Previous studies suggest that rheological changes associated with ischemia may produce postischemic hypoperfusion. We tested whether intracarotid or intravenous infusions of saline improve neurological outcome from incomplete cerebral ischemia in rats. Rats were anesthetized with 1.4% isoflurane in air, and ischemia was produced by unilateral carotid artery ligation combined with hemorrhagic hypotension to 30 mm Hg for 30 minutes. Intracarotid (n = 10) or intravenous (n = 10) saline infusion (0.3 ml/min) decreased hematocrit 20% compared with control rats (n = 10). Neurological outcome was significantly improved in rats infused with intracarotid (p less than 0.05) but not intravenous saline during ischemia without a change in brain temperature. Cerebral blood flow, measured in a separate study using laser Doppler flowmetry (n = 5), decreased 70% (p less than 0.01) during carotid ligation and hypotension but was not changed by intracarotid saline infusion (p greater than 0.30). These results show that perfusion of ischemic brain with saline improves outcome by factors not related to changes in hematocrit, brain temperature, or intraischemic tissue blood flow.

Animals↗
PubMed1991

Effects of sufentanil on cerebral blood flow, cerebral blood flow velocity, and metabolism in dogs.

The intracranial and systemic hemodynamic effects of sufentanil (20 micrograms/kg) were studied in 10 mongrel dogs. Baseline anesthesia was maintained with 0.7% end-tidal isoflurane and 50% nitrous oxide in oxygen. Catheters were inserted for blood pressure measurement, arterial and sagittal sinus blood sampling, radioactive microsphere injections, and intracranial pressure monitoring. Blood flow velocity was measured continuously in the middle cerebral artery using a transtemporal approach through a cranial window with a pulsed 8 MHz transcranial Doppler system (TCD). Cardiac output was measured using an electromagnetic flow probe on the pulmonary artery. After baseline measurements, sufentanil was injected and data were recorded at 5, 15, and 30 min. In group 1 (n = 5) blood pressure was not controlled, whereas in group 2 (n = 5) blood pressure was maintained at baseline levels with a phenylephrine infusion. Sufentanil decreased blood pressure from 120 +/- 10 mm Hg (mean +/- SEM) to 82 +/- 11 mm Hg in group 1. Cardiac output decreased 40%-50% in both groups. Intracranial pressure did not change. Cerebral blood flow (CBF) and TCD blood flow velocity decreased significantly (35%-40%) with no difference between groups. Relative decreases in CBF and TCD blood flow velocity were closely correlated (r = 0.82). The cerebral hemodynamic changes were associated with a 35%-40% decrease in cerebral oxygen consumption. We conclude that sufentanil decreases CBF in response to decreased metabolic demand without significantly affecting intracranial pressure. Relative changes in CBF can be reproducibly monitored using TCD.

Anesthesia, Inhalation↗
PubMed1991

Clonidine decreases plasma catecholamines and improves outcome from incomplete ischemia in the rat.

Clonidine decreases central sympathetic activity and anesthetic requirement. We tested whether clonidine improves outcome from incomplete ischemia of the brain in rats. Control rats were anesthetized with 25 micrograms.kg-1.h-1 of intravenous fentanyl and inhalation of 70% nitrous oxide (N2O). Clonidine-treated rats received fentanyl/N2O and 10 micrograms/kg of intravenous clonidine 10 min before ischemia, which was produced by right carotid ligation combined with hemorrhagic hypotension to 35 mm Hg for 30 min. Clonidine increased plasma glucose before ischemia and decreased blood catecholamine concentrations during ischemia compared with the control group. Neurologic outcome was evaluated daily for 3 days after ischemia and histopathology was performed at the end of this period. Clonidine significantly improved neurologic outcome on each of the 3 days after ischemia. Histopathology was severe in the control group but not enough rats survived in this group for statistical analysis. The authors conclude that clonidine decreases sympathetic activity during ischemia and that this is associated with an improvement in outcome from incomplete ischemia.

Animals↗
PubMed1991

Cerebral autoregulation in awake versus isoflurane-anesthetized rats.

We evaluated regional cerebral and spinal cord blood flow in rats during isoflurane anesthesia. Tissue blood flow was measured in cerebral cortex, subcortex, midbrain, and spinal cord using radioactive microspheres. Blood flow autoregulation was measured within the following arterial blood pressure ranges (mm Hg): 1 = less than 50, 2 = 50-90, 3 = 90-130, 4 = 130-170, 5 = greater than 170. Arterial blood pressure was increased using phenylephrine infusion and decreased with ganglionic blockade and hemorrhage. Three treatment groups were studied: 1 = awake control, 2 = 1.0 minimum alveolar anesthetic concentration (MAC) isoflurane, 3 = 2.0 MAC isoflurane. Autoregulation was seen in awake rats from 50 to 170 mm Hg in all tissues. The autoregulatory coefficient (change in blood flow/change in blood pressure) was increased in midbrain and spinal cord during 1.0 MAC isoflurane and in all tissues during 2.0 MAC isoflurane (P less than 0.05). Within the arterial blood pressure range of 90-130 mm Hg, isoflurane produced the following changes in tissue blood flow (percent of awake control): 1.0 MAC isoflurane: cortex = 87% +/- 8% (P greater than 0.30), subcortex = 124% +/- 11% (P greater than 0.05), midbrain = 263% +/- 20% (P less than 0.001), spinal cord = 278% +/- 19% (P less than 0.001); 2.0 MAC isoflurane: cortex = 137% +/- 13% (P less than 0.05), subcortex = 272% +/- 24% (P less than 0.001), midbrain = 510% +/- 53% (P less than 0.001), spinal cord = 535% +/- 50% (P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Inhalation↗
PubMed1990

Regional blood-brain glucose transfer and glucose utilization in chronically hyperglycemic, diabetic rats following acute glycemic normalization.

Regional rates of brain glucose utilization (rCMRglc) and glucose influx (rJin), along with regional brain tissue glucose concentrations, were measured in chronically hyperglycemic diabetic (CHD) rats following acute glycemic normalization. These results were compared to those obtained in nondiabetic normoglycemic controls. The diabetic rats were evaluated at 6-8 weeks following i.p. streptozotocin injection. All rats were N2O (70%) sedated, paralyzed, and artificially ventilated for study. Acutely normoglycemic (plasma glucose = 8.5 mumol/ml), demonstrated significantly higher (p less than 0.05) rCMRglc and rJin values in 8 of the 11 regions analyzed. Tissue/plasma glucose concentration ratios were significantly greater than control in 9 of 11 regions. Prior to acute glycemic normalization, rCMRglc values in CHD rats were either unchanged or moderately lower than control. These findings indicate that no blood-brain barrier glucose transport repression is present in CHD rats. In fact, the results suggest an increased transport capacity. The increased rCMRglc observed in the acutely normalized CHD rats may be a manifestation of the "hypoglycemic symptoms" observed in chronically hyperglycemic patients following acute glycemic reductions to the normal range. The present results imply that these symptoms are not related to the presence of a relative cerebral glucopenia, as others have suggested.

Animals↗
PubMed1990

Comparison of methohexital and isoflurane on neurologic outcome and histopathology following incomplete ischemia in rats.

Using a rat model of incomplete cerebral ischemia the effects of isoflurane (iso) and methohexital (metho) were compared with those of 70% nitrous oxide controls (N2O). Two levels of incomplete cerebral ischemia were produced by right carotid occlusion plus hypotension for 30 min: moderate = 30 mmHg, FIO2 = 0.30; severe = 25 mmHg, FIO2 = 0.20. The iso doses (1 and 2 MAC) and metho doses (0.01 and 0.1 mg.kg-1.min-1) were tested at each ischemic level. These iso and metho doses were selected because without ischemia they produced similar decreases in cerebral oxygen consumption (CMRO2) compared with that produced in N2O controls. In the absence of ischemia, the electroencephalogram (EEG) was suppressed by 0.01 mg.kg-1.min-1 metho and 1 MAC iso and showed burst-suppression with 0.1 mg.kg-1.min-1 metho and 2 MAC iso. The EEG was further depressed by ischemia under all anesthetic conditions. Neurologic outcome was evaluated for 3 days following incomplete cerebral ischemia by using a graded deficit score (0 = normal, 5 = death associated with stroke). Following moderate ischemia all four anesthetic treatments improved outcome compared with N2O controls, but after severe ischemia only 2 MAC iso significantly improved outcome. Neurohistopathology was evaluated on a scale of 0 to 40, 24 h after ischemia. The neurohistopathology score was significantly improved by all four anesthetic treatments compared with N2O following moderate ischemia and was better with 2 MAC iso compared with 0.1 mg.kg-1.min-1 metho after both moderate and severe ischemia. These results show that both iso and metho improve outcome from cerebral ischemia compared with that associated with N2O, but only 2 MAC iso resulted in an improved outcome following severe ischemia. This difference in outcome between the two anesthetics may be related to greater neuronal depression with iso, which may occur with little difference in cerebral metabolic depression.

Animals↗
PubMed1990

Brain lactate and neurologic outcome following incomplete ischemia in fasted, nonfasted, and glucose-loaded rats.

The neurologic outcomes following incomplete cerebral ischemia in rats treated by fasting, nonfasting, or glucose administration (6 ml/kg of 50% glucose solution intraperitoneal) were compared. Rats were anesthetized with 1.4% inspired isoflurane in air and incomplete ischemia was produced by temporary unilateral carotid occlusion and hypotension of 30 mmHg for 30 min. The rats were recovered and neurologic outcome was scored every 8 h for 3 days using a 6-point scale ranging from 0 (normal) to 5 (death associated with stroke). Brain histopathology was scored using a four-point scale on 19 of 30 rats surviving the 3-day postischemic neurologic examination and was correlated with neurologic deficit scores. Fasted rats had plasma glucose concentrations of 79 +/- 7 mg/100 ml (mean +/- SE) during ischemia and a significantly better neurologic outcome (P less than 0.001) than glucose-loaded rats (plasma glucose = 496 +/- 43 mg/100 ml). Nonfasted rats had blood glucose values (292 +/- 28 mg/100 ml) and deficit scores not significantly different from fasted but better than glucose-loaded rats (P = 0.054). Brain histology showed the greatest neuronal damage in caudate followed by hippocampus and cortical tissue. Histopathologic evaluation showed a correlation of r = 0.87 (P less than 0.01) with neurologic outcome. In separate experiments brain samples were collected at the end of the ischemic period in each of the experimental groups and regional tissue lactate and brain phosphocreatine and adenosinetriphosphate (ATP) concentrations were measured. Ischemic tissue lactate was similar in fasted, nonfasted, and glucose-loaded rats in caudate and hippocampus but was significantly higher in glucose loaded rats in cortical and thalamic tissue.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed1990

Cerebrovascular and cerebral metabolic effects of N2O in unrestrained rats.

There is controversy about whether N2O increases cerebral blood flow and cortical oxygen consumption (CMRO2) in rats. Cortical and subcortical blood flow and CMRO2 were measured in awake, unrestrained rats while awake and during 70% N2O administration using radioactive microspheres. In the awake state, cortical and subcortical blood flow were 126 +/- 10 and 98 +/- 7 ml.100 g-1.min-1, respectively, and CMRO2 (cortical) was 10.0 +/- 0.6 ml O2.100 g-1.min-1 (mean +/- SE). After 15 min of 70% N2O, cortical and subcortical blood flow increased 100% and 40%, respectively, while CMRO2 did not increase significantly. Cerebral blood flow remained increased after 60 min of N2O exposure, and CMRO2 did not change. These results show that N2O produces cerebrovasodilation in rats that is not related to a change in metabolic demand. Plasma catecholamines do not change during N2O administration, indicating that the increase in blood flow is not due to a general stress response.

Anesthesia, Inhalation↗
PubMed1990

Ganglionic blockade improves neurologic outcome from incomplete ischemia in rats: partial reversal by exogenous catecholamines.

The authors investigated the effects of nitrous oxide (N2O), ganglionic blockade, and combined infusion of epinephrine and norepinephrine (0.1 microgram.kg-1.min-1 each) on neurologic outcome and brain histopathology in a model of incomplete cerebral ischemia in the rat. Thirty-eight Sprague-Dawley rats were assigned to one of four groups: group 1 (n = 10) received 70% N2O in O2; group 2 (n = 12) received 70% N2O in O2, plus ganglionic blockade; and group 3 (n = 10) received 70% N2O in O2, plus ganglionic blockade and catecholamine infusion. In groups 1-3, ischemia was produced by right carotid occlusion combined with hemorrhagic hypotension (35 mmHg) for 30 min. Group 4 (n = 6) received 70% N2O in O2 and hemorrhagic hypotension without carotid occlusion for 30 min. At the end of ischemic and nonischemic hypotension, the carotid artery was unclamped and the blood slowly reinfused. Neurologic outcome was evaluated for a 5-day period with a graded deficit score (0 = normal to 39 = stroke-related death). Brain histopathology was evaluated in coronal section at the level of the caudate nucleus according to a 6-point scale, from 0 = normal to 5 = total hemispheric infarction. Arterial blood gases, pH, and body temperature were kept constant in all groups. Compared to N2O alone (group 1), treatment with ganglionic blockade (group 2) decreased plasma catecholamines by 75% and significantly improved neurologic outcome from incomplete cerebral ischemia (P less than 0.05). Administration of exogenous epinephrine and norepinephrine in the presence of N2O and ganglionic blockade (group 3) worsened neurologic outcome compared to group 2 (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Brain glucose utilization and transport and cortical function in chronic vs. acute hypoglycemia.

We compared regional brain capillary permeability-surface area products for glucose transfer (PSin), cerebral glucose utilization (rCMRGlc) rates, and brain tissue glucose levels (GlCbr) in N2O-sedated, paralyzed, and artificially ventilated rats during normoglycemia (NG), insulin-induced acute hypoglycemia (AH), or chronic hypoglycemia (CH) [hypoglycemic plasma glucose (Glcp) = 2.2-2.3 mumol/ml]. In addition, a comparative assessment of brain function in AH vs. CH was performed employing somatosensory-evoked response (SSER) technology. A double-label (3H and 14C) 2-deoxy-D-glucose method was used for the simultaneous assessment of PSin and rCMRGlc. Compared with normoglycemic controls, AH resulted in significant 40-50% reductions in rCMRGlc in 10 of 11 regions analyzed (cerebellum unchanged). In CH vs. AH, significantly higher values for rCMRGlc, Glcbr/Glcp ratios, and PSin were seen in 8, 8, and 5 regions, respectively. No differences in rCMRGlc were observed when comparing CH vs. NG groups. Furthermore, CH rats were able to sustain normal SSER at levels of hypoglycemia (1.5 mumol/ml) that, when imposed acutely, resulted in attenuated SSER. Thus CH is associated with an enhanced blood-brain glucose transport capacity in many (but not all) brain regions. This in turn increases rCMRGlc and improves the general cerebral function compared with that seen during AH.

Acute Disease↗
PubMed1990

Hypothermia versus ethanol: neurologic outcome after incomplete cerebral ischemia in midazolam-anesthetized rats.

We examined neurologic outcome after incomplete cerebral ischemia in rats treated with hypothermia versus ethanol, two techniques that decrease brain metabolism. All animals, including control rats, received a baseline midazolam anesthetic. Ischemia was produced by right carotid artery occlusion combined with hemorrhagic hypotension to a mean arterial pressure of 30 mm Hg for 30 min. Neurologic outcome was evaluated for 3 days after ischemia using a 5-point scale. In separate studies, cerebral blood flow (CBF) was measured using radioactive microspheres, and cortical oxygen consumption (CMRO2) was calculated from the blood flow data and the arteriovenous oxygen difference. Hypothermia to 31 degrees C decreased CBF 50% and CMRO2 52% compared with control rats, and significantly improved outcome. Although ethanol decreased CBF 35% and CMRO2 22%, it did not improve outcome from stroke compared with control rats. These results suggest that hypothermia protects the brain from ischemia and that ethanol does not, despite a decrease in CMRO2.

Journal Article↗
PubMed1989

Cerebral mitochondrial respiration in diabetic and chronically hypoglycemic rats.

The respiratory function of cerebral mitochondria harvested from genetically diabetic (BB/W) and streptozotocin-diabetic rats deprived of insulin for 3-4 weeks was found to be unchanged from control values. Furthermore, insulin-deprived BB/W rats subjected to 30 min of insulin-induced hypoglycemic coma demonstrated a normal mitochondrial respiration following a 60 min period of glucose restitution, a finding consistent with earlier results in non-diabetic rats. However, in rats exposed to 1 week of moderate hypoglycemia (plasma glucose = 3.0 mumol.ml-1), both state 3 respiration and the respiratory control ratio (RCR) were reduced from control. In fact, when the chronic hypoglycemia was imposed following a 3-4 week period of diabetic hyperglycemia, the state 3 rate and RCR were found to be reduced to a greater degree than in chronically hypoglycemic, non-diabetic, previously normoglycemic rats. Finally, when 1 week of moderate hypoglycemia preceded a 30 min period of insulin-induced hypoglycemic coma, a disturbed pattern of mitochondrial respiration (i.e. increased state 4, decreased RCR) was found at 60 min of recovery following coma. These results indicate that chronic increases in glucose (and insulin deprivation) have no effect on cerebral mitochondrial respiratory function, whereas prolonged, albeit moderate, reductions in cerebral glucose supply result in perturbations in mitochondrial respiration. These results demonstrate the importance of an adequate glucose supply for normal mitochondrial activity.

Animals↗
PubMed1989

The interaction of nitrous oxide and isoflurane with incomplete cerebral ischemia in the rat.

In rats with incomplete cerebral ischemia the effects of 70% N2O alone, isoflurane alone (0.5 and 1 MAC), and the combination of N2O + isoflurane on neurologic outcome, neurohistopathology, and EEG were compared. Moderate and severe ischemia were produced by right carotid artery occlusion combined with hemorrhagic hypotension (moderate ischemia, MAP = 30 mmHg, FIO2 = 0.30; severe ischemia, MAP = 25 mmHg, FIO2 = 0.20). Neurologic outcome was evaluated using a graded deficit score from 0 to 5 (0 = normal, 5 = death associated with stroke), and neurohistopathology was evaluated using a 40-point scale from 0 = normal to 40 = total hemisphere infarct at the level of the caudate nucleus in coronal section. Compared with N2O alone, isoflurane (0.5 and 1 MAC) improved neurologic outcome following moderate ischemia (P less than 0.05). Isoflurane also decreased histopathologic damage following moderate ischemia (N2O control = 33 +/- 1 vs. 0.5 MAC isoflurane = 11 +/- 4 and 1 MAC isoflurane = 12 +/- 3, P less than 0.05), whereas only 0.5 MAC isoflurane decreased histopathologic damage following severe ischemia (N2O control = 38 +/- 1 vs. 0.5 MAC isoflurane = 25 +/- 5; P less than 0.05) Adding N2O to 0.5 MAC isoflurane attenuated the neurologic protective effect of isoflurane alone and increased histopathologic damage following both moderate and severe ischemia (moderate = 23 +/- 5, severe = 37 +/- 2; both P greater than 0.05 compared with N2O controls). The effect of adding 70% N2O to isoflurane on cerebral blood flow (CBF) and cerebral oxygen consumption(CMRO2) was also evaluated.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Inhalation↗