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M M Todd

Publications and source records attributed to M M Todd.

At least 91 records · Page 5Linked to original sources
PubMed1991

Differences in cerebral blood flow between alpha-stat and pH-stat management are eliminated during periods of decreased systemic flow and pressure. A study during cardiopulmonary bypass in rabbits.

Prior reports suggest cerebral blood flow (CBF) responses to changing bypass (systemic) flow rates may differ between alpha-stat and pH-stat management. To compare the effect of blood gas management upon CBF responses to changing systemic flow and pressure, 15 New Zealand White rabbits, anesthetized with fentanyl and diazepam, underwent nonpulsatile cardiopulmonary bypass at 25 degrees C. One group of animals (n = 8) was randomized to alpha-stat blood gas management that maintained arterial carbon dioxide tension (PaCO2) approximately 40 mmHg when measured at 37 degrees C. A second group (n = 7) was managed with pH-stat technique, maintaining PaCO2 approximately 40 mmHg when corrected to the animal's actual temperature. Bypass was initiated at a flow rate of 100 ml.kg-1.min-1 and, after approximately 20 min, control hemodynamic and CBF measurements (radioactive microspheres) were made. Thereafter, bypass flow rate was changed in random order at 15-min intervals to 50, 70, and 100 ml.kg-1.min-1. CBF and hemodynamic measurements were repeated at the end of each period of altered bypass flow. Groups differed significantly with respect to both pHa and PaCO2. There were no significant differences between groups with respect to bypass flow rate, mean arterial pressure (MAP), central venous pressure, temperature, hematocrit, arterial oxygen tension (PaCO2), or bypass duration at any measurement point. MAP decreased significantly, from approximately 80 to approximately 65 mmHg with decreasing bypass flow (P = 0.0001). Over the entire range of bypass flows, CBF decreased with decreasing bypass flow (P = 0.001), and the degree of change was equivalent among regions and between groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Cerebral blood flow response to PaCO2 during hypothermic cardiopulmonary bypass in rabbits.

Differences in cerebral blood flow (CBF) between alpha-stat and pH-stat management depend on preserved responsiveness of the cerebral vasculature to changes in arterial carbon dioxide tension (PaCO2). We tested the hypothesis that hypothermia-induced reductions in CBF would decrease the CBF response to changing PaCO2 (delta CBF/delta PaCO2). Anesthetized New Zealand white rabbits were randomly assigned to one of three temperature groups--group 1 (37 degrees C, n = 9); group 2 (31 degrees C, n = 10); or group 3 (25 degrees C, n = 10)--and were cooled using cardiopulmonary bypass. After esophageal temperature equilibration (approximately 40 min), oxygenator gas flows were serially varied to achieve PaCO2 values of 20, 40, and 60 mm Hg (temperature-corrected). All animals were studied at all three PaCO2 levels in random order. At each level of PaCO2, CBF and masseter blood flow were determined using radiolabeled microspheres. There were no significant differences between groups with respect to mean arterial pressure (approximately 80 mmHg), central venous pressure (approximately 4 mmHg), or hematocrit (approximately 22%). Prior normothermic studies have found delta CBF/delta PaCO2 to be proportional to CBF. Nevertheless, in this study, with hypothermia-induced reductions in CBF, delta CBF/delta PaCO2 was not significantly different between temperature groups. Thus, hypothermia either increased the sensitivity of the cerebral vasculature to carbon dioxide and/or increased the effective level of cerebrospinal fluid respiratory acidosis produced by each increment of temperature-corrected PaCO2.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Secondary hypotensive insults in a rat forebrain ischemia model.

Previous studies have shown that the recently injured brain has an increased sensitivity to subsequent brief episodes of severe ischemia. This investigation was designed to assess whether less severe secondary insults, which alone would be incapable of producing injury, exacerbate brain damage resulting from a primary episode of global ischemia. Rats were subjected to either 10 min of 2-vessel forebrain ischemia (primary insult alone), 20 min of hypotension (mean arterial pressure, MAP = either 40 or 25 mmHg) without vessel occlusion (secondary insult alone), or 10 min ischemia followed 1 h later by the hypotensive challenge (primary + secondary insult). Seven days later, the animals were neurologically evaluated and the brains then prepared for histologic analysis. Neither magnitude of secondary insult alone was found to produce injury. In contrast, the primary insult alone caused moderate damage in the hippocampus, caudoputamen and neocortex. With the exception of increased neuronal necrosis in the hippocampal CA1 sector in rats receiving the primary + secondary insult (MAP = 25 mmHg), no worsening of outcome could be attributed to the secondary insults. These results indicate that the recovering brain may not be as sensitive to hypoperfusion as has previously been suggested.

Animals↗
PubMed1990

Effects of nitrous oxide on cerebral metabolic rate in rats anaesthetized with isoflurane.

It has been demonstrated in several species that a significant increase in cerebral blood flow (CBF) occurs when nitrous oxide is added to a volatile anaesthetic. This blood flow response could result from an increase in cerebral metabolic rate or from a direct effect of nitrous oxide on cerebral vessels. To investigate this, the cerebral metabolic rate for glucose (CMRglu) was determined autoradiographically in rats receiving isoflurane anaesthesia with or without nitrous oxide. An increase in anaesthetic depth from 0.5 to 1.0 MAC achieved with isoflurane alone caused a significant reduction in CMRglu (52 (SD11) mumol/100 g min-1 vs 39 (8)mumol/100 g min-1). In contrast, the addition of 70% nitrous oxide (0.5 MAC) to 0.5 MAC isoflurane anaesthesia (1 MAC total) left CMRglu unchanged (54 (4) mumol/100 g min-1). We conclude that 70% nitrous oxide does not alter cerebral metabolic rate when administered with 0.5 MAC isoflurane. Because CBF increases substantially under very similar conditions, our data indicate that the CBF effects of nitrous oxide, when administered with a volatile agent, were direct and mediated by factors other than changes in cerebral metabolic rate.

Anesthesia↗
PubMed1990

The influence of halothane, isoflurane, and pentobarbital on cerebral plasma volume in hypocapnic and normocapnic rats.

Cerebral blood volume (CBV = cerebral plasma volume [CPV] + cerebral red cell volume [CRBCV]) is one determinant of intracranial pressure. In an effort to quantitate the effects of anesthetics and PaCO2 on CBV, the authors measured cerebral plasma volume (CPV) in normocapnic (PaCO2 approximately 42 mmHg) and hypocapnic (PaCO2 approximately 22 mmHg) rats receiving 1 MAC doses of isoflurane or halothane, or given an approximately equivalent dose of pentobarbital. All animals were paralyzed, their lungs mechanically ventilated, and body temperature kept normal throughout the study. CPV was measured using 14C-labeled dextran, a large (70,000 molecular weight [M.W.]), nondiffusible compound that was given intravenously and allowed to circulate for approximately 5 min. The experiments then were terminated by freezing the brains in situ with liquid N2 poured into a funnel affixed to the exposed calvarium. Isotope concentrations in solubilized brain and in plasma were determined by scintillation counting, and CPV was calculated as the ratio between these values. CPV during both hypocapnic and normocapnic pentobarbital anesthesia was less than with either volatile agent. During normocapnia, CPV for pentobarbital = 2.1 +/- 0.26 ml/100 g (mean +/- SD, n = 8), compared with 2.96 +/- 0.44 ml/100 g (n = 9) and 3.06 +/- 0.44 ml/100 g (n = 9) for halothane and isoflurane, respectively. There were no differences in CPV between the two volatile agents during normocapnia.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Nitrous oxide does not alter infarct volume in rats undergoing reversible middle cerebral artery occlusion.

This experiment was designed to determine if nitrous oxide alters neurologic and pathologic outcome from temporary focal cerebral ischemia in spontaneously hypertensive rats deeply anesthetized with a barbiturate. Two groups of rats were given intravenous methohexital such that a stable EEG pattern of burst suppression was achieved. In one group of rats (n = 11), the lungs were mechanically ventilated with 70% N2O/30% O2, and in the other group (n = 10), ventilation was done with 70% nitrogen/30% O2. The middle cerebral artery was then occluded for 2 h, during which time mean arterial pressure, blood gases, hematocrit, plasma glucose, and head temperature were held constant between groups. The total doses of methohexital administered were similar in both groups as were the plasma methohexital concentrations immediately prior to onset of ischemia. After reperfusion of the middle cerebral artery, the animals were allowed to awaken. Neurologic evaluations were performed prior to ischemia and at 24 and 96 h postischemia. Cerebral infarct volume was measured at 96 h postischemia using triphenyl tetrazolium chloride staining and computer imaging techniques. There were no neurologic differences between the N2O and nitrogen groups at any experimental interval although both groups exhibited deficits at both 24 and 96 h postischemia relative to preischemic values. The two groups also had nearly identical cerebral infarct volumes (N2O = 231 +/- 97 mm3; nitrogen = 226 +/- 75 mm3; mean +/- SD).(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Inhalation↗
PubMed1990

Differential effect of oncotic pressure on cerebral and extracerebral water content during cardiopulmonary bypass in rabbits.

To study the effect of oncotic pressure on brain water content during cardiopulmonary bypass (CPB), 14 anesthetized New Zealand White rabbits underwent 60 min of nonpulsatile CPB at normothermia. Animals were grouped according to the composition of the circuit priming fluid. Group 1 animals (n = 7) received a priming fluid (6.5% hydroxyethyl starch in 0.72 N NaCl; 323 +/- 13 mOsm/kg [mean +/- SD]) that maintained normal colloid oncotic pressure (COP) during CPB (19.0 +/- 1.5 mmHg). Group 2 animals (n = 7) received a priming fluid (0.9 N NaCl; 324 +/- 23 mOsm/kg) that led to a hypooncotic state (COP = 6.2 +/- 1.2 mmHg). Blood chemistries and hemodynamics were recorded every 15 min during CPB. Animals were given additional priming fluid and sodium bicarbonate during CPB to maintain a circuit flow of 85 ml.kg-1.min-1 and arterial pH greater than 7.35. There were no significant differences between groups 1 and 2 with respect to temperature, central venous pressure, mean arterial pressure, PaO2, PaCO2, plasma sodium concentration, or osmolality at any time during CPB, although osmolality increased in both groups. After 60 min of bypass, animals were killed and organ water contents were determined by wet/dry weight ratios. A separate group of nine similarly prepared and anesthetized animals that did not undergo cannulation or CPB also underwent measurement of plasma chemistries and tissue water contents and served as nonbypass controls (group 3). Brain and kidney water contents were unaffected by oncotic pressure, whereas duodenum and skeletal muscle had significantly greater water content (P = 0.003 and P = 0.008, respectively) after hypooncotic CPB.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Anesthesia for craniotomy: a double-blind comparison of alfentanil, fentanyl, and sufentanil.

Using a prospective, randomized, and double-blind study design, alfentanil (n = 15), fentanyl (n = 14), or sufentanil (n = 16), in combination with N2O, were administered to patients undergoing craniotomy for supratentorial tumor resection. Physicians were given two syringes, one of which was labeled as "load" for the initial loading dose and the other as "maintenance" for continuous infusion. The concentration of drug in each syringe was adjusted to permit administration on a milliliter per kilogram basis. The target loading doses for alfentanil, fentanyl, and sufentanil were 75, 10, and 1 microgram/kg, respectively, and initial infusion rates were 33.5, 2.0, and 0.3 microgram.kg-1.h-1, respectively. Additional supplementary boluses and changes in maintenance infusion rate were made according to predetermined guidelines. Isoflurane, in increasing 0.2% inspired increments, was used only when the maximum allowed opioid dose had been given (i.e., supplementary bolus doses equal to 75% of the calculated loading dose or supplementary bolus doses equal to 50% of the calculated loading dose combined with a 50% increase in the maintenance infusion rate). Opioid infusions were stopped at the time of bone flap replacement. Antihypertensive medications and naloxone were subsequently given at the discretion of the anesthesiologist. Group demographics were not different. Total volumes of drug were similar among groups indicating equipotent preparations. Administration of isoflurane, antihypertensive medications, and naloxone were not different among groups. Although decreases in blood pressure seen with induction were similar among groups, alfentanil-treated patients received ephedrine more frequently before intubation. Thirty minutes after entry into the postanesthesia recovery area, respiratory rate and pH were lowest in sufentanil-treated patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Spinal cord blood flow in response to focal compression.

Anesthetized sheep were subjected to spinal cord compression to 200 mm Hg at T13 by means of a distensible epidural balloon. Eight animals were subjected to compression for 20 min, 10 animals for 40 min, and 12 animals for 80 min. Spinal cord blood flow (SCBF) and spinal evoked potentials (SEPs) from L7 to C7 and vice versa were measured prior to, during, and 1/2, 1 1/2, 2 1/2, and 3 1/2 h following compression. The traumatized zone manifested a hyperemic response subsequent to balloon withdrawal in the 20-min and 40-min groups. In the 80-min group, SCBF returned to baseline. With compression, SEPs were obliterated in all animals and failed to recover after 3 1/2 h following injury, irrespective of the duration of compression. These results show that reperfusion of the cord following a compressive insult is not accompanied with recovery of SEPs.

Acute Disease↗
PubMed1989

The role of cerebral metabolism in determining the local cerebral blood flow effects of volatile anesthetics: evidence for persistent flow-metabolism coupling.

The effects of equipotent doses of halothane (1.05%) versus isoflurane (1.38%) anesthesia on CMRglc were determined autoradiographically using the 2-[14C]deoxyglucose technique in the rat. Eight anatomically standardized coronal sections were selected and digitized from the autoradiographs. Mean CMRglc was determined for hemispheric, neocortical, and subcortical regions at each anatomic level, and a neocortical/subcortical CMRglc ratio was calculated. In addition, the current CMRglc autoradiographs, as well as previous CBF autoradiographs obtained under identical experimental conditions were examined to characterize and compare flow/metabolism relationships for the two anesthetics. For this analysis, CBF was determined in 80 selected anatomic areas, and the values from each area were plotted against CMRglc values obtained from identical areas. In all major regions, mean CMRglc was greater with halothane than with isoflurane. The neocortical/subcortical ratio, reflecting the pattern of CMRglc distribution, was also greater during halothane anesthesia. This suggests that isoflurane has a disproportionate effect on neocortical metabolism resembling patterns previously seen for CBF. Analysis of CBF versus CMRglc plots for each anesthetic group showed two parallel lines with nearly identical slopes, but different Y intercepts. We conclude that the distribution of CMRglc observed during 1 MAC (minimum alveolar concentration) halothane and isoflurane anesthesia parallels the distribution of CBF. This finding supports the conclusion that flow-metabolism coupling is intact during halothane and isoflurane anesthesia, and that drug induced changes in cerebral metabolism may play an important role in determining the CBF response to that drug. Furthermore, there is evidence that, at a given level of CMRglc, isoflurane may have greater vasodilating capabilities than halothane.

Anesthesia↗
PubMed1989

Effects of nitrous oxide and volatile anaesthetics on cerebral blood flow.

Nitrous oxide and halogenated anaesthetic agents are often administered concurrently during neuroanaesthesia. To assess the interactive effects of these agents on cerebral blood flow (CBF), we have measured CBF by 14C-iodoantipyrine autoradiography, in normocapnic rats receiving either 0.5 or 1.0 MAC of volatile agent alone (halothane or isoflurane) or 0.5 MAC of volatile agent + 0.5 MAC nitrous oxide. CBF (global and regional) was significantly greater at 1.0 MAC compared with 0.5 MAC, regardless of how 1.0 MAC was achieved (agent alone or agent + nitrous oxide) (P less than 0.05). The addition of 0.5 MAC nitrous oxide to 0.5 MAC halothane resulted in flows similar to those produced by 1.0 MAC halothane alone. In contrast, the addition of nitrous oxide to 0.5 MAC isoflurane resulted in flow values significantly greater than those measured during 1.0 MAC isoflurane alone. We conclude that the use of nitrous oxide, as opposed to an increased dose of volatile agent, has no advantage in respect of minimizing anaesthetic-induced increases in cerebral blood flow.

Anesthesia, Inhalation↗
PubMed1989

Prolonged reduction in colloid oncotic pressure does not increase brain edema following cryogenic injury in rabbits.

The effects of an 8-h period of reduced colloid oncotic pressure (COP) on cerebral edema formation following cryogenic brain injury were studied in 24 normothermic, normocarbic rabbits. Anesthesia was induced with halothane and catheters inserted to permit the monitoring of arterial, right atrial, and intracranial pressures (MAP, CVP, and ICP, respectively). When surgery was complete, halothane was discontinued, 40 mg/kg of pentobarbital was given iv, and ventilation continued with 66% N2O/balance O2. A left parietal cryogenic injury was then produced using liquid N2, and the animals assigned to one of three groups. In group 1 (Control, n = 8), only maintenance lactated Ringer's solution (LR) was given for the remainder of the study. Beginning 30 min after injury, animals in the other two groups (n = 8 each) underwent 45 min of plasmapheresis (arterial phlebotomy, with packed cells returned). In group 2 (Iso-COP) separated plasma was replaced with 6% hetastarch in LR, while in group 3 (Hypo-COP), plasma was replaced with LR alone. In both groups, the volume of fluid given was adjusted to maintain MAP and CVP at baseline values. After plasmapheresis, animals subsequently received only maintenance LR. Eight and one-half hours after the injury (8 h after the start of plasmapheresis), animals were killed and the brains removed. Regional tissue specific gravities (SpGr) and water contents (%H2O) were measured respectively by microgravimetry and drying. In addition, the %H2O of samples of skeletal muscle and small bowel were determined to assess peripheral edema formation. There were no important intergroup differences in MAP, CVP, ICP, blood gases, or osmolality at any time.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

A comparison of the effects of halothane, isoflurane, and pentobarbital anesthesia on intracranial pressure and cerebral edema formation following brain injury in rabbits.

To evaluate the impact of anesthetics on the evolution of a cerebral injury, 33 rabbits were subjected to a cryogenic brain lesion, followed by 10 h of anesthesia with 1 MAC halothane or isoflurane (n = 11 each) or with an equipotent dose of pentobarbital (n = 11). The lungs were ventilated to a PaCO2 = 30-35 mmHg with O2/air and normothermia was maintained. Intracranial pressure (ICP), mean arterial pressure (MAP), central venous pressure (CVP), arterial blood gases, and pH, osmolality, and other blood chemistries were recorded. Fifteen minutes after surgery, a left parietal injury was produced with liquid N2. A MAP greater than 70-75 mmHg was maintained throughout the study, using angiotensin II as needed, and CSF was removed if severe intracranial hypertension (ICP greater than 30 mmHg) threatened to reduce cerebral perfusion pressure (CPP = MAP-ICP) below 40 mmHg. 10 h after injury, the animals were killed, and edema formation assessed by: A) the wet weight of the two hemispheres; B) water content (%H2O; wet-dry weight) of the posterior aspect of the hemispheres; and C) specific gravity (SpGr) of tissue samples taken adjacent to and distant from the lesion. Animals given pentobarbital had higher MAP's until 3 h after the lesion had been induced. There were no subsequent intergroup differences in MAP, and no differences at any time in CVP, PaO2, PaCO2, pH, total fluids, or urine output. ICP increased in all animals, but with no significant intergroup differences (ICP in halothane animals was numerically lower). There were no clear differences in the incidence of ventricular drainage (1 halothane, 5 isoflurane, 3 pentobarbital; P = 0.16). In spite of CSF drainage and angiotensin, CPP

Anesthesia↗
PubMed1989

EEG changes during carotid occlusion and hypotension in the rat: the effects of nitrous oxide.

It has been suggested that N2O may alter the sensitivity of the brain to ischemia. To test this hypothesis. we examined the effects of N2O on the development of left-right hemispheric asymmetry in the electroencephalogram (EEG) during hemorrhagic hypotension in rats subjected to unilateral carotid occlusion. Rats were anesthetized with halothane/O2/air, and ventilated to normocarbia (PaCO2 approximately 40 mm Hg). Catheters were placed in the femoral artery and vein, and both common carotid arteries (CCA) were exposed. Bilateral fronto-occipital screws were then placed to record left and right hemispheric EEGs, which were processed by computer and stored on disc. Animals were then randomly assigned to one of three treatment groups (n = 8 each): group 1, 0.5 MAC (0.5%) halothane + 0.5 MAC (70%) N2O; group 2, 1 MAC (1.0%) halothane + 70% nitrogen; and group 3, 1 MAC halothane + 70% N2O. After stabilization, the left CCA were occluded. Animals with EEG changes at this point were discarded. Beginning 5 min later, venous blood withdrawal was started at a rate of 0.25 ml/min, while mean arterial blood pressure (MAP) and EEG were continuously recorded. After exsanguination was complete, EEG data (raw and processed) were re-examined by an individual who was unaware of the anesthetics administered to determine the MAP at which any evidence of EEG asymmetry appeared. There were no intergroup differences in weight, PaO2, PaCO2, pHa, blood glucose. hematocrit, or starting (prebleed) MAP. The earliest change in the EEG was typically a decrease in total amplitude over the hemisphere ipsilateral to the carotid occlusion. Adding 70% N2O to a 1 MAC halothane background (group 2 vs. group 3) had no effect on the MAP at which this EEG asymmetry appeared (54 +/- 13 vs. 53 +/- 10 mm Hg). However, this MAP was significantly higher in animals breathing 0.5 MAC halothane + 0.5 MAC N2O (group 1, 78 +/- 17 mm Hg, p = 0.0019 by ANOVA). We conclude that 70% N2O had no direct effects on the MAP at which EEG abnormalities appear (group 2 vs. 3), and that the observed differences are more closely related to the concentration of volatile agent. Whether these differences are related to anesthetic-induced differences in the brain's tolerance to reduced CBF or whether there are differences in cerebral blood flow (CBF) autoregulation are unknown.

Journal Article↗
PubMed1989

Distribution of cerebral blood flow during deep isoflurane vs. pentobarbital anesthesia in rats with middle cerebral artery occlusion.

While previous studies have identified a protective effect for barbiturate anesthesia during focal cerebral ischemia, no such effect has been demonstrated for isoflurane. To better understand the effects of these anesthetics on cerebral blood flow and metabolism that might have relevance to their respective potential for cerebral protection, fasted physiologically stable rats underwent autoradiographic determination of CBF and CMRglu during deep isoflurane or pentobarbital anesthesia (burst suppression of EEG). As expected, cerebral blood flow was significantly greater during isoflurane anesthesia (isoflurane = 157 +/- 18 and pentobarbital = 54 +/- 12 ml/100 g/min) while CMRglu values were nearly identical (isoflurane = 35 +/- 5 and pentobarbital = 33 +/- 4 mumol/100 g/min). Additional identically anesthetized rats underwent middle cerebral artery occlusion with CBF autoradiographically determined 1 h later. While the insult resulted in a significant reduction in the ipsilateral hemispheric and cortical blood flow in both anesthetic groups, flow remained at least twofold greater in isoflurane as opposed to pentobarbital-anesthetized rats. When regional flow was assessed, no difference between groups was observed with respect to the area of tissue with flow values falling between 0-10 ml/100 g/min. In contrast, isoflurane-anesthetized rats had significantly less hemispheric and cortical area with flow values in the ranges of 10-20 and 20-30 ml/100 g/min, respectively. These data, therefore, do not support the contention that isoflurane causes maldistribution of CBF during focal ischemia.

Journal Article↗
PubMed1989

Effects of elevated plasma magnesium versus calcium on cerebral ischemic injury in rats.

Both Mg2+ and Ca2+ have been implicated as having roles in the pathomechanisms of cerebral ischemia. To further study the effects of these ions on postischemic histologic outcome, fasted rats were given one of three intravenous infusions: 5.0 mmol/kg MgCl2, 5.0 mmol/kg MgCl2 + 0.035 units/kg regular insulin, or 1.0 mmol/kg CaCl2. This resulted in elevated plasma Mg2+ or Ca2+ concentrations in the corresponding groups. A fourth group received 0.9% NaCl (saline). Preinfusion plasma glucose concentration was similar for all groups and was unchanged after infusion in rats receiving either saline or MgCl2 + insulin. In contrast, postinfusion glucose concentration was increased in the MgCl2 group (p less than 0.001) and decreased in the CaCl2 group (p less than 0.001) relative to saline-treated rats. Following respective infusions, all rats underwent 10 minutes of reversible forebrain ischemia (bilateral carotid artery occlusion and systemic hypotension) followed by 7 days' recovery. Six of 12 CaCl2-treated rats died 2-3 days after ischemia; all other rats remained neurologically indistinguishable, without gross neurologic deficits. Histologic injury in the neocortex and caudate was moderate in all groups. In the hippocampus, MgCl2 + insulin resulted in 66 +/- 6% (mean +/- SD) dead CA1 pyramidal cells, which was similar to the amount in saline-treated rats (68 +/- 10%). Injury was increased in the MgCl2 group (79 +/- 4% dead cells), while in surviving CaCl2-treated rats, injury was decreased (54 +/- 13%). We conclude that the increased injury in MgCl2-treated rats and the decreased injury noted in surviving rats receiving CaCl2 are due to the plasma glucose concentrations present prior to ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗