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O Alonso

Publications and source records attributed to O Alonso.

At least 37 records · Page 2Linked to original sources
PubMed1998

Posttraumatic cerebral ischemia after fluid percussion brain injury: an autoradiographic and histopathological study in rats.

OBJECTIVES: Mild-to-moderate reductions in local cerebral blood flow (ICBF) have been reported to occur in rats after moderate (1.7-2.2 atm) fluid percussion brain injury. The purpose of this study was to determine whether evidence for severe ischemia (i.e., mean ICBF < 0.25 ml/g/min) could be demonstrated after severe brain injury. In addition, patterns of indium-labeled platelet accumulation and histopathological outcome were correlated with the hemodynamic alterations. METHODS: Sprague-Dawley rats (n = 23), anesthetized with halothane and maintained on a 70:30 mixture of nitrous oxide:oxygen and 0.5% halothane, underwent normothermic (37 degrees C) parasagittal fluid percussion brain injury (2.4-2.6 atm). Indium-111-tropolone-labeled platelets were injected 30 minutes before traumatic brain injury (TBI), while 14C-iodoantipyrine was infused 30 minutes after trauma for ICBF determination. Sham-operated animals (n = 8) underwent similar surgical procedures but were not injured. For histopathological analysis, traumatized rats (n = 5) were perfusion-fixed 3 days after TBI. RESULTS: In autoradiographic images of indium-labeled platelets, abnormal platelet accumulation that was most pronounced overlying the pial surface was commonly associated with severe reductions in ICBF within underlying cortical regions 30 minutes after TBI. For example, within the lateral parietal cortex, ICBF was significantly reduced from 1.67 +/- 0.11 ml/g per minute (mean +/- standard error of the mean) in sham-operated animals to 0.23 +/- 0.03 ml/g per minute within the traumatized group. In addition to focal severe ischemia, moderate reductions in ICBF were detected throughout the traumatized hemisphere, including the frontal and occipital cortices, hippocampus, thalamus, and striatum. Mild decreases in ICBF were also observed throughout the contralateral cerebral cortex. At 3 days after severe TBI, histopathology demonstrated intracerebral and subarachnoid hemorrhage associated with cerebral contusion and selective neuronal necrosis. CONCLUSION: These data indicate that multiple cerebrovascular abnormalities, including subarachnoid hemorrhage, focal platelet accumulation, and severe ischemia, are important early events in the pathogenesis of cortical contusion formation after TBI. Injury severity is expected to be a critical factor in determining what therapeutic strategies are attempted in the clinical setting.

Animals↗
PubMed1998

99Tc(m)-MIBI scanning of the thyroid gland in patients with markedly decreased pertechnetate uptake.

Diffusely reduced 99Tc(m)-pertechnetate uptake is a relatively infrequent but annoying finding that impairs evaluation of the thyroid gland. We studied 32 female patients aged 19-85 years with markedly reduced pertechnetate uptake. The following causes of reduced pertechnetate uptake were recognized: treatment with iodinated pharmaceuticals (n = 15), suppression therapy with T4 (n = 11), subacute thyroiditis (n = 5) and massive tumour replacement (n = 1). 99Tc(m)-MIBI thyroid scintigraphy was performed within 24 h of the pertechnetate study. The results were correlated with neck ultrasound, serum TSH (n = 25) and surgical findings in patients who had been operated on. The technique identified the following conditions: normally sized thyroids (n = 4), diffuse goitres (n = 8), multinodular goitres (n = 17) and solitary thyroid nodules (n = 3). Moreover, substernal goitres were identified in nine patients. This condition was confirmed at surgery in seven patients. Ultrasonography was concordant in 29 of 32 patients in terms of thyroid size and structure, but failed to demonstrate substernal thyroid tissue. Our results suggest that 99Tc(m)-MIBI scintigraphy may contribute to the diagnosis of thyroid pathology and treatment planning in patients with diffusely decreased 99Tc(m)-pertechnetate uptake.

Adult↗
PubMed1998

Detection of recurrent malignant melanoma with 99mTc-MIBI scintigraphy.

Initial reports suggest that 99mTc-methoxyisobutylisonitrile (MIBI) scanning may be of clinical value in staging patients with malignant melanoma. We carried out a study to evaluate the potential of this technique in the detection of recurrent disease. Whole-body 99mTC-MIBI scans were performed in 81 patients with a history of a surgically excised MM: 28 with known recurrent lesions and 53 during follow-up without evidence of disease. Images started 10 min post-injection, using a dose of 740 MBq. Diagnoses were confirmed by cytological/histological examination or at least one conventional imaging modality. Blinded interpretations of the MIBI scans were performed. Whole-body MIBI scanning correctly detected 68 (92%) of 74 metastatic lesions in the following sites: regional lymph nodes (n=23), non-regional lymph nodes (n=10), skin (n=16), brain/cerebellum (n=6), lung (n=8), bone (n=4) and breast (n=1). The technique failed to detect three subcutaneous regressive lesions (< 1 cm), one liver metastasis, one spleen metastasis and a case of multiple small lesions of the duodenal mucous membrane. In 14 patients the procedure detected previously unknown metastatic lesions. These results suggest that 99mTc-MIBI scanning is an effective imaging modality for whole-body screening of metastatic disease in malignant melanoma patients with the potential to influence treatment planning.

Adult↗
PubMed1997

Extracellular release of serotonin following fluid-percussion brain injury in rats.

Serotonin has been implicated in the pathobiology of central nervous system trauma. Using microdialysis techniques, we performed measurements of extracellular serotonin release within the traumatized cerebral cortex of rats subjected to moderate fluid-percussion (F-P) brain injury. Twenty-four hours prior to TBI, a F-P interface was positioned parasagitally over the right cerebral cortex. On the second day, fasted rats were anesthetized with 70% nitrous oxide, 1% halothane and 30% oxygen. Under controlled physiological conditions and normothermic brain temperature (37-37.5 degrees C), rats were injured (n = 6) with a F-P pulse ranging from 1.8 to 2.0 atm. Following trauma, brain temperature was maintained for 4 h at 37 degrees C. Sham trauma animals (n = 7) were treated in an identical manner. Brain trauma induced acute elevations in the extracellular levels of serotonin (p < 0.01, ANOVA) compared to sham-operated controls. For example, serotonin levels increased from 18.85 +/- 7.12 pm/mL (mean +/- SD) in baseline samples to 65.78 +/- 11.36 in the first 10 min after trauma. The levels of serotonin remained significantly higher than control for the first 90-min sampling period. In parallel to the increase in serotonin levels after TBI, a significant 71.1% decrease (i.e., 182.29 +/- 30.08 vs 52.75 +/- 16.92) in extracellular 5-hydroxyindoleacetic acid (5-HIAA) levels was observed during the first 10 min after TBI. These data indicate that TBI is followed by a prompt increase in the extracellular levels of serotonin in cortical regions adjacent to the impact site. These neurochemical findings indicate that serotonin may play a significant role in the pathophysiology of TBI.

Animals↗
PubMed1996

Posttreatment with intravenous basic fibroblast growth factor reduces histopathological damage following fluid-percussion brain injury in rats.

The purpose of this study was to determine whether treatment with intravenous basic fibroblast growth factor (bFGF) would protect histopathologically in a rat model of traumatic brain injury (TBI). Twenty-four hours prior to TBI, the fluid-percussion interface was positioned parasagittally over the right cerebral cortex. On the second day, fasted rats were anesthetized with 70% nitrous oxide, 1% halothane, and 30% oxygen. Under controlled physiological conditions and normothermic brain temperature (37-37.5 degrees C), rats were injured with a fluid-percussion pulse ranging from 1.6 to 1.9 atm. Rats were randomized into two groups where either bFGF (45 micrograms/kg/h) in vehicle (n = 7) or vehicle alone (n = 7) was infused intravenously for 3 h, beginning 30 min after TBI. Three days later, brains were perfusion-fixed for histopathological assessment and quantitative analysis of contusion volume and numbers of necrotic cortical neurons. In vehicle-treated animals, necrotic neurons were observed throughout the lateral cerebral cortex remote from the impact site. In addition, an intracerebral contusion was present in all rats at the gray-white interface underlying the injured cortical areas. Posttraumatic administration of bFGF significantly reduced the numbers of damaged cortical neuron profiles at several coronal levels and reduced the total number of damaged neurons (696 +/- 148 vs. 1,248 +/- 198, means +/- SEM), p < 0.05, ANOVA). In addition, contusion ares at several coronal levels as well as total contusion volume was significantly reduced (1.13 +/- 0.39 mm(3) vs. 3.18 +/- 0.81 mm(3), p < 0.05). These data demonstrate neuroprotection with intravenous bFGF infusion in the posttraumatic setting.

Animals↗
PubMed1996

Thyroid imaging with Tc-99m MIBI in patients with solitary cold single nodules on pertechnetate imaging.

Thyroid imaging was performed in 30 patients with the standard pertechnetate technique, as well as with Tc-99m MIBI using a double-phase acquisition protocol. All patients had normal thyroid function confirmed by hormone measurements and cold solitary thyroid nodules, which were evaluated by pertechnetate scanning. Tc-99m MIBI scans were reported as showing cold (N = 14), warm (N = 7), or hot (N = 9) nodules. Nodule classification was made according to fine needle aspiration biopsy findings in 20 patients. The remaining 10 proceeded to surgery and had histopathologic confirmation of their lesions. Although all cold nodules with Tc-99m MIBI were cystic, six of the warm nodules were benign lesions. No histologically proven benign nodule was hot with Tc-99m MIBI. Of the hot nodules, seven were suspicious for follicular carcinoma with fine needle aspiration biopsy (N = 3), or had histologically proven papillary carcinoma (N = 4). Delayed images in five of seven of these lesions showed nodular retention of the radiopharmaceutical. In conclusion, double-phase Tc-99m MIBI scanning of the thyroid gland could be helpful in the preoperative assessment of patients with cold solitary thyroid nodules in order to evaluate the malignancy probability of these lesions.

Adenocarcinoma, Follicular↗
PubMed1996

Scintigraphic detection of invasive cutaneous malignant melanoma with Tc-99m MIBI.

Malignant melanoma is a relatively uncommon cancer of increasing incidence. The authors report on two cases of malignant melanoma lesions (primary and lymph node metastasis) imaged with Tc-99m MIBI. One patient revealed intense accumulation of the radiotracer in a primary skin lesion of the thorax, whereas the other patient showed increased Tc-99m MIBI uptake in a lymph node metastasis of the neck. Tc-99m MIBI imaging could be helpful in the evaluation of patients with suspicious skin lesions and in patients with known cutaneous malignant melanoma, in the investigation of lymph nodal invasion, local recurrence, and metastatic spread.

Adult↗
PubMed1996

Widespread hemodynamic depression and focal platelet accumulation after fluid percussion brain injury: a double-label autoradiographic study in rats.

Cerebrovascular damage leading to subsequent reductions in local cerebral blood flow (lCBF) may represent an important secondary injury mechanism following traumatic brain injury (TBI). We determined whether patterns of 111-indium-labeled platelet accumulation were spatially related to alterations in lCBF determined autoradiographically 30 min after TBI. Sprague-Dawley rats (n = 8), anesthetized with halothane and maintained on a 70:30 (vol/vol) mixture of nitrous oxide/oxygen and 0.5% halothane, underwent parasagittal fluid percussion brain injury (1.7-2.2 atm). 111-Indium-tropolone-labeled platelets were injected 30 min prior to TBI while [14C]-iodoantipyrine was infused 30 min after trauma. Sham-operated animals (n = 7) underwent similar surgical procedures but were not injured. In autoradiographic images of the indium-labeled platelets, focal sites of platelet accumulation within the traumatized hemisphere were restricted to the pial surface (five of eight rats), the external capsule underlying the lateral parietal cortex (five of eight rats), and within cerebrospinal fluid (CSF) compartments (six of eight rats). In contrast, mild-to-moderate reductions in lCBF, not restricted to sites of platelet accumulation, were seen throughout the traumatized hemisphere. Flow reductions were most severe in coronal sections underlying the impact site. For example, within the lateral parietal cortex and hippocampus, lCBF was significantly reduced [p <0.01; analysis of variance (ANOVA)] from 1.71 +/- 0.34 (mean +/- SD) and 0.78 +/- 0.12 ml/g/min, respectively, versus 0.72 +/- 0.17 and 0.41 +/- 0.06 ml/g/min within the traumatized hemisphere. Significant flow reductions were also seen in remote cortical and subcortical areas, including the right frontal cortex and striatum. These results indicate that focal platelet accumulation and widespread hemodynamic depression are both early consequences of TBI. Therapeutic strategies directed at these early microvascular consequences of TBI may be neuroprotective by attenuating secondary ischemic processes.

Animals↗
PubMed1996

Delayed posttraumatic brain hyperthermia worsens outcome after fluid percussion brain injury: a light and electron microscopic study in rats.

The morphological consequences of delayed posttraumatic brain hyperthermia (39 degrees C) after fluid percussion brain injury were assessed in rats. Sprague-Dawley rats anesthetized with 4% halothane and maintained on a 70:30 mixture of nitrous oxide:oxygen and 0.5% halothane underwent moderate (1.5-2.0 atm) traumatic brain injury with the injury screw positioned parasagittally over the right parieto-occipital cortex. At 24 hours after traumatic brain injury, the rats were reanesthetized and randomized into two groups in which either a 3-hour period of brain normothermia (36.5 degrees C, n = 18) or hyperthermia (39 degrees C, n = 18) was maintained. Sham-operated controls (n = 10) underwent all surgical and temperature-monitoring procedures. After the 3-hour monitoring period, the rats were allowed to survive for 3 days for light microscopic analysis or were injected with the protein tracer horseradish peroxidase and were perfusion-fixed 15 minutes later for light and electron microscopic analysis. At 4 days after traumatic brain injury, delayed posttraumatic hyperthermia (n = 12) significantly increased mortality (47%) and contusion volume (1.7 +/- 0.69 mm3, mean +/- standard error of the mean), compared to normothermia (n = 12) (18% mortality and 0.13 +/- 0.21 mm3 contusion volume) (P < 0.01, analysis of variance). At 15 minutes after the 3-hour hyperthermic period, the area of hemorrhage and horseradish peroxidase extravasation overlying the lateral external capsule was significantly increased (2.52 +/- 0.71 mm2, mean +/- standard error of the mean, versus 0.43 +/- 0.16 mm2) (P < 0.01), compared to normothermic rats. Examination of toluidine blue-stained plastic sections demonstrated a higher frequency of abnormally swollen myelinated axons per high microscopic field with hyperthermia. For example, numbers of swollen axons within the sixth layer of the right somatosensory cortex, corpus callosum, and internal capsule were 7.3 +/- 1.3, 4.2 +/- 1.4, and 3.0 +/- 1.2 axons (mean +/- standard error of the mean) with normothermia, respectively, compared with 24.7 +/- 12.1, 33.1 +/- 4.2, and 27.3 +/- 3.1 axons with hyperthermia, respectively (P < 0.01). An ultrastructural examination of the swollen axons demonstrated a severely thinned myelin sheath containing axoplasm devoid of cytoskeletal components. These experimental results indicate that posttraumatic brain hyperthermia might increase morbidity and mortality in patients with head injury by aggravating axonal and microvascular damage.

Animals↗
PubMed1995

Glutamate release and free radical production following brain injury: effects of posttraumatic hypothermia.

Posttraumatic hypothermia reduces the extent of neuronal damage in remote cortical and subcortical structures following traumatic brain injury (TBI). We evaluated whether excessive extracellular release of glutamate and generation of hydroxyl radicals are associated with remote traumatic injury, and whether posttraumatic hypothermia modulates these processes. Lateral fluid percussion was used to induce TBI in rats. The salicylate-trapping method was used in conjunction with microdialysis and HPLC to detect hydroxyl radicals by measurement of the stable adducts 2,3- and 2,5-dihydroxybenzoic acid (DHBA). Extracellular glutamate was measured from the same samples. Following trauma, brain temperature was maintained for 3 h at either 37 or 30 degrees C. Sham-trauma animals were treated in an identical manner. In the normothermic group, TBI induced significant elevations in 2,3-DHBA (3.3-fold, p < 0.01), 2,5-DHBA (2.5-fold, p < 0.01), and glutamate (2.8-fold, p < 0.01) compared with controls. The levels of 2,3-DHBA and glutamate remained high for approximately 1 h after trauma, whereas levels of 2,5-DHBA remained high for the entire sampling period (4 h). Linear regression analysis revealed a significant positive correlation between integrated 2,3-DHBA and glutamate concentrations (p < 0.05). Posttraumatic hypothermia resulted in suppression of both 2,3- and 2,5-DHBA elevations and glutamate release. The present data indicate that TBI is followed by prompt increases in both glutamate release and hydroxyl radical production from cortical regions adjacent to the impact site. The magnitude of glutamate release is correlated with the extent of the hydroxyl radical adduct, raising the possibility that the two responses are associated.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Post-traumatic brain hypothermia reduces histopathological damage following concussive brain injury in the rat.

The purposes of this study were (1) to document the histopathological consequences of moderate traumatic brain injury (TBI) in anesthetized Sprague-Dawley rats, and (2) to determine whether post-traumatic brain hypothermia (30 degrees C) would protect histopathologically. Twenty-four hours prior to TBI, the fluid percussion interface was positioned over the right cerebral cortex. On the 2nd day, fasted rats were anesthetized with 70% nitrous oxide, 1% halothane, and 30% oxygen. Under controlled physiological conditions and normothermic brain temperature (37.5 degrees C), rats were injured with a fluid percussion pulse ranging from 1.7 to 2.2 atmospheres. In one group, brain temperature was maintained at normothermic levels for 3 h after injury. In a second group, brain temperature was reduced to 30 degrees C at 5 min post-trauma and maintained for 3 h. Three days after TBI, brains were perfusion-fixed for routine histopathological analysis. In the normothermic group, damage at the site of impact was seen in only one of nine rats. In contrast, all normothermic animals displayed necrotic neurons within ipsilateral cortical regions lateral and remote from the impact site. Intracerebral hemorrhagic contusions were present in all rats at the gray-white interface underlying the injured cortical areas. Selective neuronal necrosis was also present within the CA3 and CA4 hippocampal subsectors and thalamus. Post-traumatic brain hypothermia significantly reduced the overall sum of necrotic cortical neurons (519 +/- 122 vs 952 +/- 130, mean +/- SE, P = 0.03, Kruskal-Wallis test) as well as contusion volume (0.50 +/- 0.14 vs 2.14 +/- 0.71 mm3, P = 0.004).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Early microvascular and neuronal consequences of traumatic brain injury: a light and electron microscopic study in rats.

The purpose of this study was to document the early morphologic consequences of moderate traumatic brain injury (TBI) in anesthetized Sprague-Dawley rats. Normothermic rats (37 degrees C) were injured with a fluid percussion pulse (1.7-2.1 atm) administered by an injury cannula positioned parasagittally over the right cerebral cortex (n = 7). At 45 min following TBI, rats were injected with the protein tracer horseradish peroxidase (HRP) and perfusion fixed or immersion fixed 15 min later for light and electron microscopic analysis. Blood-brain barrier (BBB) breakdown to HRP was present overlying the pial surface and superficial cortical layers of the injured hemisphere. A focal area of severe HRP leakage was also present at the gray-white interface of the lateral cortex. Light microscopic examination of this site revealed petechial hemorrhages associated with small venules. Dark shrunken neurons and swollen astrocytes were detected within cortical areas overlying the evolving contusion, CA3 and CA4 hippocampal subsectors, and lateral thalamus. Ultrastructural studies obtained evidence for irreversible neuronal injury and mechanical damage to vessel walls at this early posttraumatic period. In nonperfused traumatized rats, luminal platelet aggregates were also detected at sites of hemorrhage. In this model of TBI, a consistent pattern of microvascular and neuronal abnormalities can be documented in the early posttraumatic period. Pathomechanisms underlying these early changes are discussed in terms of primary and secondary injury processes.

Animals↗
PubMed1994

Widespread metabolic depression and reduced somatosensory circuit activation following traumatic brain injury in rats.

The effects of fluid percussion brain injury on the basal metabolic state and responsiveness of a somatosensory circuit to physiologic activation were investigated with [14C]2-deoxyglucose autoradiography. Under controlled physiologic conditions and normothermic brain temperature (37 degrees C), rats were injured with a moderate fluid percussion pulse ranging from 1.7 to 2.1 atm. At 4 or 24 h after traumatic brain injury (TBI), unilateral vibrissae stimulation was carried out, resulting in the metabolic activation of the whisker-barrel circuit. In sham-operated control animals, whisker stimulation resulted in the metabolic activation of the ipsilateral trigeminal medullary complex (177% of control), contralateral ventrobasal thalamus (143% control), and primary somatosensory cortex (153% control). At 4 h after injury, local cerebral metabolic rates of glucose (ICMRglu) were significantly depressed throughout the traumatized hemisphere. Although depressed ICMRglu was most pronounced in cortical regions adjacent to the evolving contusion (53% of control), significant decreases were also seen in more remote areas, including the frontal cortex (75% of control), hippocampus (79% control), and lateral thalamus (68% of control). At 24 h following TBI, ICMRglu remained significantly reduced at the impact site, within the ipsilateral somatosensory cortex and lateral thalamus. Stimulus-evoked increases in ICMRglu were depressed within all three relay stations of the vibrissae-barrel-field circuit at 4 and 24 h after TBI. These results demonstrate both focal and diffuse metabolic depression after moderate TBI. Although the most severe and longer lasting metabolic consequences occurred in cortical and thalamic regions destined to exhibit histopathologic damage, milder abnormalities, most prominent in the early posttraumatic period, were also seen in noninjured areas. The inability to activate the somatosensory circuit metabolically indicates that circuit dysfunction is an acute consequence of TBI. Widespread circuit or synaptic dysfunction would be expected to participate in the functional and behavioral consequences of TBI.

Animals↗
PubMed1993

Intraischemic but not postischemic brain hypothermia protects chronically following global forebrain ischemia in rats.

We investigated whether postischemic brain hypothermia (30 degrees C) would permanently protect the hippocampus following global forebrain ischemia. Global ischemia was produced in anesthetized rats by bilateral carotid artery occlusion plus hypotension (50 mm Hg). In the postischemic hypothermic group, brain temperature was maintained at 37 degrees C during the 10-min ischemic insult but reduced to 30 degrees C starting 3 min into the recirculation period and maintained at 30 degrees C for 3 h. In normothermic animals, intra- and postischemic brain temperature was maintained at 37 degrees C. After recovery for 3 days, 7 days, or 2 months, the extent of CA1 hippocampal histologic injury was quantitated. At 3 days after ischemia, postischemic hypothermia significantly protected the hippocampal CA1 sector compared with normothermic animals. For example, within the medial, middle, and lateral CA1 subsectors, the numbers of normal neurons were increased 20-, 13-, and 9-fold by postischemic hypothermia (p < 0.01). At 7 days after the ischemic insult, however, the degree of postischemic hypothermic protection was significantly reduced. In this case, the numbers of normal neurons were increased an average of only threefold compared with normothermia. Ultrastructural analysis of 7-day postischemic hypothermic rats demonstrated CA1 pyramidal neurons showing variable degrees of injury surrounded by reactive astrocytes and microglial cells. At 2 months after the ischemic insult, no trend for protection was demonstrated. In contrast to postischemic hypothermia, significant protection was seen at 2 months following intraischemic hypothermia. These data indicate that intraischemic, but not postischemic, brain hypothermia provides chronic protection to the hippocampus after transient brain ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Moderate hyperglycemia worsens acute blood-brain barrier injury after forebrain ischemia in rats.

BACKGROUND AND PURPOSE: Clinical and experimental data indicate that hyperglycemia can aggravate the consequences of stroke and cerebral ischemia. The purpose of this study was to examine the effects of moderate hyperglycemia on the response of the blood-brain barrier to normothermic (37 degrees C) and hypothermic (30 degrees C) global forebrain ischemia. METHODS: Sixteen rats underwent 20 minutes of four-vessel occlusion followed by 30 minutes of postischemic recirculation. We used the protein tracer horseradish peroxidase as an indicator of increased vascular permeability, and rats were perfusion-fixed for microscopic analysis. To produce moderate hyperglycemia, we gave an intraperitoneal injection of 50% dextrose 15 minutes before the ischemic insult. RESULTS: After normothermic brain ischemia, normoglycemic rats (plasma glucose level, 115 +/- 3 mg/dl) demonstrated extravasated horseradish peroxidase mainly restricted to the cerebral cortex. In contrast, more severe and widespread protein extravasation was documented throughout the neuraxis of hyperglycemic (plasma glucose level, 342 +/- 27) rats. Sites of protein leakage included the cerebral cortex, striatum, hippocampus, thalamus, and cerebellum. Foci of protein extravasation were associated with pial and large penetrating vessels. Intraischemic hypothermia significantly attenuated the blood-brain barrier consequences of hyperglycemic brain ischemia. CONCLUSIONS: Under normothermic ischemic conditions, hyperglycemia significantly worsens the degree of acute blood-brain barrier breakdown compared with normoglycemia. Postischemic blood-brain barrier disruption may play an important role in the pathogenesis of increased brain damage associated with systemic hyperglycemia.

Animals↗