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Both heart and brain are at risk for damage from asphyxia. However, these 2 organs' relative injury-thresholds have remained poorly defined. The present study using 16 anesthetized newborn piglets attempts to separate brain and heart damaging exposures from those that leave these organs unaffected. The hypoxic exposure (mean PaO2 = 3.6 +/- 0.6 kPa (27 mmHg) lasted for an average duration of 40 minutes and was associated with hypotension less than 4.7 kPa (35 mmHg) MABP. For brain damage assessment, 9 piglets that survived greater than 12 hours following resuscitation permitting histologic evaluation were used. For heart outcome assessment, those piglets that developed a postexposure, secondary hypotension to less than 4.7 kPa (35 mmHg) were compared to those without excluding 3 with uncertain cause of death. BRAIN-RESULTS: Six piglets remained brain intact while 3 exhibited brain edema and diffuse neuronal damage. The damaged animals' exposures differed from those that remained brain intact in sustaining significantly lower lowest MABPs (1.6 +/- 0.1 vs 3.3 +/- 0.4 kPa (12 vs 25 mmHg] and longer durations of MABP below 3.3 kPa (25 mmHg): 6 vs 1 min. and below 2.7 kPa (20 mmHg): 4 vs 0 min. HEART-RESULTS: Six of 13 animals developed marked delayed post-exposure hypotension requiring 5 to be killed prior to complete cardiovascular collapse. The only significant difference observed during exposure differentiating the two outcome groups (blood pressure maintenance vs cardiogenic shock) was the latter's more marked systemic acidosis (lowest mean arterial blood pH: 6.61 +/- 0.10 vs 6.91 +/- 0.10). These results suggest the brain is at risk for damage during hypoxia only when accompanied by an extreme lowering of blood pressure and the heart when accompanied by a severe acidosis. Further, the heart and brain need not both be damaged by the same hypoxic exposure. Contrary to common belief, the brain is not readily damaged from hypoxia alone absent marked circulatory changes.
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PMID:Hypoxic brain and heart injury thresholds in piglets. 273 Jun 1

Acute, bilateral pneumothorax (PT) was produced in 14 newborn piglets. The clinical status of the operated and 14 control animals was monitored by measuring the arterial blood gases, acid-base balance and mean arterial blood pressure. Different brain regions were processed for electron microscopy and albumin immunohistochemistry; water and electrolyte contents were also determined at the end stage of experimental intervention. Electron microscopy showed more intense pinocytotic activity in the endothelium of brain capillaries from PT animals evaluated by morphometry. Statistically significant (p less than 0.01) differences were found in the distribution of pinocytotic vesicles in different brain areas of PT animals. The blood-brain barrier seemed to be impermeable to albumin in all brain regions both in the controls and in the PT group. Parallel with the changes observed in pinocytosis, the water and sodium contents were also increased in the PT group in the parietal cortex (water content 85.18 +/- SD 0.81% vs. 84.10 +/- SD 0.52%, p less than 0.01; sodium content in wet brain tissue 70.94 +/- SD 8.44 mmol/kg vs. 65.09 +/- SD 4.43 mmol/kg, p less than 0.05, in dry brain tissue 481.70 +/- 75.70 mmol/kg vs. 410.15 +/- SD 35.45 mmol/kg, p less than 0.05) and in the cerebellum (water content 83.95 +/- SD 1.08% vs. 83.02 +/- SD 0.89%, p less than 0.05; sodium content in wet brain tissue 60.67 +/- SD 3.16 mmol/kg vs. 55.90 +/- 6.26 mmol/kg, p less than 0.01). However, in other brain regions--especially in the water-shed area--there was no correlation between the changes of pinocytosis and water-electrolyte contents of the tissues. It is suggested that the type of edema developing in this severe cardiovascular/hypoxic collapse is cytotoxic of origin and this fact should be more seriously taken into account in the treatment of the disease.
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PMID:Modulation of the blood-brain barrier permeability in neonatal cytotoxic brain edema: laboratory and morphological findings obtained on newborn piglets with experimental pneumothorax. 648 89

We present a case of acute lethal poisoning by oil of "epazote" (oil of chenopodium), in a 2 y 9 m female. The volatile oil was administered according to the advice of a "curandera" (female healer), in a total quantity of 40 ml. Clinical features of the poisoning were: vomiting, deep coma, seizures, mydriasis, apnea, metabolic acidosis, neurogenic shock and death. The EEG suggested a diffuse encephalopathy, the CT scan with an image of severe brain edema and ventricular collapse. Relevant postmortem findings were brain edema and neuronal necrosis, pneumonia, enteritis, pericholangitis, mild pancreatitis and tubular necrosis. The phytochemical analysis of volatile oil identified ascaridol, the main active compound of the chenopodium herbs, in a quantity of 39 mg/ml (1,560 mg in the dose administered), and Chenopodium graveolens as the plant employed to prepare it. According to the age of the patient, 60 mg of ascaridol would be the recommended dose formerly used in the treatment of parasitic disease. Thus 1,560 mg was 26 times higher than the recommended dose, and exceeded by 56% the dose of 1,000 mg reported as lethal in humans.
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PMID:[Fatal poisoning caused by oil of epazote, Chenopodium graveolens]. 896 84

Adult rats intubated with a single dose of ethanol (alcohol; approximately 5 g/kg) for 5 to 10 successive days incur neurodegeneration in the entorhinal cortex, dentate gyrus, and olfactory bulbs accompanied by cerebrocortical edema and electrolyte (Na+, K+) accumulation. The brain damage is not lessened by cotreatment with the NMDA receptor antagonist MK-801; also, as reported elsewhere, MK-801 as well as non-NMDA receptor and Ca2+ channel antagonists are not neuroprotective in a similar, but more compressed, intoxication protocol. However, cotreatment with the electrolyte transport inhibitor/diuretic furosemide reduces alcohol-dependent cerebrocortical damage by 75-85% while preventing brain hydration and electrolyte elevations; olfactory bulb neurodegeneration is not attenuated. In parallel in vitro studies, rat organotypic entorhinal/hippocampal slice cultures exposed to alcohol (50-200 mM) 15 h/day for 6 days, mirroring episodic intoxication in vivo, demonstrate concentration-related release of the cytotoxic indicator, lactate dehydrogenase. Analogous to the in vivo findings, furosemide blocks this alcohol-induced in vitro cytotoxicity. Our results showing neuroprotection by furosemide indicate that brain edema and swelling are essential events in the brain damage induced by episodic alcohol exposure. Furosemide and related agents might be useful as neuroprotective agents in alcohol abuse. We suggest that the neurodegeneration is elicited in part by edema-dependent oxidative stress, but the regional selectivity of the damage may be best explained by physical (mechanical) compression of the limbic cortex against the adjacent tympanic bulla and subsequent neuronal cytoskeletal collapse. A scheme for these apparently nonexcitotoxic metabolic and mechanical pathways initiated by repeated alcohol exposure is proposed.
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PMID:Brain damage due to episodic alcohol exposure in vivo and in vitro: furosemide neuroprotection implicates edema-based mechanism. 947 87

This case reports on a fatal craniocerebral trauma involving numerous ruptured cerebral bridging veins that did not bleed subdurally, despite approximately 15 hours of survival. A 15-year-old girl was severely injured as the passenger of a car that crashed sideways into a tree. She-suffered a cerebral trauma of the "diffuse injury" type and was unconscious after the accident. Her computed tomographic scan at admission showed massive brain edema, axial herniation, and marked hypodensity of the bilateral carotid flow area. Despite intensive care measures, the clinical course was characterized by central decompensation with therapy-resistant cardiocirculatory insufficiency. The autopsy revealed ruptures of numerous parasagittal bridging veins. The injured vessels were not thrombosed, and yet there was absolutely no subdural bleeding. This unusual combination of findings is assumed to be caused by an isolated collapse of cerebral circulation occurring shortly after the accident and primarily attributed to a rapid increase of intracranial pressure.
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PMID:Rupture of several parasagittal bridging veins without subdural bleeding. 1049 29

The study was held in order to analyze the main causes of death in cases of rheumatic diseases (RD) in Moscow. The authors studied the pathology records of autopsies performed in 1999-2002 in two pathology departments of Moscow clinics. Cases with RD were selected. The study found 165 cases of RD, which constituted 2% of all autopsies performed in these departments. There were 99 cases (60%) of rheumatic heart disease (RHD), 4 cases (2.4%) of rheumatic fever (RF) relapse, 28 cases (17%) of rheumatoid arthritis (RA), 8 cases (4.8%) of systemic lupus erythematosus (SLE), 3 cases (1.8%) of scleroderma systematica (SS), 2 cases (1.2%) of ankylosing spondylitis (AS), 2 cases (1.2%) of systemic vasculitis (SPV), 11 cases (7.3%) of osteoarthrosis, 3 cases (1.8%) of gout, 1 case (0.6%) of polymyositis. The death of patients with RHD had been caused by hemodynamic decompensation (HD) in 54% of the cases, acute cardiovascular collapse (ACC) in 14% of the cases, 6% of the patients had died from thromboembolism (TE) and 26%--from other conditions (intoxication, uremia, brain and lung edema etc). The death of patients with RF was caused by TE in 2 cases, by HD in 1 case and by ACC in 1 case. Secondary amyloidosis resulting in chronic renal failure and uremia occurred in 5 out of 28 cases of RA, HD--in 3, ACC--in 7, TE--in 1, infectious complications--in 5, other complications--in 7 cases. Patients with SLE died from various conditions: uremia in 2 cases, acute adrenal failure in 1 case, infectious complications in 2, ACC--in 2, brain edema--in 1 case. The complications of SS were uremia and intoxication. ACC was the cause of death in cases of gout and SS. The majority of RD cases were patients with RHD. The main cause of death in RD was cardiovascular disorders.
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PMID:[The causes of death of patients with rheumatic diseases in Moscow]. 1575 89

Emotional stress aggravates the course of brain ischemia that has developed in the presence of the former. The investigation studied the functional state of parietooccipital leptomeningeal anastomoses by vital biomicroscopy, as well as the linear blood flow velocity in the a. cerebri media and a. basilaris by high-frequency (38.5 MHz) Doppler ultrasonography before and after occlusion of the common carotid artery in normal (control) Wistar rats and ones that had experienced 18-hour aggressively conflict emotional stress and that were sensitive to the latter. Hemodynamic differences were found in the rats having a varying sensitivity to the used model of cerebral ischemia. Inadequate collateral blood supply along the circle of Willis was shown when this model of brain ischemia was used in the control animals. It was ascertained that in emotional stress, blood flow considerably reduced in the a. basilaris; the contiguous blood supply area displayed evolving brain edema that compressed leptomeningeal anastomoses and prevented the formation of collateral circulation, followed by occlusion of the common carotid arteries. With this, unilateral occlusion was followed by a short-term reduction in systemic blood pressure (BP) that was not seen in the controls and bilateral occlusion was by the development of collapse. Cerebral blood flow became dependent of systemic BP. The obtained experimental data suggest that it is expedient to include antistressor agents into therapy for chronic cerebrovascular diseases. This is particularly relevant to patients with occlusive carotid artery lesion and Willis circle anomalies since emotional stress may be fatal to them.
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PMID:[Hemodynamic mechanisms of negative impact of emotional stress on the development of cerebral ischemia in stressor load-sensitive rats]. 1991 10

The collapse of the blood-brain barrier (BBB) is one of the fundamental pathophysiology changes during cerebral ischemia reperfusion injury. Resveratrol has been recently reported to reduce cerebral ischemic damage by regulating the matrix metalloproteinase-9 (MMP-9). But, more direct evidence for the explanation of the BBB protected by resveratrol against cerebral ischemia reperfusion is still lacking. Therefore, the present study was aimed to investigate the regulation of BBB integrity by resveratrol after cerebral ischemia reperfusion and to determine the role of the MMP-9 and its endogenous inhibitor TIMP-1 balance in this process. Cerebral ischemia was induced by middle cerebral artery occlusion in rats. The BBB function was evaluated by brain water content and the Evans blue dye extravasation; the activities of MMP-9 and TIMP-1 were detected by using gelatin zymography analysis, and cellular apoptosis was examined by TUNEL staining. We confirmed that resveratrol reduced the cerebral ischemia reperfusion damage, brain edema, and Evans blue dye extravasation. Moreover, we found that resveratrol improved the balance of MMP-9/TIMP-1 in terms of their expressions and activities. A TIMP-1 neutralizing antibody reversed those neuroprotective effects of resveratrol. In conclusion, resveratrol attenuated the cerebral ischemia by maintaining the integrity of BBB via regulation of MMP-9 and TIMP-1.
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PMID:Resveratrol attenuates the blood-brain barrier dysfunction by regulation of the MMP-9/TIMP-1 balance after cerebral ischemia reperfusion in rats. 2533 Aug 60

Chiari type 1 malformation (CM1) rarely causes papilloedema, which is indicative of high intracranial pressure with or without ventricular dilatation. Furthermore, concomitant brain parenchymal abnormalities have not been reported to date. In this paper, the authors report on a young woman of CM1-induced intracranial hypertension (ICH) with diffuse brain edema with a focus on venous sinus assessment, and discuss the surgical strategy. A 24-year-old woman presented to Nagoya University Hospital complaining of 4-year history of severe occipital headache and blurry vision with slowly progressive worsening. Head and whole spine MRI showed a CM1 with diffuse white matter hyperintensities (WMH) on T2-weighted imaging and narrowed brain sulci without hydrocephalus. Lumbar puncture revealed extremely high opening pressure. Detailed blood examination and other radiographical imaging studies denied the presence of tumor, collagen disease, encephalitis and other entities. Head magnetic resonance venography and angiography demonstrated severe transverse sinus stenosis on both sides. Foramen magnum decompression was performed to alleviate the ICH by restoration of cerebrospinal fluid (CSF) stagnation at the foramen magnum with successful outcome. The patient completely recovered from preoperative symptoms immediately after surgery. The diffuse WMH and narrowing brain sulci have been resolving. The most feasible explanation for this complicated pathophysiology was ICH induced by CM1 led to transverse sinus collapse, resulting in diffuse WMH as a result of venous hypertension. This case report is the first illustration of successful surgical treatment of CM1 with diffuse brain edema with a focus on venous sinus assessment.
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PMID:Chiari Type 1 Malformation-induced Intracranial Hypertension with Diffuse Brain Edema Treated with Foramen Magnum Decompression: A Case Report. 2901 53

Intracerebral hemorrhage (ICH) is a primary cause of death and disability in adults worldwide. Secondary brain injury (SBI) induced by ICH can lead to impaired mitochondrial function, which ultimately contributes to apoptosis and necrosis. Mitochondrial Rho GTPase 1 (Miro1) is a key regulator of mitochondrial movement and motor protein binding. Although Miro1 has been demonstrated to be implicated in various types of central nervous system damage, its potential effect on ICH-induced SBI has not been studied in detail. Hence, in the present new study, we explored the effect of Miro1 on SBI in vivo and in vitro. Self-body heart blood was injected into the right basal ganglia of the rat brain in vivo. Meanwhile, our in vitro model of ICH was based on the stimulation of oxygen hemoglobin (OxyHb) to neurons. Then, Miro1 was overexpressed both in the brains of rats after ICH in vivo and in OxyHb-treated cultured neurons in vitro. Miro1 overexpression in vivo reduced several pathological indexes such as brain edema, neurobehavioral impairment, and neuronal death. Immunofluorescent staining in vitro showed that overexpression of Miro1 ameliorated neuronal damage via facilitation of mitochondrial transport and distribution. JC-1 staining indicated that overexpression of Miro1 reduced the collapse of mitochondrial membrane potential and enhanced mitochondrial mass. Additionally, live-dead cellular staining and flow cytometry analysis revealed that Miro1 overexpression in cultured neurons reduced both necrotic and apoptotic rates. In contrast, inhibition of Miro1 expression yielded opposite effects to those of Miro1 overexpression. Above all, the upregulation of Miro1 significantly alleviated pathological symptoms on SBI in vivo and in vitro.
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PMID:Miro1 Regulates Neuronal Mitochondrial Transport and Distribution to Alleviate Neuronal Damage in Secondary Brain Injury After Intracerebral Hemorrhage in Rats. 3250 Mar 52


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