hypercapnia/infarto

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Cardioprotective effect of chronic hypoxia is blunted by concomitant hypercapnia.

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The effect of chronic hypercapnia on cardioprotection induced by chronic hypoxia was investigated in adult male Wistar rats exposed to isobaric hypoxia (10 % O(2)) for three weeks. In the first experimental group, CO(2) in the chamber was fully absorbed; in the second group, its level was increased

Altered cerebral inhibition of respiratory and cardiac responses to hypercapnia in acute stroke.

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Ventilatory and heart-rate responses to hypercapnia were evaluated by a CO2 rebreathing technique in 56 patients with acute ischemic stroke and 14 normal controls. Both ventilatory and heart-rate responses were increased in patients with hemispheral lesions, but not in patients with brainstem

[Hyperbaric oxygenation in myocardial infarct].

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A total of 52 patients with myocardial infarction have been examined. The patients have been subjected to HBO procedures. 40-62 min sessions with a working pressure of 0.3-1.1 atm were performed. The optimal pressure during the first days is 0.3 atm with a gradual increase to 0.7 atm. It is

Hypercapnic alteration of visual evoked responses in acute cerebral infarction.

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To determine the effect of inhaled carbon dioxide on acute ischemic cerebral injury, we have compared occipital visual evoked responses (VER) at baseline and during hypercapnia in 20 patients with acute unilateral cerebral infarction (ten with and ten without homonymous hemianopsia) and in ten

Vascular response to carbon dioxide in areas with and without diaschisis in patients with small, deep hemispheric infarction.

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The reactivity of cerebral blood vessels to changes in PaCO2 in areas of the cerebral cortex with or without diaschisis was investigated in 13 patients in a subacute or chronic stage after a small capsular infarct. A focal area of hypoperfusion (area of diaschisis) was detected in the ipsilateral

Effect of extreme hypercapnia on hypoxic-ischemic brain damage in the immature rat.

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To ascertain the effect of extreme hypercapnia on perinatal hypoxic-ischemic brain damage, 7-d-postnatal rats were exposed to unilateral common carotid artery occlusion followed by hypoxia with 8% oxygen combined with 3, 12, or 15% carbon dioxide (CO2) for 2 h at 37 degrees C. Survivors underwent

Cerebral vasomotor reactivity is significantly reduced in low-flow as compared to thromboembolic infarctions: the key role of the circle of Willis.

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To test the hypothesis that cerebral vasomotor reactivity (CVMR) is significantly more reduced in patients with hemispheric low-flow infarctions than in brain infarctions due to arterio-arterial embolism, a series of 64 consecutive patients with internal carotid artery occlusions were studied. CVMR

Evaluation of MR-derived cerebral oxygen metabolic index in experimental hyperoxic hypercapnia, hypoxia, and ischemia.

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OBJECTIVE A noninvasive MRI method to measure cerebral oxygen metabolism has the potential to assess tissue viability during cerebral ischemia. The purposes of this study were to validate MR oxygenation measurements across a wide range of global cerebral oxygenation and to examine the spatiotemporal

[Two cases of severe cytomegalovirus pneumonitis treated with permissive hypercapnia].

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Two patients with severe cytomegalovirus (CMV) pneumonitis were treated with permissive hypercapnia. Case 1 was a 66-year-old male who suffered ventricular septal perforation caused by acute myocardial infarction. Case 2 was a 54-year-old male who sustained a blunt chest injury. In both cases,

Chronic parasympathetic sectioning decreases regional cerebral blood flow during hemorrhagic hypotension and increases infarct size after middle cerebral artery occlusion in spontaneously hypertensive rats.

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Regional cerebral blood flow (rCBF) during controlled hemorrhagic hypotension (140-20 mm Hg) was assessed 10-14 days after chronic unilateral sectioning of parasympathetic and/or sensory fibers innervating pial vessels in spontaneously hypertensive rats (SHR). rCBF was measured in the cortical

Migrainous Infarction in a Patient With Sporadic Hemiplegic Migraine and Cystic Fibrosis: A 99mTc-HMPAO Brain SPECT Study.

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Genetic mutations of sporadic hemiplegic migraine (SHM) are mostly unknown. SHM pathophysiology relies on cortical spreading depression (CSD), which might be responsible for ischemic brain infarction. Cystic fibrosis (CF) is caused by a monogenic mutation of the chlorine transmembrane conductance

Vasoreactivity and peri-infarct hyperintensities in stroke.

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OBJECTIVE It is unknown if impaired cerebral vasoreactivity recovers after ischemic stroke, and whether it compromises perfusion in regions surrounding infarct and other vascular territories. We investigated the regional differences in CO2 vasoreactivity (CO2 VR) and their relationships to

Inhibition of Apoptosis is a Potential Way to Improving Ischemic Brain Tolerance in Combined Exposure to Hypercapnia and Hypoxia.

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We compared the intensity of apoptosis in the peri-infarction area of the brain after isolated and combined exposure to hypoxia and hypercapnia prior to focal ischemic stroke modeling. Hypoxia and hypercapnia reduced the number of TUNEL-positive cells in the peri-infarction area, and their

Protection of Myocardial Ischemia-Reperfusion by Therapeutic Hypercapnia: a Mechanism Involving Improvements in Mitochondrial Biogenesis and Function.

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Previous studies proposed that acidic reperfusion may be a protective strategy for myocardial ischemia-reperfusion therapy with potential of clinical transformation. In this study, we investigated whether therapeutic hypercapnia could mimic acidosis postconditioning in isolated hearts with a 30-min

Impaired cerebral vasoreactivity in a transgenic mouse model of cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy arteriopathy.

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OBJECTIVE Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is an inherited small vessel disease causing stroke and dementia. The disease is caused by highly stereotyped mutations in NOTCH3, which is restrictively expressed in vascular smooth muscle

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