Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0264733 (ventricular dilatation)
 2,163 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Eighty-five studies of regional cerebral blood flow (rCBF) were performed on 49 patients with ruptured intracranial aneurysms. The changes in rCBF were analyzed under various pathophysiological conditions, The degree of flow abnormalities correlated well with the clinical severity of neurological deficits. All of the patients with diffuse vasospasm of severe grade, to less than half of their control value, showed focal areas of decreased flow below 30 ml/100 gm/min, in addition to a reduction in mean CBF. The relief or disappearance of vasospasm in angiograms was followed by the increase of rCBF in the ischemic focus and mean CBF. Marked reduction in rCBF was found in patients with intracerebral hematoma and ventricular dilatation. Impaired CO2 response and autoregulation were found in patients with severe neurological deficits, a severe degree of vasospasm and marked depression of CBF. In this series direct operation was delayed in patients with impaired vascular reactivity as well as marked decrease of mean CBF below 30 ml/100 gm/min; good clinical results were obtained in thses patients.
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PMID:Regional cerebral blood flow in patients with ruptured intracranial aneurysms. 43 Jan 52

Eleven cases of acute carbon-monoxide poisoning in various stages were observed with the computerized tomography for 17 times and analysed their correlation between intracranial lesion and their clinical courses. Five of 11 cases revealed characterististic pathologic findings in CT scan, however complete recovery of consciousness was observed in only 4 of 6 cases with normal CT findings. In early stage of acute carbon-monoxide poisoning, CT scans showed typical diffuse subcortical low absorption with no obvious ventricular dilatation. The entity of this typical finding was supposed to be the so called "vasogenic edema" attributed to increased extracellular fluid caused by increased permeability of vessels due to hypoxic process of the poisoning. While this diffuse subcortical edema was subsiding gradually in about 2 weeks, progressive brain atrophy was supervening and resulted finally in severe dilatation of the ventricular system. In spite of two exceptional cases of vegetative state with normal CT scan in early stage seemed suggestive of poor prognosis in most of cases. Pathogenesis of subcortical brain edema and the effect of hyperbaric therapy in the cases of acute carbon monoxide poisoning were also discussed.
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PMID:[Dynamic aspect of brain edema in cases of acute carbon-monoxide poisoning (author's transl)]. 66 19

Cerebral blood flow and metabolism were studied in experimental hydrocephalus which was produced by intracisternal injection of kaolin in cats, rabbits and rats. Measurements were carried out in varied stages of hydrocephalus. Local cerebral blood flow (l-CBF) was measured by the hydrogen clearance method. Assessment of cerebral metabolism was made biochemically in the brain tissues of various regions, including water content, Na, K, lactate, pyruvate, lipids, ATP, cyclic AMP, catecholamines and monoamine metabolites. Blood flow studies were performed in the cerebral cortex, periventricular white matter, thalamus and midbrain reticular formation in hydrocephalic cats. In all of these regions, l-CBF decreased to about half of the control in both acute and chronic stages of hydrocephalus. CO2 reactivity to CBF was impaired only in the acute stage, while autoregulation of CBF was preserved in the hydrocephalic brain. Water content of the brain tissue increased temporarily only within the periventricular white matter of hydrocephalic rabbits concomitant with increase in Na and decrease in K. Transient increase in the lactate and lactate/pyruvate ratios was also observed in the frontal lobe tissue. In hydrocephalic rats, decrease in phospholipids and cholesterol was observed parallel with the degree of ventricular dilatation. ATP and cyclic AMP decreased biphasically in both acute and chronic stages. On the other hand, increase in concentrations of norepinephrine, dopamine, homovanillic acid, and 5-hydroxyindoleacetic acid became evident in the chronic stage of hydrocephalus. From the above results, it is concluded that the hydrocephalic brain sustained considerable disturbance of metabolism in all modalities in association with decreased blood flow, which is sufficient to explain the clinical symptoms of hydrocephalus.
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PMID:Cerebral blood flow and metabolism in experimental hydrocephalus. 287 11

The aim of this study was to assess the result of surgical repair of Fallot's tetralogy (FT) and to advise physical and sporting activities. Thirty-two patients (20 boys and 12 girls) underwent correction of FT either before 4 years of age (14 cases) or after (18 cases). The patients were assessed on average 7.5 years postoperatively (range 4 to 13 years). All but one were class I of the NYHA classification. Radiological cardiomegaly was observed in 3 cases (CTI greater than 0.55). Sinus rhythm was present in all cases: 27 out of 30 had complete right bundle branch block without bifascicular block. Holter monitoring was performed in 22 cases: occasional monomorphic VES (1 to 15/hour) were observed in 7 cases. Frequent polymorphic VES were observed during exercise in one adult. Echocardiography and cardiac catheterization revealed pulmonary regurgitation and right ventricular dilatation in over half the cases, with an infundibular aneurysm in 2 cases and a residual pressure gradient of 55 and 66 mmHg in 2 other cases requiring reoperation. Left ventricular function was satisfactory in all cases. Treadmill exercise testing was performed in 28 patients. However, for statistical analysis 12 boys aged 7 to 15 years were compared with 11 controls of the same age. There was a significant decrease in maximal O2 consumption, of CO2 excretion, of ventilation, of heart rate, of work developed and total work in the operated patients. Clinical assessment and complementary investigations are essential 5 to 10 years after correction of FT to detect latent abnormalities and to better advise patients on physical and sporting activities.
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PMID:[Long-term evaluation, physical and sports activities after correction of Fallot's tetralogy]. 642 51

The brains of 34 patients at the chronic stage of acute carbon monoxide poisoning (CO poisoning) were examined using computerized tomography (CT). Ventricular and sulcal dilatations were measured quantitatively, with picture analysis of CT for the measurement of ventricular dilatation. Significant ventricular and sulcal dilatations were found in all cases of the CO group compared with age-matched controls, and bilateral low density areas in the globus pallidus were seen in 9 of the patients. There were significant correlations between duration of initial unconsciousness and the ventricular dilatation or cortical atrophy. Such dilatations were considered to be due to the cerebral damage in the acute stage.
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PMID:Computerized tomographies of 34 patients at the chronic stage of acute carbon monoxide poisoning. 663 21

Hypoxia is sensed by all mammalian cells and elicits a variety of adaptive and pathophysiological responses at the molecular and cellular level. For the pulmonary vasculature, hypoxia causes increased vasoconstriction and vessel-wall remodeling. These responses are mediated by complex intracellular cascades leading to altered gene expression and cell-cell interaction. Hypoxia transiently increases the transcriptional rate of the heme oxygenase-1 (HO-1) gene, resulting in increased production of carbon monoxide (CO) and bilirubin. CO has vasodilatory and antiinflammatory properties in the vasculature, whereas bilirubin is an antioxidant. Both enzymatic products could thus modulate the hypoxic cellular response. Accumulating data suggest that CO inhibits the hypoxic induction of genes encoding vasoconstrictors and smooth muscle cell mitogens in the early hypoxic phase. During chronic hypoxia, low CO levels tilt the balance toward increased production of growth factors and vasoconstrictors that promote vessel-wall remodeling. Mice null in the HO-1 gene manifest decreased tolerance to hypoxia with right ventricular dilatation and infarction, whereas targeted lung overexpression of HO-1 prevents hypoxia-induced inflammatory responses and protects against the development of pulmonary hypertension. Such observations point to CO as a critical modulator of the body's adaptive responses to hypoxia.
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PMID:Hypoxia and carbon monoxide in the vasculature. 1200 80

Cardiac hypertrophy occurs in a number of disease states associated with chronic increases in cardiac work load. Although cardiac hypertrophy may initially represent an adaptive response of the myocardium, ultimately, it often progresses to ventricular dilatation and heart failure. Much investigation has focused on the signaling pathways controlling cardiac hypertrophy at the level of the single cardiac myocyte. One prohypertrophic pathway that has received much attention involves the ubiquitously expressed Ca2+/calmodulin-activated phosphatase calcineurin. Upon activation by Ca2+, calcineurin dephosphorylates nuclear factor of activated T cell (NFAT) transcription factors, leading to their nuclear translocation. As common in complex biological systems, cardiac hypertrophy is controlled simultaneously by stimulatory (prohypertrophic) and counter-regulatory (antihypertrophic) pathways. Given the potent prohypertrophic effects of the Ca2+-calcineurin-NFAT pathway in cardiac myocytes, it is not surprising that the activity of this pathway is tightly controlled at multiple levels. Inhibitory mechanisms upstream (nitric oxide (NO), cGMP, cGMP-dependent protein kinase type I (PKG I), heme oxygenase-1 (HO-1), biliverdin, carbon monoxide (CO)) and downstream from calcineurin (glycogen synthase kinase-3 (GSK3), c-Jun N-terminal kinases (JNKs), p38 mitogen-activated protein kinase (MAPKs)) have been described. Moreover, several inhibitors directly target calcineurin enzymatic activity (cyclosporine A (CsA), tacrolimus (FK506), calcineurin-binding protein-1 (Cabin-1)/calcineurin-inhibitory protein (Cain), A-kinase-anchoring protein-79 (AKAP79), calcineurin B homology protein (CHP), MCIPs, VIVIT). Considering the dominant role of the calcineurin pathway in cardiac hypertrophy and failure, calcineurin-inhibitory strategies may lead to the identification of novel therapeutic approaches for patients with cardiac disease.
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PMID:Interference of antihypertrophic molecules and signaling pathways with the Ca2+-calcineurin-NFAT cascade in cardiac myocytes. 1527 70

A 4-year-old boy was found unconscious due to carbon monoxide poisoning, and required cardiopulmonary resuscitation, mechanical ventilation and inotropic support. Examination revealed cerebral edema, myocardial injury with left ventricular dilatation, depressed contractility and positive biomarkers. Complete recovery was seen at 4-month follow-up.
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PMID:Transient cardiomyopathy secondary to carbon monoxide poisoning. 1875 10