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)

In cases of Parkinson's disease, a high incidence of dementia and simultaneous pathologic changes of Alzheimer's type have been reported. X-ray CT and MRI have such good spatial resolution that they can be expected to be useful for evaluation of brain atrophy. Positron emission tomography (PET) used with 18F-2-deoxy-2-fluoro-D-glucose is considered to reflect regional function. By these techniques, brain atrophy and local cerebral metabolic rate of glucose (LCMR-glc) in patients with Parkinsonism with dementia was studied, and also compared with age-matched normal controls and senile dementia of Alzheimer type. In seven cases of Parkinson's disease with dementia, LCMRs-glc were statistically decreased in all regions in comparison with ten normal controls. LCMRs-glc in six Parkinson's disease without dementia were higher than those of demented Parkinson's disease, but significantly lower than normal controls in all regions except basal ganglia. Some aged normal controls presented cortical atrophy and a significant difference could not be seen in evaluation by MRI among these three groups. There was also no correlation between LCMR-glc and cortical atrophy. There was no significant difference of LCMR-glc between six Guamnian cases of Parkinsonism-Dementia complex (PD complex) without ALS and four cases of PD complex with ALS, and these values were significantly lower than five Guamanian and ten Caucasian normal controls. In PD complex with and without ALS, remarkable cortical atrophy and ventricular dilatation were recorded in comparison with normal controls, and correlation between decrement of LCMR-glc and cortical atrophy was indicated in frontal, parietal and temporal lobe. In Parkinson's disease with dementia and PD complex in Guam, LCMRs-glc in all regions of brain were generally lower than normal controls. These findings were different from Alzheimer's disease in which LCMR-glc have been reported to be low especially in cerebral cortex. On the other hand, cortical atrophy and ventricular dilatation evaluated by MRI and CT was apparent in PD complex, but these changes were not remarkable in Parkinson's disease. Cortical atrophy did not always correlate with the decrease of LCMR-glc and changes of LCMR-glc could reflect clinical signs such as Parkinsonism and dementia. Both PET as a functional imaging method and MRI, CT as an anatomical imaging method are useful to access the study of these diseases.
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PMID:[Comparison study of positron emission tomography, X-ray CT and MRI in parkinsonism with dementia]. 279 56

Blood pressure, which ist the product of cardiac output and peripheral vascular resistance is regulated by a complex feedback mechanism involving the sympathetic and parasympathetic systems and hormones. An acute disturbance of regulation may lead to a life-threatening increase in blood pressure. Diagnosis is based upon a careful measurement of blood pressure, which must be performed under internationally standardized conditions. Hypertensive crisis refers to a rapid blood pressure increase greater than 30 mmHg above the age-related 95th percentile. The main causes of hypertension in childhood are renal diseases, which may be aggravated by additional conditions either by the clinician himself (e.g. cyclosporin, steroids) or by the patient (lack of compliance). Crisis affects the brain (hypertensive encephalopathy), the heart (left ventricular insufficiency), the retina (visual disturbances) and the mucous membranes (epistaxis). Hypertensive encephalopathy is induced by a break-through of the autoregulation of brain flow, leading to hyperperfusion and, thus to cerebral oedema. The clinical manifestations are characterized by restlessness, severe and diffuse headache, vomiting, nystagmus, impaired vision, dizziness, paraesthesia, seizures and palsies, which may lead - if untreated - to coma and death. The course is usually prolonged and reversible by adequate treatment. The morphological consequences are purpura cerebri, fresh retinal haemorrhages and papillary oedema, apart from left ventricular dilatation and hypertrophy. The diagnostic procedure rests on the quick realization of essential anamnestic (blood pressure, renal disease, drugs), clinical (oedema, cardiac action, central nervous system, fundus) and laboratory parameters (serum creatinine, electrolytes, glucose, blood count, urine). Treatment should start before the manifestation of clinical signs (hypertensive emergency) with rapidly acting antihypertensive drugs.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The hypertensive crisis in childhood]. 305 87

Since elevation of plasma concentrations of free fatty acids (FFA) increases myocardial oxygen consumption without influencing mechanical performance in normal hearts, it was the purpose of this study to determine whether FFA would modify mechanical performance at limited oxygen supply. Left coronary blood flow was reduced by gradual clamping of a shunt from the left carotid artery until moderate ventricular dilatation supervened. Left ventricular systolic pressure (LVSP), its maximal rate of rise (dP/dt) and stroke volume (SV) were unchanged or slightly reduced. The ischemia resulted in a decrease in myocardial oxygen consumption (MVO(2)) from 9.7+/-1.1 ml/min to 7.9+/-0.8 ml/min, and myocardial lactate uptake was reduced or reversed to excretion. Increasing the plasma concentrations of FFA from 359+/-47 muEq/1 to 3688+/-520 muEq/1 by intravenous infusion of a triglyceride emulsion and heparin resulted in further ventricular dilatation, accompanied by increased excretion of lactate. The ventricular decompensation and enhancement of anaerobic myocardial metabolism associated with increased uptake of FFA was not related to changes in coronary flow, MVO(2), or LVSP. dP/dt and SV were virtually unchanged. Intravenous infusion of glucose/insulin, which lowered plasma concentrations of FFA, reversed ventricular dilatation and lactate excretion. The data support the hypothesis that high concentrations of FFA play a significant role in increasing myocardial oxygen requirement and thereby promote depression of contractility of the hypoxic heart in experimental animals.
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PMID:Effect of free fatty acids on myocardial function and metabolism in the ischemic dog heart. 503 25

A 72-year-old woman, previously in good health, suffered for 2 years from attacks of a complex neuropsychiatric syndrome lasting from 2 days to 4 weeks. These episodes, which were followed by intervals of nearly complete recovery, were usually marked by fever, headache, mental confusion, vomiting ataxia, anisocoria, epileptic seizures and stiffness of the neck. Neuroradiological investigation revealed only slight ventricular dilatation. In 13 CSF examinations, there was reduced glucose, increased protein, considerable rise of the IgG index and constant oligoclonal bands. There was also an increase of polymorphonuclear leucocytes, lymphocytes or epithelial-like cells. As all microbial, viral or mycotic tests were negative and the patient recovered, the case was considered to be benign recurrent meningitis of Mollaret. The nosological position of this rare disease, as well as its probable pathogenetic mechanisms, are discussed.
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PMID:A case of benign recurrent meningitis of Mollaret. 616 85

The review deals with neonatal seizures, perinatal hypoxic-ischemic brain injury, and neonatal intraventricular hemorrhage. neonatal seizures are the most prominent signals of the largest number of neonatal neurological disorders. The convulsive phenomena may be subtle. The predominant etiological process is hypoxic-ischemic encephalopathy. Prognosis is related primarily to the neurological disease responsible for the seizures. Treatment may be specific for the underlying disorder (e.g., glucose or calcium) or less specific (i.e., therapy with anticonvulsant drugs). Prompt control of the seizures is important to avoid brain injury secondary to the effects of the seizures on ventilation, perfusion, and brain metabolism. Hypoxic-ischemic encephalopathy in the newborn most often is a consequence of intrauterine asphyxia. Diagnosis depends primarily on recognition of the clinical syndrome but also on a variety of neurodiagnostic techniques, including radionuclide and CT brain scans. Prognosis is estimated best by a combination of clinical analysis and specialized neurodiagnostic studies. management is based principally on vigorous support, particularly of ventilation and perfusion, maintenance of adequate glucose influx, and control of seizures. Intraventricular hemorrhage is the most common type of neonatal intracranial hemorrhage. The neuropathology is characterized by bleeding from capillaries of the subependymal germinal matrix. Secondary rupture of the ependymal lining then causes intraventricular hemorrhage. Pathogenesis relates to the anatomy of the germinal matrix, the distribution and regulation of cerebral blood flow, and the structure and vulnerability of periventricular capillaries. Precise diagnosis requires a brain imaging procedure; portable, real-time ultrasound is the preferred approach for critically ill infants. Prognosis relates to the severity of the hemorrhage as well as any preceding hypoxic-ischemic insults and the subsequent occurrence of hydrocephalus. Choice of therapy for posthemorrhagic ventricular dilatation depends upon severity and rapidity of progression and ranges from close observation only to ventriculoperitoneal shunting.
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PMID:Seizures, hypoxic-ischemic brain injury, and intraventricular hemorrhage in the newborn. 728 98

Survivors of perinatal intraventricular hemorrhage often develop a distinct clinical syndrome characterized by hydrocephalus and biochemical abnormalities in cerebrospinal fluid. The authors investigated six neonates with post-hemorrhagic obstructive hydrocephalus in order to identify cerebral metabolic disturbances responsible for the hypoglycorrhachia observed in this disorder. Lactic acid concentraions and lactate/pyruvate ratios in ventricular fluid were significantly elevated in infants with post-hemorrhagic hydrocephalus compared with the values in five with congenital (non-hemorrhagic) obstructive hydrocephalus. Comparable degrees of ventricular dilatation and intracranial hypertension were present in the two groups. There is evidence that neither residual cellular elements in ventricular fluid nor a disrupted blood-CSF barrier can fully explain the observed alterations in ventricular-fluid glucose, lactate or lactate/pyruvate ratios. It is suggested that when periventricular hemorrhage occurs, the associated cerebral ischemia leads to focal anaerobic glycolysis and increased glucose requirement. With inadequate cerebral glucose glycolysis and increased glucose requirement. With inadequate cerebral glucose delivery from the blood, glucose diffuses into the brain from the ventricular fluid, resulting in hypoglycorrhachia. Cerebral lactic acid production is enhanced, which accumulates in ventricular fluid in the presence of ventricular obstruction.
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PMID:Cerebral oxidative metabolism in perinatal post-hemorrhagic hydrocephalus. 739 28

L-Carnitine can affect cardiac function principally by improving fatty acid and/or glucose metabolism, by increasing perfusion due to modulation of the deformability of erythrocytes and/or vasodilatation, and by stabilising mitochondrial and plasma membranes of cardiomyocytes. While short-term administration of L-carnitine in vivo does not increase the muscular and probably also not the cardiac L-carnitine content, it improves the function of perfused rat or pig hearts in the reperfusion phase after ischemia. Long-term administration of L-carnitine increases the cardiac L-carnitine content in mice and has been shown to improve surrogate markers of coronary heart disease such as arrhythmias, nitrate consumption, and left ventricular dilatation and infarct size in patients after myocardial infarction. The only clear indication for L-carnitine in cardiology is to date cardiomyopathy associated with primary L-carnitine deficiency.
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PMID:[Physiologic bases for the use of L-carnitine in cardiology]. 952 39

A case of primary coccidiodal meningitis without pulmonary, osseous or dermic affection due to Coccidioides immitis in a 27 years old male patient with hypertensive brain of one month of evolution, was reported. The patient was resident of Northern California, and he was previously healthy. The cerebrospinal fluid (CSF) showed a glucose of 22 mg/dL, proteins 62 mg/dL, white blood cells 100/mm3 (97% PMN, 3% MN). CT SCAN showed bilateral ventricular dilatation. Diagnosis of coccidioidal meningitis was made based on antibodies against anticoccidioides (IgM 6.8 mg/dL and IgG 4.9 mg/dL, normal < 2 mg/dL) and growth of Coccidioides immitis. The chest radiograph was normal and the detection of antibodies against human immunodeficiency virus was negative. A VP shunt was placed and the patient was treated with intravenous amphotericin B and intratecal amphotericin B through on Ommaya reservoir. Even with antifungal treatment the patient deteriorated neurologically after an initial transient improvement, he died two weeks later in his hometown.
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PMID:[Coccidioides immitis: primary infection of the central nervous system. Case report and literature review]. 1034 67

We examined the effect of six doses of dexamethasone (Dex) administered daily (2-7 days of age) to postnatal rats on body weight gain, food and water intake, peripheral hormonal/metabolic milieu, and hypothalamic neuropeptides that regulate food intake. We observed a Dex-induced acute (3 days of age) suppression of endogenous corticosterone and an increase in circulating leptin concentrations that were associated with a decrease in body weight in males and females. Followup during the suckling, postsuckling, and adult stages (7-120 days of age) revealed hypoleptinemia in males and females, and hypoinsulinemia, a relative increase in the glucose-to-insulin ratio, and a larger increase in skeletal muscle glucose transporter (GLUT 4) concentrations predominantly in the males, reflective of a catabolic state associated with a persistent decrease in body weight gain. The increase in the glucose-to-insulin ratio and hyperglycemia was associated with an increase in water intake. In addition, the changes in the hormonal/metabolic milieu were associated with an increase in hypothalamic neuropeptide Y content in males and females during the suckling phase, which persisted only in the 120-day-old female with a transient postnatal decline in alpha-melanocyte-stimulating hormone and corticotropin-releasing factor. This increase in neuropeptide Y (NPY) during the suckling phase in males and females was associated with a subsequent increase in adult food intake that outweighed the demands of body weight gain. In contrast to the adult hypothalamic findings, cerebral ventricular dilatation was more prominent in adult males. We conclude that postnatal Dex treatment causes permanent sex-specific changes in the adult phenotype, setting the stage for future development of diabetes (increased glucose:insulin ratio), obesity (increased NPY and food intake), and neurological impairment (loss of cerebral volume).
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PMID:Postnatal glucocorticoid exposure alters the adult phenotype. 1500 31

Insulin resistance (IR) and diabetes increase the risk of acute myocardial infarction (MI). Angiotensin receptor blockers (ARBs) have been shown to reduce the risk of cardiovascular events in patients with hypertension and diabetes, and to be beneficial after a large MI. Whether pretreatment with ARBs is beneficial in acute MI is unknown. We evaluated whether pre-, peri-, and post-MI treatment with the ARB losartan improved the outcome in the IR Zucker fatty rat (ZFR). ZFR (n=264) received either losartan (3 mg/kg daily) or vehicle for 7 d prior to MI. Early (24 h) protocol (n=31): ventricular arrhythmias were evaluated post-MI using continuous ambulatory ECG monitoring. Late (38 d) protocol (n=233): losartan was increased to 10 mg/kg daily 10 d post-MI and to 30 mg/kg daily 20 d post-MI. Blood glucose, cardiac hemodynamics and remodeling, GLUT-4, fetal gene expression, and survival were evaluated. In large-MI rats, losartan improved early survival (43% vs. 27% in controls, p=0.01) and late survival (23% vs.15% in controls, p=0.02). Improved early survival was associated with a reduction in ventricular arrhythmias. Losartan reduced pulmonary congestion, cardiac hypertrophy, and fetal gene expression in the absence of statistically significant changes in ventricular dilatation and hemodynamics. Blood glucose and cardiac GLUT-4 expression did not change with losartan. In IR ZFR, losartan improves post-MI survival, likely as a result of an early reduction in ventricular arrhythmias. There was also an associated reduction in pulmonary congestion, hypertrophy, and fetal gene expression.
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PMID:Losartan and acute myocardial infarction in insulin-resistant Zucker fatty rats: reduced ventricular arrhythmias and improved survival. 1639 7


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