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)

Infantile hydrocephalus is most often caused by an obstruction in the cerebrospinal fluid flow pathway and results in ventricular dilatation and chronic trauma to the surrounding brain. Surgical treatment alleviates the condition but does not cure or prevent neurological deficits. The H-Tx rat has severe hydrocephalus due to a spontaneous aqueduct obstruction in late gestation. In order to determine how hydrocephalus affects brain metabolism in tissue adjacent to the expanded ventricles, cortical extracts have been made from groups of hydrocephalic and control littermates with early, intermediate, and advanced hydrocephalus at 4, 11, and 21 days after birth. Extracts were analyzed with 1H and 31P NMR spectroscopy and metabolite peaks were quantified using an external standard. Metabolite concentrations were calculated relative to tissue wet weight and subsequently expressed relative to tissue dry weight, using values for water content obtained from additional groups of rats. In early hydrocephalus there was a significant decrease in the phosphomonoester phosphorylcholine, and there were small, nonsignificant changes in other compounds. By 11 days, in addition to phosphomonoesters, there were significant decreases in ATP, phosphocreatine, and in inorganic phosphate, but with no change in lactate. By 21 days there were also substantial decreases in cholines, inositol, creatine, glutamate, glutamine, aspartate, N-acetylaspartate, alanine, and taurine. It is concluded that the sequence of pathological events starts with changes in membrane lipids. This is followed by reductions in energy metabolite which leads to cell swelling with loss of intracellular osmolytes and neurotransmitters. These changes are discussed in relation to hydrocephalus pathophysiology and to prevention and reversibility with shunt treatment.
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PMID:Progressive changes in cortical metabolites at three stages of infantile hydrocephalus studied by in vitro NMR spectroscopy. 933 22

We hypothesized, that with atrophy, the correlation between water content and specific gravity of brain solids would break down signifying the onset of the atrophic process. The correlation between tissue water content, specific gravity of solids and ventricular size was studied in an impact acceleration model of closed head injury of the rat. Adult Sprague Dawley rats weighing 350 to 375 grams (n = 63) were separated into two groups: Group 1: Sham (n = 21), Group II: Trauma (n = 42). Water content was assessed using both gravimetric method and drying-weighing method at 1 hour, on days 1, 3, 7, 14, 28, and 42 in the trauma group as well as in the control group. Ventricular size was measured in cm2 on the MRI computer console in the coronal section at the coronal suture at the same time points. In the trauma group we found a significant increase (p < 0.01) in water content during the first week except on day 3 and there was a good correlation between the results of water content using both methods (p < 0.001). However, this relationship was poorly correlated after day 14 (p = 0.25). Although the ventricular size was the smallest at 1 hour post trauma, it significantly increased over the next 3 days (p < 0.001). On day 7 and 14 ventricular size decreased to normal size, yet gradually increased and then reached a significantly larger size on 42 days post trauma again (p < 0.01). We may consider, that brain edema following CHI begins immediately following trauma and resolves within 2 weeks. After 14 days degenerative change occurs in the cortex, as detected by specific gravity measurements which signifies the onset of the atrophic process and subsequent post traumatic ventricular dilatation.
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PMID:Detection of brain atrophy following traumatic brain injury using gravimetric techniques. 941 83

Hydrocephalus is characterized by enlargement of the cerebral ventricles. The behavioral disturbances are, in some cases, rapidly reversible by surgical treatment suggesting that there may be a functional impairment of neurons. Hydrocephalus was induced in 3-week old rats by kaolin injection into the cisterna magna. Parietal cerebrum and striatum content of monoamine neurotransmitters and amino acids were assayed by high performance liquid chromatography (HPLC), 1, 2, or 4 weeks after induction of hydrocephalus. The ventricles exhibited progressive enlargement which was partially reversed by surgical treatment. Cerebral water content was increased at all stages. Increased levels of cerebral aspartate and glutamate suggest that there is the potential for excitatory neurotoxicity. The increase in cerebral taurine correlated negatively with the increase in water content. Cerebral concentrations of norepinephrine and serotonin, and its metabolite 5-HIAA, were increased at 1 and 2 weeks suggesting an increase in their turnover during the early stages of ventricular dilatation. Dopamine and its metabolite DOPAC were transiently diminished in the striatum at 1 and 2 weeks, respectively, suggesting that axonal projections from the brainstem may be impaired. We conclude that the effect of hydrocephalus on amino acids and monoamines varies regionally. Due to increased water content, there may be dilution effects in whole tissue, therefore, it is important to make determinations on the basis of protein content.
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PMID:Monoamine neurotransmitters and amino acids in the cerebrum and striatum of immature rats with kaolin-induced hydrocephalus. 966 99

The relation between increased cerebrospinal fluid (CSF) pressure and ventricular enlargement in infantile hydrocephalus is uncertain, variable, and probably dependent on the etiology of the condition. The HTx rat has early-onset hydrocephalus due to aqueduct stenosis in late gestation with ventricular dilatation present in fetuses. Increased CSF pressure, however, is first detected at postnatal day 10 or later. How the transition from low pressure to raised pressure hydrocephalus takes place, is not clear. In order to study this, we investigated how CSF pressure is related to the magnitude of ventricular dilatation using hydrocephalic and control HTx rats at postnatal days 15 and 21. At 15 days, the CSF pressure for hydrocephalics was 31.1 +/- 3.6 mm H2O (mean +/- SEM) which was not significantly higher than the controls at 19.9 +/- 2.8 mm H2O. At 21 days, the pressure was significantly higher in hydrocephalics at 50.9 +/- 7.5 mm H2O compared to 24.3 +/- 3.6 mm H2O for controls, p < 0.05. The mean volume of the lateral ventricles was 409.3 mm3 at day 15 and 478.8 mm3 at day 21, whereas age-matched control rats in a previous study had ventricles of 14 and 25 mm3. At each age there was a significant linear relationship between CSF pressure and ventricle volume, p < 0.05 at day 15 and p < 0.01 at day 21. Closer examination of the data, however, showed that 5/10 hydrocephalics at day 15 and 4/10 at day 21 had CSF pressures that were within the 95% confidence limits of the mean pressures for the control groups. The ventricle volumes of these low pressure hydrocephalics were between 100 and 280 mm3 which was several times larger than the ventricles in control rats. CSF pressure in the remaining 15 day rats ranged from 30 to 53 mm H2O and in the 21 day rats from 46 to 90 mm H2O and the ventricles were between 280 and 1050 mm3. The results suggest that up to a critical volume the infant rat brain can accommodate additional CSF without an increase in pressure. At this volume there is a "break point" beyond which additional fluid results in further expansion along with an increase in CSF pressure.
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PMID:The relation between CSF pressure and ventricular dilatation in hydrocephalic HTx rats. 992 28

To estimate the usefulness of the bedside swallowing assessment proposed by Smithard et al and neuroimaging findings characteristic for dysphagia, we studied the outcome of 102 patients with chronic cerebral infarction after assessment of swallowing by this test with brain computerized tomography (CT). All patients had a variety of motor disturbance and were admitted on a long-term medicare basis. They were divided into two groups according to the findings: the positive group (n = 33), who showed any of the listed types of difficulty in swallowing water, and the negative group (n = 69). Followed up to 2.2 years, their outcomes were studied. CT findings were studied on type of infarction, number and laterality of infarction, grade of periventricular lucency (PVL), presence of ventricular dilatation (VD), and severity of cortical atrophy (CA). The mean age was 76.4 years at registration and 61 were men. The frequency of severe dementia and disturbed ADL were significantly higher in the positive group. Eighteen patients died during the observation period and 15 of those were in the positive group, indicating higher annual death rate (29.9% vs 2.2% in the negative group). All of the 15 patients in the positive group died of pneumonia. CT findings showed high incidence of multiple infarction, bilateral hemispheric lesion, severe PVL, VD, and severe CA in the positive group. These findings indicated that this evaluation method was useful in screening swallow function for patients with cerebral infarction in the chronic phase. Furthermore, CT findings suggested that severe white matter lesion, VD, and severe CA as well as multiple infarction seen in bilateral hemisphere was related to dysphagia, probably due to multiple factors involving pyramidal- and extrapyramidal-tracts with higher brain function.
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PMID:[Findings of bedside swallowing assessment and brain computerized tomography in patients with chronic cerebral infarction, and their outcome]. 1160 14

Mast cells contain proteases capable of activating matrix metalloproteinases (MMPs). However, given the relatively low density of mast cells in the myocardium (i.e., 1.5-5.3 cells/mm(2)), it is unknown whether these enzymes are present in sufficient quantities in the normal heart to mediate MMP activation. Accordingly, this study sought to determine whether chemically induced degranulation of cardiac mast cells (with compound 48/80) would have an effect in isolated, blood-perfused, functioning rat hearts. Mast cell degranulation produced a 15% increase in histamine levels present in the coronary efflux, a significant increase in myocardial water (i.e., edema) relative to normal values (80.1 +/- 3.4% vs. 77.4 +/- 1.08%, P < or = 0.03), a substantial activation of MMP-2 (126% increase relative to controls, P < or = 0.02), and a marked decrease in myocardial collagen volume fraction (0.46 +/- 0.10% vs. 0.97 +/- 0.33%, P < or = 0.001). Furthermore, although an increase in ventricular stiffness was expected due to the extent of edema resulting from mast cell degranulation, modest ventricular dilatation was observed. These findings clearly demonstrate that the number of mast cells present in normal hearts is sufficient to mediate activation of MMPs and produce extracellular matrix degradation, thereby potentially causing subsequent ventricular dilatation.
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PMID:Cardiac mast cell-mediated activation of gelatinase and alteration of ventricular diastolic function. 1200 23

Despite a variety of biological roles for nitric oxide (NO) in the cardiovascular system, little is known about whether NO is involved in cardiac hypertrophy. We hypothesized that NO production following a sustained increase in shear stress by volume-overload modifies the level of cardiac hypertrophy independent of hemodynamic changes. Volume-overload was induced by shunt formation between the left common carotid artery and the external jugular vein in 21 rabbits. These shunt rabbits were randomly assigned to 3 groups: shunt with no treatment (n = 8), shunt treated with a low dose of N(G)-nitro-L-arginine methyl ester (L-NAME. 0.5 g/L in drinking water, n=8), and shunt with a high dose of L-NAME (1.5 g/L, n = 5). Eight sham operated rabbits were used as controls. Treatments were started immediately after operation and were continued for 6 weeks. Chronic volume-overload by shunt formation caused left ventricular dilatation and arterial enlargement proximal to the fistula. The relative wall thickness of the left ventricle was decreased, indicating eccentric cardiac hypertrophy. L-NAME elevated mean arterial blood pressure (P < 0.01) and reduced the increment of cardiac output (P < 0.05). L-NAME attenuated ventricular weight (P < 0.01) ventricular cavity dilatation (P < 0.01). and arterial enlargement (P < 0.05). The re-capitulation of atrial natriuretic factor mRNA in the hypertrophied left ventricular myocardium by volume-overload was attenuated with L-NAME. In this model with chronic volume-overload, NO plays a pivotal role in the progression of cardiovascular remodeling by regulating the loading conditions of the heart.
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PMID:Role of nitric oxide in the progression of cardiovascular remodeling induced by carotid arterio-venous shunt in rabbits. 1262 44

Long-term prognosis in dialysis is poor compared to that in healthy control persons. A worsening of the prognosis is noted especially for patients who at initiation of dialysis have congestive heart failure, ischemic heart disease, or left ventricular dysfunction or hypertrophy. This is the main reason that cardiovascular causes are the most common for morbidity in these patients. The weight obtained when normal urine output is present is the dry weight. With reduced ability to excrete the volume by the kidneys in end-stage renal disease (ESRD), the body will retain water and the patient will gain weight. This extra weight is due to volume overload. While volume overload may induce a rise in blood pressure, if the heart is in acceptable condition, a fast removal of fluid by ultrafiltration (UF) during dialysis may instead cause hypotension. Ultrafiltration failure in peritoneal dialysis (PD) patients may lead to successive water retention and overhydration with subsequent cardiac failure, while volume overload may occur over a few days in hemodialysis (HD) patients. Anemia or even too-high hematocrit may impair cardiac function further and worsen conditions caused by wrong dry weight. Thus, during long-term and sustained volume overload, left ventricular (LV) hypertrophy will occur in an eccentric manner. A sustained overload then may lead to cell death and LV dilatation and, eventually, systolic dysfunction. Once a severe left ventricular dilatation has developed, the blood pressure may decrease during volume overload. A worsened prognosis is seen if malnutrition and low albumin levels are present. Volume overload necessitates ultrafiltration to achieve dry weight. Thereby, volume contraction contributes to exaggerated stimulation of or response to activation of the RAS and alpha-adrenergic sympathetic systems. If ultrafiltration goes beyond these compensatory mechanisms, hypotension will occur and increase the risk for hypoperfusion of vital organs. Such episodes may cause cardiac morbidity, aspiration pneumonia, vascular access closure, or neurological complications (seizures, cerebral infarction), besides a more rapid lowering of residual renal function. Preventive measures are, first, finding the right dry weight; second, minimizing interdialytic weight gain; third, optimizing the target for hemoglobin (110-120 g/l); fourth, lowering dialysate calcium (1.25 mmol/l); and fifth, eventually using higher dialysate potassium if long dialyses are performed.
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PMID:Ultrafiltration and dry weight-what are the cardiovascular effects? 1266 7

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

The objective of this study was to determine whether elevated circulating levels of endothelin (ET)-1 are capable of mediating left ventricular (LV) mast cell degranulation and thereby induce matrix metalloproteinase (MMP) activation. After the administration of 20 pg/ml ET-1 to blood-perfused isolated rat hearts, LV tissue was analyzed for signs of mast cell degranulation and MMP activation. Relative to control, ET-1 produced extensive mast cell degranulation as well as a significant increase in myocardial water content (78.8 +/- 1.5% vs. 74.2 +/- 2.2%, P <0.01), a marked 107% increase in MMP-2 activity (P <0.05), and a substantial decrease in collagen volume fraction (0.69 +/- 0.09% vs. 0.99 +/- 0.04%, P <0.001). Although the myocardial edema would be expected to increase ventricular stiffness, compliance was not altered, and moderate ventricular dilatation was observed (end-diastolic volume at end-diastolic pressure of 0 mmHg of 330.2 +/- 22.1 vs. 298.9 +/- 17.4 microl in ET-1 treated vs. control, respectively, P=0.07). Additionally, pretreatment with the mast cell stabilizer nedocromil prevented ET-1-induced changes in MMP-2 activity, myocardial water content, collagen volume fraction, and end-diastolic volume. These findings demonstrate that ET-1 is a potent cardiac mast cell secretogogue and further indicate that ET-1-mediated mast cell degranulation is a potential mechanism responsible for myocardial remodeling.
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PMID:Endothelin-1 mediates cardiac mast cell degranulation, matrix metalloproteinase activation, and myocardial remodeling in rats. 1523 95


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