bluuebunny/crossref_metadata_2025_split huggingface dataset:
Myocardial and Hepatic Free Carnitine Concentrations in Pups of Diabetic Female Rats
Authors: Akısu Mete , Kultursay Nilgun , Coker Isıl , Huseyınov Afig 
Published: April 2003

<i>Background/Aims:</i> Adequate carnitine levels are required for normal fatty acid and energy metabolism in heart muscle. It is well known that streptozotocin-induced diabetic rats develop myocardial carnitine deficiency and that carnitine therapy may be beneficial to the diabetic heart. Infants of diabetic mothers (IDM) are known to be at risk for developing a hypertrophic type of cardiomyopathy. In the present investigation, we examined the free carnitine concentration from cardiac and hepatic tissue in pups of streptozotocin-induced diabetic female rats. We also assessed the effect of maternal <i>L</i>-carnitine supplementation on the free carnitine concentration in pups of diabetic rats. <i>Method:</i> Three groups, each consisting of 4 Wistar albino female rats, were studied, Group 1 (untreated diabetic; n = 4) and group 2 (<i>L</i>-carnitine-treated diabetic; n = 4) rats were given streptozotocin (60 mg/kg) by intraperitoneal injection; group 3 were controls. During pregnancy, <i>L</i>-carnitine was given at a dose of 150 mg/kg by intraperitoneal injection once a day for 14 days. Cesarean section was carried out, and 113 newborn rats (group 1 n = 36; group 2 n = 38; group 3 n = 39) were obtained from all the pregnant rats. <i>Results:</i> The free carnitine concentration in myocardial tissue was significantly decreased in the female diabetic rats (p < 0.001). However, the free carnitine concentration from hepatic tissue in diabetic female rats was similar to that in controls. In pups of group 1 diabetic rats, a significantly decreased free carnitine concentration was found in both myocardial and hepatic tissue compared to group 2 and controls. The free carnitine content from myocardial and hepatic tissue was significantly elevated in the maternal <i>L</i>-carnitine-supplemented group when compared to group 1 and control pups (p < 0.001 and p < 0.05, respectively). <i>Conclusions:</i> The present study has demonstrated that the free carnitine concentration from myocardial and hepatic tissue is significantly reduced in pups of streptozotocin-induced diabetic female rats. This study has also shown that administration of maternal <i>L</i>-carnitine improves the carnitine level in pups of diabetic rats. A decreased myocardial carnitine concentration may be partly responsible for the development of cardiomyopathy in IDM.
Clinical Trials of Postnatal Corticosteroids: Inhaled and Systemic
Authors: Halliday Henry L. 
Published: April 2003

Chronic lung disease (CLD) remains a common problem in neonatal intensive care units. Corticosteroids are being used increasingly to prevent or treat CLD. Uncertainties remain including the timing, duration and route of administration, and ratio of benefits to costs. This paper reviews the outcome of 39 randomized clinical trials of postnatal corticosteroid treatment. Twenty-five trials studied systemic steroids at three different postnatal ages; early (<96 h), moderately early (7–14 days), and delayed (>3 weeks). Fourteen-trials studied inhaled steroids (early: <7 days; late: >14 days) and inhaled versus systemic steroids. Systemic steroids have short-term beneficial effects improving gas exchange and lung mechanics to facilitate earlier extubation when used at any postnatal age in infants who are ventilator dependent. Early and moderately early steroids also reduce the risk of CLD at both 28 days and 36 weeks. For moderately early steroid use, there is also a reduction in neonatal mortality with 1 extra survivor for approximately every 16 babies treated (95% confidence interval 9–55). Proven adverse effects are either gastro-intestinal (bleeding) or metabolic (hyperglycaemia and hypertension). Unproven but potential adverse effects include decreased brain and lung growth. Inhaled steroids have been studied less thoroughly. Some studies report improvement in gas exchange and lung mechanics, but long-term benefits are not apparent to date in the published material. Trials comparing inhaled and systemic steroids suggest a more rapid response with the latter, but no significant differences in the rate of CLD at either 28 days or 36 weeks were found. Further research is necessary to define the roles of systemic and inhaled steroids in the prevention and treatment of CLD and to allow comparison of benefits to costs.
Plasma Cortisol, Cortisone and Urinary Glucocorticoid Metabolites in Preterm Infants
Authors: Midgley P.C. , Holownia P. , Smith J. , Moore M. , Russell K. , Oates N. , Shaw J.C.L. , Honour J.W. 
Published: April 2003

<i>Objective and Methods: </i>In the fetal circulation, there is a low cortisol:cortisone (F:E) ratio (∼0.3) suggesting high activity of 11β-hydroxysteroid dehydrogenase type 2 (11βHSD2). The circulating F:E ratio rises after birth in term infants, but little is known about infants born prematurely. Our hypothesis was that the low fetal plasma F:E ratio would persist in infants born prematurely, due to persistently high tissue 11βHSD2 activity. To test this hypothesis, a longitudinal observational study of plasma F, E levels and urinary F and E metabolites was performed in 22 preterm infants of 24–31 weeks gestation. <i>Results:</i> Median plasma F was 234–380 nmol l<sup>–1</sup>, median 124–177 nmol l<sup>–1</sup> from 1 to 14 days age. Plasma F fell with increasing postnatal and postconceptional age. The F:E ratio was 3 in the first week of life, and thereafter was 1–2, falling with postnatal age. Urinary glucocorticoid metabolites were low in quantity (∼48–120 µg kg<sup>–1</sup> day<sup>–1</sup>), consisted of E metabolites until term, and did not reflect the plasma F:E ratio. <i>Conclusions:</i> The fetal plasma F:E ratio did not persist in these preterm infants, due to tenfold higher levels of F. The F:E ratios were similar to those reported in term infants. These data suggest that the low F:E ratio in utero is due to low fetal production of cortisol, and effective placental inactivation of maternal F by 11βHSD2.
Effect of N<sup>G</sup>-Nitro-<i>L</i>-Arginine Methyl Ester on Intestinal Permeability following Intestinal Ischemia-Reperfusion Injury in a Rat Model
Authors: Luo Chih-Cheng , Chen Han-Ming , Chiu Cheng-Hsun , Lin Jer-Nan , Chen Jeng-Chang 
Published: April 2003

Subclinical intestinal ischemia-reperfusion injury (IRI) causes an increase in mucosal permeability and may represent an early event in the pathogenesis of necrotizing enterocolitis in premature infants. Previous studies suggested that continuous, endogenous formation of nitric oxide (NO) maintains the mucosal integrity of the intestine, thus protecting the gut from injuries from blood-borne toxins and tissue-destructive mediators. This study was undertaken to assess whether the inhibition of NO production causes an increase in intestinal permeability in rats following IRI. Sprague-Dawley rats weighing 200–300 g were divided into 4 groups: (1) untreated group (normal control); (2) ischemia-reperfusion group; (3) early N<sup>G</sup>-nitro-<i>L</i>-arginine methyl ester (<i>L</i>-NAME), a specific inhibitor of NO production, treatment group, and (4) late <i>L</i>-NAME treatment group. Transient IRI was induced by 30-min occlusion, followed by reperfusion of the isolated ileal loop. The <i>L</i>-NAME was administered 15 min before and after mesenteric ischemia as a 25-mg/kg bolus. Fluorescein isothiocyanate-dextran (FITC-D) was used to quantitatively assess the alteration in mucosal permeability of the intestine. There was no significant increase in the portal vein FITC-D level among normal controls, ischemia-reperfusion group and late <i>L</i>-NAME-treated group, but there was an approximately 6-fold increase in the early <i>L</i>-NAME treatment group. The pathological features of the intestine following IRI include denudation of the villus epithelium and reduction of villus height, associated with marked inflammatory cell infiltration over the lamina propria. These results suggest that endogenous NO may play a role in the protecting intestinal integrity after IRI.
Auditory Brainstem Response and Unbound Bilirubin in Jaundiced (jj) Gunn Rat Pups
Authors: Ahlfors Charles E. , Shapiro Steven M. 
Published: April 2003

The role of plasma bilirubin-albumin binding in the pathogenesis of kernicterus in human newborns is controversial. Kernicterus in the jaundiced (jj) Gunn rat pup, an animal model for kernicterus, prolongs interwave intervals and decreases wave amplitude in the auditory brainstem response (ABR). Plasma total bilirubin concentration (TBC), albumin concentration, and unbound bilirubin concentration (UBC), a measure of bilirubin-albumin binding, were measured in 16-day-old jj Gunn rat pups (n = 21) and compared with ABR wave latencies, interwave intervals, and wave amplitudes by linear correlation. The UBC, but not the TBC or TBC/albumin ratio, correlated positively and significantly with ABR I–II and I–III interwave intervals (r = 0.55, p = 0.009, and r = 0.60, p = 0.004, respectively). The UBC, but not the TBC or TBC/albumin ratio, predicts bilirubin toxicity, as measured by bilirubin-induced ABR changes in jj Gunn rat pups.
Hormonal Factors in the Morbidities Associated with Extreme Prematurity and the Potential Benefits of Hormonal Supplement
Authors: Yeung Melinda Y. , Smyth John P. 
Published: April 2003

Cortisol and thyroid hormones are known to modulate the maturation of various fetal organ systems, enzymes, and biochemical pathways. The cortisol furnished by the structural and biochemical immature fetal adrenal gland renders the extremely premature infants relatively cortisol deficient in comparison with the term newborns. The premature infants also have elevated fetal androgens, the production of which persists until &#8776;42 weeks of postconceptional age. The androgens produced by the fetal adrenal cortex and the müllerian inhibiting substance produced by the fetal testis have antiglucocorticoid and inhibitory effects on human fetal lung growth and maturation in vitro. Hypothalamic-pituitary-thyroid axis and thyroid function are also immature in extreme prematurity. In addition, there is reduced tissue thyroid hormone responsiveness. Superimposed on this is the reduced thyroid function seen in non-thyroidal illness in which elevated cytokine levels have been implicated. Repeated courses of antenatal steroids and high-dose postnatal dexamethasone appear to be deleterious to lung and brain development. This may be through inhibition of cell replication and catabolism as well as decreased thyroid-stimulating hormone secretion and reduced peripheral conversion of T<sub>4</sub> to T<sub>3</sub>. Furthermore, dexamethasone has been found to enhance neurosteroid production in the immature brain, potentially altering brain development. Considered together, the relative cortisol deficiency/androgen excess and reduced thyroid function as well as prolonged high-dose postnatal dexamethasone therapy in these infants may be important factors in their high degree of morbidity. We propose to restrict antenatal steroids to a single course and hypothesize that the overall outcome of low-gestation infants would be improved with (1) hydrocortisone (i.v./p.o.) supplement at a fixed dose of 0.5 mg/kg birth weight every 12 h in infants <30 weeks of gestation from birth till 32 weeks of postconceptional age and (2) T<sub>3</sub> (i.v./p.o.) supplement at a fixed dose of 0.4 µg/kg birth weight every 12 h in those <27 weeks of gestation from birth till 32 weeks of postconceptional age.
Anti-Anginal and Anti-Ischemic Effects of Mibefradil, a New T-Type Calcium Channel Antagonist
Authors: Kobrin Isaac , Bieska Gabriele , Charlon Vincent , Lindberg Elisabet , Pordy Robert 
Published: April 2003

Mibefradil is the first of a new class of calcium antagonists (CAs), the tetralol derivatives, that selectively blocks the T-type calcium channel. The anti-anginal and anti-ischemic efficacy of mibefradil in patients with chronic stable angina pectoris was established in five placebo-controlled trials (2 monotherapy trials, 3 trials with background β-blocker or long-acting nitrate therapy). At the recommended doses of 50 and 100 mg, mibefradil treatment was associated with a significant dose-related increase in exercise test variables regardless of demographic subpopulation or background therapy. Significant reductions in weekly anginal attacks, silent ischemic parameters, heart rate (HR) and rate-pressure product were also observed. Two active-controlled trials compared mibefradil 100 mg with amlodipine 10 mg or diltiazem SR 120 mg b.i.d., respectively. Patients receiving mibefradil showed significantly larger improvements than did those treated with amlodipine and similar improvements as those treated with diltiazem SR in all variables measured. In both studies, treatment with mibefradil was associated with a greater decrease in HR and rate-pressure product. Mibefradil was found to be well tolerated and safe; this held true for patients on chronic anti-anginal background therapy. The overall incidences of adverse events and premature withdrawals were only slightly higher than those of placebo-treated patients. Asymptomatic sinus bradycardia and first-degree atrioventricular block were the most frequently occurring mibefradil dose-related ECG changes. Mibefradil was better tolerated than amlodipine (mainly with regard to leg edema) and similarly well tolerated as diltiazem CD.
Angiotensin II Antagonism and the Heart: Valsartan in Left Ventricular Hypertrophy
Authors: Thürmann Petra A. 
Published: April 2003

Left ventricular hypertrophy (LVH) represents an independent risk factor for cardiovascular morbidity and mortality, and normalization of left ventricular mass has become a desirable goal of antihypertensive treatment. In a randomized, double-blind study the angiotensin II (AT<sub>1</sub> receptor) antagonist valsartan (Diovan<sup>®</sup>; 80 mg/160 mg q.d.) was compared with the beta-blocker atenolol (50 mg/100 mg q.d.) over 8 months in predominantly previously untreated patients with essential hypertension and LVH. Sixty-nine patients were randomized, of whom 58 were evaluated with echocardiographic data. After 8 months of treatment in the atenolol group [n = 8 with additional hydrochlorothiazide (HCTZ)], initial blood pressure was reduced from 160/103 to 147/92 mm Hg (p < 0.0001), and in the valsartan group (n = 9 with additional HCTZ) blood pressure decreased from 163/101 to 146/90 mm Hg (p < 0.0001). Left ventricular mass index decreased from 127 to 117 g/m<sup>2</sup> in the atenolol group and from 127 to 106 g/m<sup>2</sup> in the valsartan group. Long-term treatment with valsartan resulted in a significant reduction of LVH in patients with essential hypertension.
Altered Regulation of the Myocardial Microcirculation in Young Smokers
Authors: Madsen Mette M. , Bøttcher Morten , Nielsen Torsten Toftegaard , Czernin Johannes 
Published: April 2003

Smoking is known to affect microcirculatory function in a middle-aged population. However, the effects of smoking on myocardial perfusion in young smokers have not been studied. Myocardial perfusion was measured in 15 smokers (24 ± 2 years) and 15 nonsmokers (24 ± 3 years) using positron emission tomography. Myocardial perfusion was measured at rest, during cold stress and during dipyridamole. Resting myocardial blood flow was similar in the two groups. The well-described correlation between rate-pressure product and myocardial blood flow was present only in the nonsmokers (r<sup>2</sup> = 0.61, p < 0.001). Myocardial blood flow corrected for the rate-pressure product declined during cold by 20% in the smokers [1.11 ± 0.28 vs. 0.92 ± 0.20 ml·g<sup>–1</sup>·min<sup>–1</sup> (p = 0.012)], but remained unchanged in nonsmokers [1.11 ± 0.25 vs. 1.09 ± 0.30 ml·g<sup>–1</sup>·min<sup>–1</sup> (p = NS)]. Dipyridamole-induced hyperemia was similar in the two groups [2.23 ± 0.78 vs. 2.42 ± 0.65 ml·g<sup>–1</sup>·min<sup>–1</sup> (p = NS)]. In conclusion, smoking induces abnormalities in myocardial microcirculatory regulation in young otherwise healthy smokers. The coronary flow reserve, however, is not significantly altered.
Role of Intraventricular Dispersion of Early Diastolic Filling in Indicating Left Ventricular Diastolic Dysfunction: Assessment by Color M-Mode Inflow Propagation Velocity
Authors: Voon Wen-Chol , Huang Chih-Hsin , Sheu Sheng-Hsiung 
Published: April 2003

The intraventricular to mitral E velocity ratio (IvE/MvE) and the color M-mode Doppler inflow propagation velocity (LVIPV) were evaluated in 36 healthy controls and 33 patients with hypertension and/or ischemic heart disease. The intraventricular E velocity was significantly lower than the mitral E velocity in the control group (52 vs. 68 cm/s, p < 0.001), but they are similar in the disease group (59 vs. 63 cm/s, p = nonsignificant). Compared with the control group, the disease group had a higher IvE/MvE (0.95 ± 0.28 vs. 0.78 ± 0.23, p < 0.01). Nevertheless, the LVIPV was not significantly different between the disease and control groups (53 ± 14 vs. 56 ± 13 cm/s, p = nonsignificant). The LVIPV did not correlate with the IvE/MvE (r = 0.202, p = nonsignificant). Therefore, an intraventricular dispersion of early diastolic filling does not seem to indicate impaired left ventricular relaxation.
Is There a Need to Reclassify Acute Stroke Patients?
Authors: Schwartz A. , Gass A. , Hennerici M.G. 
Published: April 2003

During the last decade classification of stroke patterns has been a need not only for a common scientific language but also for early clinical and therapeutic stratification. The underlying idea was to find a tool to determine the causal pathology from the stroke pattern. Confirmation of the origin of stroke as early as possible (preferably already during the first hours, <3–6 h) by definition of a pattern opened the door to a differentiated therapy by e.g. thrombolysis, anticoagulation, thrombendarterectomy and many others.
Amantadine Increases Gait Steadiness in Frontal Gait Disorder due to Subcortical Vascular Encephalopathy: A Double-Blind Randomized Placebo-Controlled Trial Based on Quantitative Gait Analysis
Authors: Baezner H. , Oster M. , Henning O. , Cohen S. , Hennerici M.G. 
Published: April 2003

In a randomized, double-blind placebo-controlled trial, 40 patients diagnosed as subcortical vascular encephalopathy (SVE) were given a daily dose of 500 ml i.v. amantadine vs. placebo for 5 days. Both groups were treated with physiotherapy on a daily basis. Quantitative gait analyses were performed at days 1 and 6 to evaluate gait steadiness from cadence, length of heel-to-toe movements, variability of centre of gravity (COG) and double support time. Both placebo- and amantadine-receiving patient groups showed mild improvement in gait parameters after study, which failed to show the superiority of amantadine, when comparing drug-induced changes between both groups. However, analysing the treatment effects from day 0 to day 6 in both groups separately, statistically significant changes could be found in the amantadine group for cadence, length of heel-to-toe movements in single support phase as well as for variability in double support phase and double support time (two-tailed paired t-test, p < 0.05), whereas in the placebo group, a statistically significant effect could only be seen for double support time (p < 0.05). In this small pilot study, amantadine tends to improve gait steadiness as evaluated by cadence, length of heel-to-toe movements in single support phase, variability in double support phase and double support time, in patients with moderate frontal gait disorder due to SVE. Improvements in the placebo group can be interpreted as physiotherapy effect, which improved gait steadiness slightly, however, this was statistically significant only for double support time.
Recovery of Motor Functions following Hemiparetic Stroke: A Clinical and Magnetic Resonance-Morphometric Study
Authors: Binkofski F. , Seitz R.J. , Hackländer T. , Pawelec D. , Mau J. , Freund H.-J. 
Published: April 2003

Predictors for the degree of clinical recovery after stroke are still poorly defined. In this study we tried to assess the predictive value of clinical data and of lesion size for motor recovery after ischemic stroke. In 52 hemiparetic patients we monitored the course of clinical recovery by a dedicated score of sensorimotor hand function after their first stroke. The course of the lesion size was measured in proton density magnetic resonance images. Three groups of patients were identified. Patients with moderate initial motor deficit recovered almost completely within 9 days (17/17, group 1). From the patients with severe initial motor deficit, about equal numbers recovered (16/35, group 2) or remained severely impaired during the entire observation period of more than 6 months (19/35, group 3). There was no correlation between changes of lesion size and motor deficit. Logistic regression of probability of good clinical outcome on initial lesion size, initial motor score and subcortical versus cortical location of lesion showed that only the initial motor score was predictive (p = 0.006). A relative improvement of the initial motor score of about 20% in the first 4 weeks after stroke appeared to be a relevant cut point for good outcome. The data indicate that patients with mild initial motor deficits recover well, whereas severely affected patients may differ in outcome. Since lesion size was not correlated with outcome the amount of spared residual function appeared as major determinant for the capacity for motor recovery.
Poststroke Depression in Acute Phase after Stroke
Authors: Berg Anu , Palomäki Heikki , Lehtihalmes Matti , Lönnqvist Jouko , Kaste Markku 
Published: April 2003

We studied factors associated with acute poststroke depression in 100 patients, aged 27–70, 2 weeks after their first clinically significant stroke. Depressive symptoms were relatively common (27% Beck Depression Inventory ≧10), but the prevalence of major depression was only 5.6%. Older patients were most vulnerable to poststroke depression. Patients with left hemisphere lesion had no more depression than other patients, but when the lesion was in the left hemisphere or in the brainstem, stroke severity was associated with depression.
Bone Blood Flow and Vascular Reactivity
Authors: Fleming John T. , Barati Michelle T. , Beck Dennis J. , Dodds James C. , Malkani Arthur L. , Parameswaran Dushi , Soukhova Galia K. , Voor Michael J. , Feitelson Jeremy B.A. 
Published: April 2003

Blood flow is essential for normal bone growth and bone repair. Like other organs, the regulation of blood flow to bone is complex and involves numerous physiologic mechanisms including the sympathetic nervous system, circulating hormones, and local metabolic factors. Our studies addressed the following questions: (1) Which endogenous vasoconstrictor agents regulate in vivo blood flow to bone? (2) Does a decrease in bone vascular reactivity to vasoconstrictor hormones account for the increase in blood flow during bone healing? (3) Does the endothelium influence bone arteriolar function? An intact bone model was developed in the rat to assess hormonal regulation of in vivo bone blood flow and in vivo bone vascular reactivity. An isolated, perfused bone arteriole preparation was employed to characterize the responsiveness of small resistance-size arterioles (diameter < 100 µm) to vasoconstrictor hormones and to evaluate the role of the vascular endothelium to modulate vascular smooth muscle reactivity. Our results indicate that: (1) though exogenous endothelin is a potent constrictor of the in vivo bone vasculature, endogenous endothelin does not actively regulate in vivo blood flow; (2) the increase in blood flow to a bone injury site is not due to a decrease in bone vascular sensitivity to norepinephrine, and (3) isolated bone arterioles of young rats are very sensitive to vasoconstrictor hormones but exhibit only modest endothelium-mediated vasodilation.