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Biomedical subjects

L Chen

Publications and source records attributed to L Chen.

At least 973 records · Page 54Linked to original sources
PubMed1996

Blood in the gastric lumen increases splanchnic blood flow and portal pressure in portal-hypertensive rats.

BACKGROUND & AIMS: In portal-hypertensive humans, portal blood flow and pressure increase after a meal. These hemodynamic changes may increase variceal rupture risk. The aim of this study was to determine whether blood in the stomach lumen increases splanchnic flow and portal pressure (PP) in portal-hypertensive rats. METHODS: superior mesenteric artery flow and PP were measured in conscious, unrestrained, fasted partial portal vein-ligated rats with chronically implanted Doppler flow probes or portal vein catheters before and after gavage with heparinized, warmed blood from donor rats, air, standard meal, or empty tube. RESULTS: Percentage of changes in flow and pressure from baseline were significantly greater after gavage with blood (an increase of 22.6% +/- 3.5% and an increase of 16.4% +/- 3.1%, respectively) than empty tube (an increase of 3.4% +/- 0.6% and a decrease of 5.4% +/- 3.5%, respectively) (P < 0.005). Percentage of changes in flow and pressure were slightly but insignificantly greater after gavage with air vs. empty tube (P < 0.005). CONCLUSIONS: In portal-hypertensive rats, blood in the stomach lumen significantly increases splanchnic blood flow and PP. Splanchnic hyperemia from absorption of blood's calories probably contributes to these hemodynamic changes. In patients with variceal hemorrhage, blood in the stomach may increase the risk of persistent variceal bleeding or rebleeding.

Animals↗
PubMed1996

Effects of beta-blockade and atropine on ischemic responses in left ventricular regions subtending coronary stenosis during dobutamine stress echocardiography.

OBJECTIVES: This study was designed to examine the effects of a beta-adrenergic blocking agent on the ischemic response to dobutamine stress and to determine the degree to which these effects can be abolished by the addition of atropine. BACKGROUND: Whether beta-blockade affects the sensitivity of dobutamine stress echocardiography for the diagnosis of coronary artery disease has been controversial. METHODS: In nine pigs, a left anterior descending coronary artery stenosis was created to reduce flow reserve (maximal/rest flow) to 1.1 to 1.9 without baseline regional wall motion abnormalities. This corresponded to a 50% to 90% diameter stenosis. Wall thickening was measured using epicardial echocardiography. Regional lactate production and coronary venous pH were monitored from an adjacent cardiac vein. A standard protocol of dobutamine stress echocardiography was first performed. After normalization of the ischemic abnormalities elicited with this infusion, esmolol was infused at 50 micrograms/kg body weight per min and the dobutamine test was repeated, with 1.0 mg of atropine added at the maximal dobutamine dose. RESULTS: Without esmolol, dobutamine stress induced myocardial ischemia with a reduction in regional wall thickening and lactate production in all nine pigs. Multiple regression analysis revealed that coronary flow per heartbeat (p < 0.01) and lactate production (p < 0.05) independently correlated with regional wall thickening during dobutamine stress. The beta-blocker significantly reduced heart rate and regional oxygen consumption and altered the relation between coronary flow per heartbeat and regional wall thickening (p < 0.05) during dobutamine stress. Esmolol prevented dobutamine-induced ischemia (lactate production and wall motion abnormalities) in seven of nine pigs. The addition of atropine induced lactate production and a reduction in wall thickening in five of seven pigs in which ischemia had been prevented by beta-blockade. However, lactate production was higher and regional venous pH was lower with the baseline dobutamine infusion than with that performed after esmolol with atropine added at the maximal dobutamine dose (p < 0.05). CONCLUSIONS: A correlation between regional wall thickening and coronary flow per heartbeat was demonstrated during baseline dobutamine stress. Beta-blockade shifted this relation so that dobutamine stress-induced myocardial ischemia was attenuated. The mechanisms by which beta-blockade prevents dobutamine-induced ischemia appeared to be mainly through decreases in heart rate and rate of rise in left ventricular pressure, improvement of regional coronary flow per heartbeat and attenuation of regional ischemic lactate production. Adding atropine in conventional doses enhanced the ability of dobutamine stress to induce myocardial ischemia but did not completely abolish the effects of beta-blockade on either the severity of dobutamine-induced wall thickening abnormalities or regional metabolic disturbances.

Adrenergic beta-Antagonists↗
PubMed1996

Effects of continuous positive airway pressure on cardiac output and plasma norepinephrine in sedated pigs.

Continuous positive airway pressure (CPAP) increases cardiac output (CO) in congestive heart failure (CHF). In six sedated pigs that were normovolemic (NV) and hypervolemic (HV), and seven previously instrumented pigs with pacing-induced CHF, we tested the hypothesis that this is associated with decreased total body sympathetic nerve activity (SNA). Hemodynamic variables and plasma norepinephrine level measurements were measured at baseline, CPAP 5 and 10 cm H2O, and recovery. Arterial O2 saturation was maintained at greater than or equal to 90% and PCO2 did not change. For NV baseline plasma norepinephrine level (PNE) was 97 +/- 61 pg/mL, CO 2.4 +/- .5 L/min, and pulmonary wedge pressure (Pw) 10.1 +/- 2.4 mmHg and did not change with CPAP. HV and CHF were associated with increased baseline Pw (18-21 mmHg). Baseline CO was increased with HV and unchanged with CHF. Baseline PNE was increased 4 to 5-fold with both HV and CHF. CO increased at CPAP 5 compared with baseline with both HV and CHF. However, PNE decreased with CPAP in HV, and increased with CPAP in CHF. Increased CO was always associated with decreased systemic vascular resistance. We conclude the following: (1) increased CO with CPAP can be associated with either increasing or decreasing SNA; (2) CPAP can produce increases in CO when the heart is distended whether baseline LV function is relatively normal (HV) or depressed (CHF); and (3) there are probably a number of different mechanism increasing CO with CPAP and these may vary from condition to condition.

Animals↗
PubMed1996

The effects of high dose NG-nitro-L-arginine-methyl ester on myocardial blood flow and left ventricular function in dogs.

PURPOSE: Nitric oxide (NO) synthase inhibition has been reported to cause elevation in mean arterial pressure (MAP) and a decrease in cardiac index (CI), the cause of which is not completely understood. It has been shown that increased concentrations of NO synthase inhibitors cause a further drop in cardiac output without a corresponding increase in arterial pressure, prompting the conclusion that NO inhibition results in direct myocardial depression. However, myocardial ischemia was not completely ruled out as a cause for myocardial dysfunction in these studies. The purpose of this study was to examine the effects of 30 mg/kg of the NO synthase inhibitor NG-nitro-L-arginine-methyl ester (L-NAME) to those of 300 mg/kg and assess the effects on coronary ischemia and myocardial function. MATERIALS AND METHODS: Eight anesthetized dogs underwent median sternotomy and pericardiectomy. L-NAME 30 mg/kg was administered and the effects were recorded at 5, 15, and 30 minutes. Thereafter, 300 mg/kg was administered and the effects were observed for 5, 15, and 30 minutes. We measured MAP, heart rate (HR), CI, left ventricle (LV) and systolic and diastolic pressures, the first derivative of LV pressure (dP/dt), left anterior descending artery blood flow, regional LV contraction, gas tensions, and lactates. A coronary sinus catheter allowed for measurements of coronary sinus pressure, lactate, and gas tensions. Stroke volume, percent myocardial shortening (dL/dt) myocardial oxygen consumption, and net lactate myocardial production were calculated. RESULTS: Whereas 30 mg/kg had minimal effects on coronary blood flow and LV function, 300 mg/kg resulted in profound hypotension, drop in CI, and acidocsis. CONCLUSIONS: L-NAME at 30 mg/kg caused a rise in MAP and systemic vascular resistance; however, it had no effect on ventricular function. High dose NO synthase inhibition causes myocardial depression not related to increased afterload, coronary vasoconstriction, or myocardial ischemia.

Animals↗
PubMed1996

Deficient cerebellar long-term depression, impaired eyeblink conditioning, and normal motor coordination in GFAP mutant mice.

Mice devoid of glial fibrillary acidic protein (GFAP), an intermediate filament protein specifically expressed in astrocytes, develop normally and do not show any detectable abnormalities in the anatomy of the brain. In the cerebellum, excitatory synaptic transmission from parallel fibers (PFs) or climbing fibers (CFs) to Purkinje cells is unaltered, and these synapses display normal short-term synaptic plasticity to paired stimuli in GFAP mutant mice. In contrast, long-term depression (LTD) at PF-Purkinje cell synapses is clearly deficient. Furthermore, GFAP mutant mice exhibited a significant impairment of eyeblink conditioning without any detectable deficits in motor coordination tasks. These results suggest that GFAP is required for communications between Bergmann glia and Purkinje cells during LTD induction and maintenance. The data support the notion that cerebellar LTD is a cellular mechanism closely associated with eyeblink conditioning, but is not essential for motor coordination tasks tested.

Animals↗
PubMed1996

Synthesis and structure determination of the adducts formed by electrochemical oxidation of 1,2,3,4-Tetrahydro-7,12-dimethylbenz[a]anthracene in the presence of deoxyribonucleosides or adenine.

Study of DNA adducts formed with aromatic hydrocarbons is part of the strategy to elucidate the mechanisms of tumor initiation by these compounds. 1,2,3,4-Tetrahydro-7,12-dimethylbenz[a]anthracene (THDMBA) is of special interest because it allows discrimination between the pathways of bioactivation by one-electron oxidation and monooxygenation. To study and identify adducts formed biologically, synthetic adducts are needed as reference standards. THDMBA was electrochemically oxidized in the presence of deoxyadenosine (dA), adenine (Ade), deoxyguanosine (dG), or deoxycytidine (dC). In the presence of dA, four adducts were isolated: 7-methyl-1,2,3,4-tetrahydrobenz[a]anthracene-12-CH2-N7Ade (7-MTHBA-12-CH2-N7Ade, 3.6%), 12-MTHBA-7-CH2-N7Ade (4.2%), 7-MTHBA-12-CH2-N6dA (5.8%), and 12-exo-methylene-7-MTHBA-7-N6dA (22.8%); a dehydrogenated product, 7,12-di-exo-methylene-THBA (44.2%), was also obtained. In the presence of Ade, nine adducts were synthesized: 7-MTHBA-12-CH2-N7Ade (1.1%), 12-MTHBA-7-CH2-N7Ade (2.4%), 7-MTHBA-12-CH2-N1Ade (10.2%), 12-MTHBA-7-CH2-N1Ade (13.2%), 7-MTHBA-12CH2-N3Ade (1.7%), 12-MTHBA-7-CH2-N3Ade (1.7%), 7-exo-methylene-12-MTHBA-12-N3Ade (11.2%), 12-exo-methylene-7-MTHBA-7-N3Ade (27.9%), and 12-exo-methylene-7-MTHBA-7-N6Ade (12.1%), as well as the dehydrogenated product 7,12-di-exo-methylene-THBA (16.7%). In the presence of dG, three adducts were produced: 7-MTHBA-12-CH2-N7Gua (24.2%), 12-MTHBA-7-CH2-N7Gua (12.2%), and 7-MTHBA-12-CH2-N2dG (3.7%), as well as the dehydrogenated product 7,12-di-exo-methylene-THBA (38.9%). Anodic oxidation in the presence of dC yielded a large amount of 7,12-di-exo-methylene-THBA (80.4%), but no adducts. The structure of the adducts was elucidated by using UV, NMR, and MS. The N-7 positions in dG, dA, and Ade, the 2-NH2 in dG, and the N-1 position in Ade form exclusively methyl-linked adducts. In contrast, the 6-NH2 group of dA and Ade and the N-3 of Ade prefer to attack the meso-anthracenic positions rather than the methyl groups. The order of reactivity of dG and dA in the formation of methyl-linked THDMBA adducts agrees well with that previously found for 7,12-dimethylbenz[a]anthracene [RamaKrishna et al. (1992) J. Am. Chem. Soc. 114, 1863-1874.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1996

The development of metacognitive knowledge of basic motor skill: walking.

The development of children's metacognitive knowledge of walking was investigated. Sixty elementary school children (30 boys and 30 girls), 9, 11, and 13 years of age, viewed a video presentation of an adult performing normal walking and six different forms of partial walking (varying in terms of the presence or absence of four essential features of normal walking: arm swing, leg swing, arm-leg coordination, and distance traveled). Then the children were asked to rate the partial walking. A repeated measures ANOVA revealed that children of all these ages appreciated the differences between normal walking and partial walking. As age increased, the degree of importance of the four features became more differentiated. By 13 years of age, the children considered leg swing to be the most important feature of walking, arm swing the second, arm-leg coordination the third, and distance traveled the least important feature.

Adolescent↗
PubMed1996

The effect of interferon-alpha on the pituitary-adrenal axis.

This report concerns the use of a minimum stress animal model for evaluating the neuromodulatory effects of interferon-alpha (IFN-alpha). Male Sprague-Dawley rats, 350-450 g, received jugular catheters and were habituated to handling and sampling arenas. These procedures will minimize stress usually associated with i.v. injections and blood sampling. Natural rat IFN-alpha/beta (RaIFN-alpha/beta) endotoxin free (Lee Biomolecular Research Laboratories, San Diego, CA) or recombinant human IFN-alpha, (rHuIFN-alpha) (a gift from Hoffman La Roche, Nutley, NJ) was injected into rats via catheter at various IFN concentrations. Controls were injected with either (1) vehicle (saline), (2) human or bovine serum albumin in saline, or (3) heat-denatured RaIFN-alpha/beta. Experiments were begun (0 h) at about 0900 h, and blood samples were withdrawn at intervals up to 2 h after IFN or control injections and replaced by the same volume of saline. The concentrations of corticosterone and ACTH in peripheral plasma were measured by radioimmunoassay. Both IFN, when injected at concentrations of 300 or 600 U/g body weight (U/gbw), stimulated an increase above 0 h levels of both hormones in the same animals. Additionally, the stimulation was also evident when compared with plasma hormone levels in animals injected with control substance in a parallel time course. After administration of 150 U/gbw of either IFN, only the increase in the blood corticosterone was significant. These studies demonstrate that both homospecific (RaIFN-alpha/beta) and heterospecific (rHuIFN-alpha) IFN preparations are capable of stimulating the pituitary-adrenal axis.

Adrenal Cortex↗
PubMed1996

Coronary stenosis progression differs in patients with stable angina pectoris with and without a previous history of unstable angina.

OBJECTIVES: To compare the evolution of stenoses responsible for acute coronary events with those not associated with acute coronary syndromes. METHODS AND RESULTS: We prospectively studied angiographic stenosis progression in 190 stable angina patients, with single vessel disease, who were awaiting non-urgent coronary angioplasty. Sixty four patients had a previous history of unstable angina (Group 1) and 126 patients had no history of unstable angina (Group 2). Culprit stenoses were classified as "complex' or "smooth'. At restudy, 8 +/- 4 months after the first angiogram, 12 of 63 culprit stenoses in Group 1 had progressed and seven of 125 in Group 2 (19% vs 6%, P = 0.0044). Thirteen of 68 complex culprit stenoses had progressed, compared with only 6 of 120 smooth culprit stenoses (19% vs 5%, P = 0.003). Coronary events occurred in 12 Group 1 patients and nine Group 2 patients (P = 0.02). CONCLUSIONS: In patients with stable angina, stenoses associated with previous episodes of unstable angina are more likely to progress than stenoses not associated with previous unstable angina. Unstable coronary atherosclerotic plaques, even those that have been clinically stable for more than 3 months, may retain the potential for rapid progression to total occlusion.

Adult↗
PubMed1996

Predictors of persistence and remission of ADHD into adolescence: results from a four-year prospective follow-up study.

OBJECTIVE: To evaluate the predictors of persistence and the timing of remission of attention-deficit hyperactivity disorder (ADHD). METHOD: Subjects were 6- to 17-year old Caucasian, non-Hispanic boys with and without ADHD. DSM-III-R structured diagnostic interviews and blind raters were used to examine psychiatric diagnoses, cognitive achievement, social, school, and family functioning at a 4-year follow-up assessment. RESULTS: At the 4-year follow-up assessment, 85% of children with ADHD continued to have the disorder and 15% remitted. Of those who remitted, half did so in childhood and the other half in adolescence. Predictors of persistence were familiality of ADHD, psychosocial adversity, and comorbidity with conduct, mood, and anxiety disorders. CONCLUSIONS: The findings prospectively confirm that the majority of children with ADHD will continue to express the disorder 4 years later. For a minority of children, ADHD was a transient disorder that remits early in development. In addition, we have shown that persistence of ADHD is predictable. Familiality, adversity, and psychiatric comorbidity may be clinically useful predictors of which children with ADHD are at risk for a persistent disorder.

Achievement↗
PubMed1996

Attention-deficit hyperactivity disorder and juvenile mania: an overlooked comorbidity?

OBJECTIVE: To evaluate the psychiatric, cognitive, and functional correlates of attention-deficit hyperactivity disorder (ADHD) children with and without comorbid bipolar disorder (BPD). METHOD: DSM-III-R structured diagnostic interviews and blind raters were used to examine psychiatric diagnoses at baseline and 4-year follow-up in ADHD and control children. In addition, subjects were evaluated for cognitive, academic, social, school, and family functioning. RESULTS: BPD was diagnosed in 11% of ADHD children at baseline and in an additional 12% at 4-year follow-up. These rates were significantly higher than those of controls at each assessment. ADHD children with comorbid BPD at either baseline or follow-up assessment had significantly higher rates of additional psychopathology, psychiatric hospitalization, and severely impaired psychosocial functioning than other ADHD children. The clinical picture of bipolarity was mostly irritable and mixed. ADHD children with comorbid BPD also had a very severe symptomatic picture of ADHD as well as prototypical correlates of the disorder. Comorbidity between ADHD and BPD was not due to symptom overlap. ADHD children who developed BPD at the 4-year follow-up had higher initial rates of comorbidity, more symptoms of ADHD, worse scores on the CBCL, and a greater family history of mood disorder compared with non-BPD, ADHD children. CONCLUSIONS: The results extend previous results documenting that children with ADHD are at increased risk of developing BPD with its associated severe morbidity, dysfunction, and incapacitation.

Adolescent↗
PubMed1996

Is childhood oppositional defiant disorder a precursor to adolescent conduct disorder? Findings from a four-year follow-up study of children with ADHD.

OBJECTIVE: To evaluate the overlap between attention-deficit hyperactivity disorder (ADHD) and oppositional defiant disorder (ODD), addressing whether ODD is subsyndromal form of conduct disorder (CD) and, if so, whether it is a precursor or prodrome syndrome of CD. METHOD: Assessments from multiple domains were used to examine 140 children with ADHD and 120 normal controls at baseline and 4 years later. RESULTS: Of children who had ADHD at baseline, 65% had comorbid ODD and 22% had CD. Among those with ODD, 32% had comorbid CD. All but one child with CD also had ODD that preceded the onset of CD by several years. ODD+CD children had more severe symptoms of ODD, more comorbid psychiatric disorders, lower Global Assessment of Functioning Scale scores, more bipolar disorder, and more abnormal Child Behavior Checklist clinical scale scores compared with ADHD children with non-CD ODD and those without ODD or CD. In addition, ODD without CD at baseline assessment in childhood did not increase the risk for CD at the 4-year follow-up, by midadolescence. CONCLUSIONS: Two subtypes of ODD associated with ADHD were identified: one that is prodromal to CD and another that is subsyndromal to CD but not likely to progress into CD in later years. These ODD subtypes have different correlates, course, and outcome.

Adolescent↗
PubMed1996

Electrophysiological mechanisms for the antiarrhythmic action of (-)-caryachine in rat heart.

(-)-Caryachine (CNMe) is a pavine derivative, isolated from Cryptocarya chinensis Hemsl. We wished to illustrate the electrophysiological effect and antiarrhythmic potential of this compound on rat cardiac tissues. Action potential and ionic currents in single ventricular cells were examined by current clamp or voltage clamp in a whole-cell configuration. CNMe concentration-dependently suppressed the maximum rate of rise of the action potential upstroke (V(max)) and prolonged the action potential duration at 50% of repolarization (APD(50)). A voltage-clamp study showed that the suppression of V(max) by CNMe was associated with an inhibition of sodium inward current (I(Na), IC(50), O = 4.1 microM). The prolongation of APD(50) was associated with an inhibition of transient outward current (I(to), IC(50) = 16.1 microM). CNMe reduced the I(Na) with a negative shift of its voltage-dependent steady-state inactivation curves and slowing of its recovery from inactivation. The use-dependent inhibition of I(Na) by CNMe was enhanced at a higher stimulation rate or at a longer prepulse duration. The fraction of fast recovery of I(Na) was reduced, but the recovery time constant of fast recovery component remained unaffected. The inhibition of I(to) by CNMe (10-30 microM) was associated with an acceleration of its time constant of inactivation. According to the analysis of the time course of inhibition of I(to), CNMe inhibited I(to) in a time-dependent manner. In isolated heart, CNMe could effectively inhibit ischemia/reperfusion-induced ventricular tachycardia with an EC(50) of 3.9 microM. The results indicate that CNMe is a strong I(Na) blocker with some I(to) blocking activity. The inhibition of I(Na), and I(to) may contribute to its antiarrhythmic activity against ischemia/reperfusion arrhythmia.

Action Potentials↗
PubMed1996

Injury to vascular endothelial cells and the change of plasma endothelin level in dogs with gunshot wounds.

The purpose of this study was to evaluate the relationship between injury to endothelial cells and the plasma endothelin level after gunshot wounds. Forty dogs were divided into four groups. The dogs in group 1 served as a control. The dogs in groups 2,3, and 4, respectively, were shot in both hind legs, in the hypogastric part of the abdomen, or in the right chest by military bullets (5.56 mm or 7.62 mm). After wounding, blood samples were taken at different intervals and the number of circulating endothelial cells (CEC), an indicator of injury to vascular endothelial cells (VEC), and the level of plasma endothelin were measured. Results showed that the CEC number increased in all groups immediately after wounding and showed a peak value at 10 minutes and at 6 hours. The change in plasma endothelin level paralleled that of the change of CEC number, and a linear relationship was found between them. These results suggest that, in gunshot wounds, extensive injury to VEC may be the result of the temporary cavity and shock waves produced by high velocity missiles striking the body and causing secretions of endothelin. The mechanism of injury to VEC after a gunshot wound in discussed in this paper.

Animals↗