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Biomedical subjects

W Tang

Publications and source records attributed to W Tang.

At least 235 records · Page 13Linked to original sources
PubMed1996

Effects of buffer agents on postresuscitation myocardial dysfunction.

OBJECTIVES: Earlier studies demonstrated that hypertonic buffer agents administered during cardiopulmonary resuscitation (CPR) altered neither myocardial pH nor cardiac resuscitability. The rationale for the routine use of buffer agents for CPR has therefore been challenged. However, when these buffer agents are administered during CPR, they may have favorable effects on the postresuscitation course. Postresuscitation myocardial dysfunction has more recently emerged as a potentially fatal complication after successful cardiac resuscitation. Options for prevention and management of this complication have prompted the present studies, in which the effects of buffer agents administered during CPR are evaluated as to their effects on postresuscitation myocardial function and survival. DESIGN: Prospective, randomized, controlled animal study. SETTING: University animal laboratory. SUBJECTS: Forty male Sprague-Dawley rats (450 to 570 g). INTERVENTIONS: Ventricular fibrillation was induced electrically. Mechanical Ventilation and percordial compression were initiated after either a 4- or an 8-min interval of untreated cardiac arrest. Sodium bicarbonate as a CO2-generating buffer, Carbicarb and tromethamine as CO2-consuming buffers, or hypertonic saline placebo were injected as a bolus into the right atrium during CPR. Defibrillation after 10 mins of cardiac arrest and CPR was successful in each instance. No differences in the electric power required for successful resuscitation were documented. Left ventricular pressure, rate of left ventricular pressure increase measured at a left ventricular pressure of 40 mm Hg (dP/dt40), rate of left ventricular pressure decline (-dP/dt), and end-tidal PCO2 were continuously measured for 240 mins after successful resuscitation. MEASUREMENTS AND MAIN RESULTS: Decreases in coronary perfusion pressure were observed after each buffer or placebo injection. As anticipated, end-tidal PCO2 increased after bicarbonate and decreased after Carbicarb or tromethamine. Postresuscitation left ventricular function was significantly decreased in all animals. However, there was significantly less depression in rate of left ventricular pressure increase measured at a left ventricular pressure of 40 mm Hg (dP/dt40), rate of left ventricular pressure decline (-dP/dt), and a lower left ventricular diastolic pressure with both Carbicarb and tromethamine in association with significant increases in postresuscitation survival rate. When the duration of untreated cardiac arrest was increased to 8 mins, the severity of postresuscitation left ventricular dysfunction was magnified and postresuscitation myocardial function and survival were significantly improved with both CO2-generating and CO2-consuming buffer agents. CONCLUSION: Although buffer agents may not improve the success of resuscitation when administered during CPR, they may ameliorate postresuscitation myocardial dysfunction and thereby improve postresuscitation survival.

Animals↗
PubMed1996

Conjugation of glutathione with a toxic metabolite of valproic acid, (E)-2-propyl-2,4-pentadienoic acid, catalyzed by rat hepatic glutathione-S-transferases.

The hepatotoxic metabolite of the anticonvulsant drug valproic acid (VPA), namely (E)-2-propyl-2,4-pentadienoic acid (E)-2,4-diene VPA), is known to react with glutathione (GSH) in vivo. Although glutathione-S-transferase (GST) was suspected of being the catalyst for this conjugation reaction, this was yet to be confirmed. In this study, GST activities were detected in the hepatic cytosolic and sonic-disrupted mitoplast fractions isolated from male Sprague-Dawley rats by using 1-chloro-2,4-dinitrobenzene as a substrate. An elevation of GST activities by 45 to 100% was observed after pretreatment of rats with phenobarbital (PB). Subsequently, these apparent GST activities were examined for their effects on the in vivo conjugation of GSH with N-acetyl-S-((E)-2-propyl-2,4-pentadienoyl)cysteamine (2,4-diene VPA-NACA), a structural mimic of (E)-2,4-diene VPA coenzyme A thioester. Reaction products were identified and quantitated by combined liquid chromatography-tandem mass spectrometry. The GST-mediated conjugation of GSH with 2,4-diene VPA-NACA produced two structural isomers via either 5,6- or 1,6-addition of GSH. Only the 1,6- addition product was found for the spontaneous conjugation reaction (control). Quantitatively, GSH conjugates formed in the cytosolic fraction were 23-fold that of control. An additional 1.5-fold enhancement was observed in the cytosolic fraction from PB-treated rats. The production of the GSH conjugates was increased by 2-fold for reactions involving the sonic-disrupted mitoplasts, either from untreated or PB-treated rats. Partially purified GST was found to catalyze the conjugation reactions in a fashion similar to that of the isolated subcellular fractions. No reaction with GSH could be detected for the free acid form of (E)-2,4-diene VPA. As was the case with the in vitro data, two structural isomers of GSH conjugates were detected in the bile of rats that received (E)-2,4-diene VPA. These results indicate that in vivo production of the GSH conjugates of (E)-2,4-diene VPA is most likely catalyzed by GST enzymes, with the esterified diene being essential for the conjugation reaction. In a separate experiment, 2,4-diene VPA-NACA was observed to alkylate reduced oxytocin through one or both cysteine residues. Thus, the toxicity of (E)-2,4-diene VPA might be produced via either GST-promoted depletion of cellular GSH, or a direct modification of key proteins, or both.

Animals↗
PubMed1996

Experimental extrinsic allergic alveolitis and pulmonary angiitis induced by intratracheal or intravenous challenge with Corynebacterium parvum in sensitized rats.

Extrinsic allergic alveolitis and pulmonary sarcoidosis are granulomatous diseases of the lung for which clinical presentation and anatomic site of granuloma formation differ. Extrinsic allergic alveolitis is caused by inhaled antigens, whereas the nature and source of the inciting antigen in sarcoidosis is unknown. To test the hypothesis that the route via which antigen is introduced to the lung contributes to the clinicopathological presentation of pulmonary granulomatous disease, rats immunized with intravenous (i.v.) Corynebacterium parvum were challenged after 2 weeks with either intratracheal (i.t.) or i.v. C. parvum. The granulomatous inflammation elicited by i.t. challenge predominantly involved alveolar spaces and histologically simulated extrinsic allergic alveolitis. In contrast, the inflammation induced by i.v. challenge was characterized by granulomatous angiitis and interstitial inflammation simulating sarcoidosis. Elevations of leukocyte counts and TNF levels in bronchoalveolar fluid, which reflect inflammation in the intra-alveolar compartment, were much more pronounced after i.t. than after i.v. challenge. Tumor necrosis factor, interleukin-6, CC chemokine, CXC chemokine, and adhesion molecule mRNA and protein expression occurred in each model. In conclusion, i.t. or i.v. challenge with C. parvum in sensitized rats caused pulmonary granulomatous inflammation that was histologically similar to human extrinsic allergic alveolitis and sarcoidosis, respectively. Although the soluble and cellular mediators of granulomatous inflammation were qualitatively similar in both disease models, the differing anatomic source of the same antigenic challenge was responsible for differing clinicopathological presentations.

Alveolitis, Extrinsic Allergic↗
PubMed1996

Cloning and function determination of promoter region of glucoamylase gene from Aspergillus niger T21.

A 850 bp fragment of the 5' flanking region of the glucoamylase gene (glaA) was synthesized from A. niger T21 genome using PCR. The function detection vector was constructed by fusing this fragment to E. coli hygromycin B phosphotransferase gene (hph) and was used to transform A. niger. The high hygromycin resistance transformants thus obtained verified that the synthesized fragment functioned as a promoter in filamentous fungi. Southern blot analysis showed the hph gene has been integrated into genomic DNA of A. niger transformant.

Anti-Bacterial Agents↗
PubMed1996

[Lipoprotein (a) and non-insulin dependent diabetes mellitus].

To study the relationship of the concentration of serum lipoprotein (a) [Lp(a)] with diabetic complications in non-insulin dependent diabetes mellitus (NIDDM), 100 non-diabetics with 150 patients with NIDDM were compared. There was no difference in Lp(a) concentration (P > 0.5) between the two groups. Lp(a) concentration was not significantly correlated with the levels of total cholesterol, low-density lipoprotein cholesterol, triglyceride, high-density lipoprotein cholesterol (HDL-C), HDL2-C, HDL3-C, apolipoprotein A-I, apolipoprotein B in both groups. In NIDDM group, patients with hypertension, macro- and microangiopathy had higher levels of Lp(a) than those without these complications (P < 0.001 and P = 0.002 respectively). Lp(a) level was positively related to presence of macroangiopathy (r = 0.185, P = 0.024) and proteinuria (r = 0.316, P < 0.001) in NIDDM.

Adult↗
PubMed1996

[Tolerance to rat parathyroid allograft induced by depletion of Ia+ donor cells plus short course cyclosporine].

In this study, Ia+ donor cells of rat parathyroid allografts were depleted by anti-Ia monoclonal antibody plus complement. The secreting function of treated glands as well preserved. Then we transplanted the treated glands into subcapsular of the recipient kindey, and the median survival time (MST) of the allografts were 60 days, compared with 14 days in the fresh PTG group (P < 0.01). If the recipients received 25 mg/kg cyclosponine for three days before transplantation, the MST of about 60% PTG allografts was more than 150 days, with P < 0.01 in comparison with the control group (short course CyA alone, MST: 70 days). These results indicate that long-term survival of rat parathyroid allografts can be achieved by depletion of Ia+ donor cells and short course pretreatment of the recipient with CyA.

Animals↗
PubMed1996

[The role of amylase in abdominal fluid in evaluating severity of acute pancreatitis and its prognosis].

Acute pancreatitis (AP) was induced on 22 cats, by injecting the mixture of bile and trypsin at different doses into the main pancreatic duct (MPD). In Group A, 7 cats revealed pancreatic interstitial edema after the injection of the mixture at 0.8 mg/kg. In Group B, 8 cats received the injection of the MPD at 1.0 mg/kg which resulted in significant extensive necrosis of the pancreas. The same pathological change was found in Group C (7 cats), combined with lesions of the lung and the liver. The survival time was different, more than 7 days in Group A, 50.4 hours in Group B and 10.4 hours in Group C (P < 0.001). Amylase concentration also showed marked difference in different groups, 4,890 U/L in Group A; 13 952 U/L in Group B and 23,810 U/L (P < 0.001) in Group C. These results are directly proportional to the severity of AP, but inversely proportional to the survival time. It suggests that amylase concentration in abdominal fluid can be used as an important marker to evaluate the severity of AP and its prognosis.

Acute Disease↗
PubMed1996

[Minilaparotomy cholecystectomy with clinical analysis of 50 cases].

Fifty cases of gallbladder disease operated with minilaparotomy cholecystectomy (MC) and fifty cases operated with conventional cholecystectomy (CC) were reviewed and compared in terms of their need of postoperative analgesic and hospitalization days. The results showed that the MC was better than the CC. The merits and demerits of MC. CC and LC were discussed. The operative indexes of MC were presented by author.

Adult↗
PubMed1995

Epinephrine increases the severity of postresuscitation myocardial dysfunction.

BACKGROUND: Epinephrine has been the mainstay for cardiac resuscitation for more than 30 years. Its vasopressor effect by which it increases coronary perfusion pressure is likely to favor initial resuscitation. Its beta-adrenergic action, however, may have detrimental effects on postresuscitation myocardial function when administered before resuscitation because it increases myocardial oxygen consumption. In the present study, our focus was on postresuscitation effects of epinephrine when this adrenergic agent was administered during cardiopulmonary resuscitation. Postresuscitation myocardial functions were compared with those of a selective alpha-adrenergic agent, phenylephrine, when epinephrine was combined with a beta 1-adrenergic blocking agent, esmolol, and saline placebo. METHODS AND RESULTS: Ventricular fibrillation was induced in 40 Sprague-Dawley rats. Mechanical ventilation and precordial compression was initiated either 4 or 8 minutes after the start of ventricular fibrillation. The adrenergic drug or saline placebo was administered as a bolus after 4 minutes of precordial compression. Defibrillation was attempted 4 minutes later. Left ventricular pressure, dP/dt40, and negative dP/dt were continuously measured for an interval of 240 minutes after successful cardiac resuscitation. Except for saline placebo, comparable increases in coronary perfusion pressure were observed after each drug intervention. The number of countershocks required for restoration of spontaneous circulation was significantly greater for epinephrine-treated animals (10 +/- 8) when compared with phenylephrine-treated animals (1.8 +/- 0.4, P < .01) and with animals treated with epinephrine combined with esmolol (1.6 +/- 0.9, P < .01). After resuscitation, dP/dt40 and negative dP/dt were significantly decreased and left ventricular end-diastolic pressure was significantly increased in each animal when compared with prearrest levels. However, the greatest impairment followed epinephrine, and this was associated with significantly greater heart rate and the shortest interval of postresuscitation survival of 8 +/- 4 hours, whereas placebo controls survived for 12 +/- 11 hours. Phenylephrine-treated animals survived for 41 +/- 10 hours (P < .01 versus epinephrine), and animals that received a combination of epinephrine and esmolol survived for 35 +/- 11 hours (P < .01 versus epinephrine). When the duration of untreated cardiac arrest was increased from 4 to 8 minutes, the severity of postresuscitation left ventricular dysfunction was magnified, but disproportionate decreases in postresuscitation survival were again observed with placebo and epinephrine when compared with alpha-adrenergic agonists. CONCLUSIONS: In an established rodent model after resuscitation following cardiac arrest, epinephrine significantly increased the severity of postresuscitation myocardial dysfunction and decreased duration of survival. More selective alpha-adrenergic agonist or blockade of beta 1-adrenergic actions of epinephrine reduced postresuscitation myocardial impairment and prolonged survival.

Adrenergic Agonists↗
PubMed1995

Effects of axial ligand replacement on the redox potential of cytochrome c.

The formal potentials (E0') and electron transfer numbers (n) of imidazole (Im), 1-methylimidazole (1-MeIm), and 1-ethylimidazole (1-EtIm) complexes of cytochrome c have been determined for the first time using optically transparent thin-layer spectroelectrochemistry. In comparing these results with the E0' value of the cytochrome c, their potentials at infinite dilution have been calculated, which indicate that axial replacement of methionine-80 by Im, 1-MeIm, and 1-EtIm gives rise to 426, 359, and 327 mV negative shifts relative to that of native cytochrome c, respectively. Thereby, the origins of the effects of axial substitution on redox potential are discussed.

2,6-Dichloroindophenol↗
PubMed1995

Racial differences in coronary calcium prevalence among high-risk adults.

A total of 1,461 asymptomatic high-risk adult subjects were studied with digital subtraction fluoroscopy and conventional cinefluoroscopy to detect coronary calcium. Ethnicity and risk factor data were recorded. No subject had a history or electrocardiographic evidence of prior myocardial infarction. The prevalence of coronary calcium by digital subtraction fluoroscopy was high (58%). Substantial ethnic differences in prevalence were noted: 36% of African American subjects, 60% of Caucasian subjects, and 60% of Asian American subjects had definite radiographic evidence of coronary calcium. The difference in prevalence between African American and other subjects was significant (p < 0.0001) by chi-square test for all 3 races. These differences persisted in the unsubtracted cinefluoroscopic images (p < 0.0001) and after controlling for age, gender, and other risk factors (p = 0.003). After 20 +/- 11 months of follow-up, African Americans had more coronary artery disease events (13%) than Caucasians (6%) or Asian Americans (5%) (p = 0.04). Thus, African Americans have a significantly lower prevalence of coronary calcium than do Caucasians or Asian Americans. Based on the follow-up results, these differences in prevalence are not explained by differences in coronary artery disease risk.

Aged↗
PubMed1995

Binding of 1-methylimidazole to cytochrome c: kinetic analysis and resonance assignments by two-dimensional NMR.

The binding of 1-methylimidazole to the heme iron by displacing Met-80 of cytochrome c has been studied by two-dimensional (2D) exchange spectroscopy. Two components of cytochrome c ligated by 1-methylimidazole (1-MeIm-cyt c) are first identified, which are related to the sterically hindered orientation of 1-methylimidazole by the heme pocket. Based on a matrix formalism, the kinetic parameters are calculated from the 2D peak amplitudes. With the known resonance assignments of cytochrome c, some hyperfine shifted resonances arising from heme peripheral protons and two axial ligands, and some side-chain resonances of the aliphatic and aromatic protons of 1-MeIm-cyt c have been straightforwardly assigned, which provide a clue to ligand-induced electronic and molecular structural changes of the protein.

Cytochrome c Group↗
PubMed1995

Differential sensitivity of p53(-) and p53(+) cells to caffeine-induced radiosensitization and override of G2 delay.

Most drug discovery efforts have focused on finding new DNA-damaging agents to kill tumor cells preferentially. An alternative approach is to find ways to increase tumor-specific killing by modifying tumor-specific responses to that damage. In this report, we ask whether cells lacking the G1-S arrest in response to X-rays are more sensitive to X-ray damage when treated with agents that override G2-M arrest. Mouse embryonic fibroblasts genetically matched to be (+) or (-) p53 and rat embryonic fibroblasts (+) or (-) for wild-type p53 function were irradiated with and without caffeine, a known checkpoint inhibitor. At low doses (500 microM), caffeine caused selective radiosensitization in the p53(-) cells. At this low dose (where no effect was seen in p53(+) cells), the p53(-) cells showed a 50% reduction in the size of the G2-M arrest. At higher doses (2 mM caffeine), where sensitization was seen in both p53(+) and p53(-) cells, the radiosensitization and the G2-M override were more pronounced in the p53(-) cells. The greater caffeine-induced radiosensitization in p53(-) cells suggests that p53, already shown to control the G1-S checkpoint, may also influence aspects of G2-M arrest. These data indicate an opportunity for therapeutic gain by combining DNA-damaging agents with compounds that disrupt G2-M arrest in tumors lacking functional p53.

Animals↗