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Biomedical subjects

J Duan

Publications and source records attributed to J Duan.

At least 73 records · Page 4Linked to original sources
PubMed1996

A novel renal hypertensive guinea pig model for comparing different inhibitors of the renin-angiotensin system.

The present study describes a novel renal hypertensive guinea pig model for comparing different inhibitors of the renin-angiotensin system (RAS). Renal hypertension was induced by a two-step procedure consisting of ligation of the left caudal renal artery and right nephrectomy. Sham-operated animals were used as controls. Arterial blood pressure and heart rate were monitored in conscious animals. Left caudal renal artery ligation and subsequent right nephrectomy led to a significant increase (32% over sham-operated controls, p < .05) in mean arterial blood pressure (MABP), 3 to 4 weeks following surgery. Renal hypertensive animals had increased urine production (from 63 +/- 8 mL/kg per day to 143 +/- 29 mL/kg per day, p < .05) and an increased incidence of proteinuria (11/13 animals had urine protein levels higher than 20 mg/kg per day). Five of the 13 renal hypertensive animals also had hematuria. On autopsy, an 83% increase in the left kidney/body weight ratio and a 37% increase in the heart/body weight ratio were observed in the renal hypertensive animals, compared to the sham-operated controls. Changes in blood pressure and heart rate were assessed before and after an intravenous bolus injection of the drug to be tested. Captopril reduced MABP in both sham-operated and renal hypertensive animals with equal efficacy (up to a maximum of 42%). In contrast, BILA 2157 BS, one of our human renin inhibitors, produced a similar maximum MABP decrease but only in renal hypertensive animals. This selective antihypertensive effect was also observed with enalkiren, another renin inhibitor. These results indicate that the renal hypertensive guinea pig is an useful model for comparing and contrasting different RAS inhibitors.

Animals↗
PubMed1996

[The research of radioimmunoassay using double Abs for bradykinin].

Bradykinin (BK) is a potent vasodilative substance, and plays great physiological and pathological roles in animals and human beings. To measure the quantity of BK, the radioimmunoassay (RIA) has been devised, but the traditional RIA method has certain defects, such as presence of numerows interfering factors and errors and time consuming. Now, we produce anti-BK serum in rabbits by using BK-ovalbumin conjugate as an immunogen, and the 125I labeled Tyr8-BK by using a modified chloramine-T method. High specific activity has been obtained after purification with DEAE-Sephadex A-25 column chromatography. We use the donkey anti-rabbit Ab and PEG 6000 to separate the bound from the free 125I-Tyr8-BK. The limitation range of standard curve is from 25 to 1600 pg, NSB is 3.1% affinity constant (K) is 0.8 x 10(10) L/mol, and there is no significant interference with other biological BK analogues. The blood samples are treated by adding Polybrene (inhibitor) and PEG 6000 to deposit the big serum proteins in order to reduce the disturbing substances. This method has been shown to be a sensitive, specific, reliable, simple and convenient measure of the serum BK level. By this method, the serum BK quantities in men, women and rats are respectively 1584 +/- 347 pg/ml, 1642 +/- 302 pg/ml and 1805 +/- 225 pg/ml, the recycling rate is 95%, the intergroup CV is 5.0% and outergroup CV = 9.2%.

Animals↗
PubMed1996

[Effects of gossypol acetic acid on human ejaculated sperm Ca2+ influx and rat vas deferens contraction action].

It has been reported that gossypol acetic acid (GAA) inhibits sperm motility and calcium plays an important role in regulating the function of the sperm flagella. In order to explore the mechanism by which GAA inhibits sperm motility, the effects of GAA on human ejaculated sperm Ca2+ influx and isolated rat vas deferens contraction action were studied. The results showed that GAA inhibited sperm Ca2+ influx in a dose-dependent manner, and breaked the dynamic equilibrium of sperm internal and external Ca2+ gradient concentrations. It may be one of important mechanism by which GAA inhibits sperm motility. But GAA exerts no effect on the high K+ induced contraction of smooth muscle of isolated rat vas deferens. It is likely that GAA has selective action on the sperm membrane of the rats.

Adult↗
PubMed1995

Age-related changes in electrophysiological responses to muscarinic receptor stimulation in rat myocardium.

Recent studies have demonstrated that the negative chronotropic and inotropic responses of the heart to cholinergic muscarinic receptor stimulation are strikingly enhanced with aging in the rat model. The present study investigated the electrophysiological basis of this phenomenon by determining the effects of a muscarinic receptor agonist, carbachol, on transmembrane action potential parameters in right atrial tissue and right ventricular free wall preparations from adult (6-8 months old) and aged (26-28 months old) Fischer 344 rats. In addition, the effect of carbachol on atrioventricular conduction time (AVT) was determined in isolated perfused beating hearts. The results showed the following. The baseline maximum diastolic potential (MDP: adult, -76.4 +/- 1.8 mV; aged, -66.8 +/- 1.5 mV; p < 0.05; n = 5) but not the action potential duration measured at 95% repolarization (APD95: adult, 40.0 +/- 5.0 ms; aged, 47.4 +/- 6.7 ms; n = 5) differed significantly in aged compared with adult atrium. No significant age-related difference was evident in baseline MDP measured in ventricular epicardium (adult, -69.8 +/- 0.5 mV; aged, -69.0 +/- 1.1 mV; n = 6) or endocardium (adult, -72.5 +/- 1.4 mV; aged, -73.0 +/- 1.2 mV; n =6). The baseline action potential duration measured at 50% repolarization (APD50) differed significantly with age in ventricular endocardium (adult, 11.6 +/- 2.2 ms; aged, 23.0 +/- 4.6 ms; p < 0.05; n =6) but not in epicardium (APD50: adult, 8.1 +/- 0.4 ms; aged, 13.0 +/- 2.3 ms; n = 6). Superfusion with carbachol (0.1 nM - 10 mu M) resulted in concentration-dependent hyperpolarization of MDP in atrium; the magnitude of hyperpolarization differed significantly with age (2.5-fold higher in the aged; p < 0.05; n = 5). Carbachol caused concentration-dependent shortening of APD50; this effect differed significantly with age in the ventricle (2-fold greater in the aged; p < 0.05; n = 6) but not in the atrium. Carbachol prolonged the AVT in atrial-paced (240 beats/min) hearts; the magnitude of carbachol-induced increase in AVT did not differ significantly with age. These results are consistent with the possibility that in the aging heart, greater hyperpolarization at the level of the right atrium (likely involving pacemaker cells) and greater shortening of APD50 at the level of ventricular myocytes may contribute to the enhanced cholinergic-triggered bradycardia and negative inotropic response, respectively.

Action Potentials↗
PubMed1995

Comparative studies on differential inhibition of the renin - angiotensin system in the anesthetized guinea pig.

The present study compares the hemodynamic effects and mechanisms of action of angiotensin II (AngII) antagonists, angiotensin converting enzyme (ACE) inhibitors, and renin inhibitors in the guinea pig, an animal with high similarity to primates in terms of in vitro and in vivo responses to several human renin inhibitors. Animals were anesthetized with urethane and ketamine. The carotid artery was catheterized for monitoring blood pressure and heart rate. After 30 min stabilization, drug (or vehicle) effects were monitored for 1 h following each increasing dose (i.v. bolus injection). Drugs tested include losartan, an AngII receptor antagonist; two renin inhibitors, BILA 2157 BS and PD-134672; and captopril, an ACE inhibitor. All drugs dose dependently decreased blood pressure. Diastolic blood pressure was reduced more than systolic blood pressure, suggestive of vasodilation. The maximum decrease (32 +/- 6%, p < 0.05 vs. vehicle) in mean arterial blood pressure (MABP) by losartan was achieved with a dose of 1 mg/kg. A similar decrease in MABP was observed with renin inhibitors at a dose of 3 mg/kg, without affecting heart rate. A further increase in the dose of renin inhibitors (6 mg/kg) decreased not only blood pressure but also heart rate. Captopril decreased MABP with a maximum of 48 +/- 3% (p < 0.05 vs. vehicle, losartan, and PD-134672). In the presence of HOE-140, a bradykinin antagonist, the MABP decrease by captopril was only 35 +/- 4%, (p < 0.05 vs. captopril alone). Bilateral nephrectomy reduced the peak MABP effect of PD-134672 by 67%, while the effects of captopril on MABP were affected to a lesser degree (57%). Therefore, captopril remains more effective in reducing MABP (p < 0.05 vs. that of PD-134672). These results suggest that renin inhibitors and AngII antagonists act more specifically on the renin - angiotensin system cascade, while captopril acts partially by a bradykinin-dependent mechanism. The small animal model described provides a novel tool for the comparative pharmacologic assessment of different renin - angiotensin system inhibitors.

Alanine↗
PubMed1995

Expression of human interleukin-11 cDNA in E. coli.

A 551-bp hIL-11 gene fragment that includes no nucleotide sequences encoding signal polypeptide and the initial 8 amino acids of the mature protein was cloned into a high-level expression vector pEx31B of E. coli. The authors identified the recombinant plasmid, designated pEx31-IL11, by restriction endonucleases digestion and DNA sequencing. The resulting recombinant plasmids were then used to transform E. coli strain HB101, and expression in the PL promoter system, which is temperature-regulated, was achieved. The expressed fusion protein amounts to 50% of total bacterial proteins. The hIL-11 protein expressed in E. coli was fused to the N-terminal 99 amino acids of the MS2 polymerase to form the inclusion body. These recombinant proteins can be purified to about 80% by extracting inclusion body with urea. One IL-6-dependent cell line 7 TD1 was used for bioassay. The recombinant hIL-11 protein was preliminarily purified and renatured to a specific activity of 10(5)U/mg, even in the presence of an excess of a neutralizing anti-IL-6 antibody.

DNA, Complementary↗
PubMed1995

The modality of huoxue-huayu in treatment of retinal vein occlusion.

BACKGROUND: There were some reports in China about Huoxue-Huayu therapy on retinal vein occlusion (RVO), but prospective and systematic studies are very few. The curative effect and mechanism of this therapy on RVO have not been reported previously. METHODS: 80 patients with RVO were randomly divided into 2 groups, Fundus III (group A) and urokinase group (group B). Group A was treated by Fundus III oral liquid (a composite herbal recipe for Huoxue-Huayu or invigoration of blood circulation and reduction of blood stasis) 10ml/time P.O. t.i.d. The treatment course was 1 mouth. Group B was treated by urokinase. The urokinase that produced in China was used 10,000 u + 5% glucose 500ml/day i.v. drip for 5 days in a course, the rest 5 days going on another course. The total treatment courses lasted 1 month, too. RESULTS: The visual acuity in group A was remarkably improved while that in group B did not change. The extravasated retinal blood was evidently absorbed in 92.7% of the cases in group A and in 66.7% of those in group B. The difference was significant. Fundus III also improved the retinal circulation, decreased the whole blood viscosity and fibrinogen and reduced leakage of the retinal capillaries. The total effective rates were 83.7% in group A and 53.7% in group B with significant statistical difference between the 2 groups (P < 0.01). CONCLUSION: Fundus III may alleviate retinal edema and necroses, improve the recovering of visual acuity, the retinal microcirculation, the rate of absorbing of retinal haemorrhage and treat RVO, and the curative effect is better than urokinase.

Adult↗
PubMed1995

[Chemical constituents of Clematis intricata Bunge].

Five compounds were isolated from the aerial part of Clematis intricata for the first time. On the basis of spectral data (UV, IR, MS, 1HNMR and 13CNMR), they were identified as scopoletin, caffeic acid, inositol, 1-tria-contanol and beta-sitosterol.

Caffeic Acids↗
PubMed1995

Cloning, expression and purification of the ligand-binding region of human IL-6R in E. coli and its preliminary functional identification.

The ligand-binding region of human IL-6R is taken as the target gene fragment to be cloned and expressed. With pET-3b as expressing vector, two recombinants pET-6R(B) and pET-6R(B)4 have been constructed encoding the ligand-binding region (28 kD) of hIL-6R and its dimmer (53 kD), respectively. After induction with IPTG, they produced two proteins rIL6R-28 of 28 kD and rIL6R-53 of 53 kD amounting to 50% and 30% of total bacteria proteins, respectively. The expressed products were mainly recovered as inclusion bodies. After purification and renaturation, both of them were capable of augmenting the growth-stimulating effect of IL-6 on 7TD1 cells, an IL-6 dependent cell line. The result of ELISA also revealed that both rIL6R-28 and rIL6R-53 had the obvious ligand-binding activity.

Antigens, CD↗
PubMed1994

Electro-oculogram of retinal vein occlusion.

Twenty five cases, including 26 eyes with retinal vein occlusion (RVO) were examined by means of the electro-oculogram. The results showed that 23 of the 26 eyes suffering from RVO exhibited abnormalities of the electro-oculogram (EOG). The potential difference and Arden ratio in the RVO eyes were lower than those in the normal eyes (P < 0.01). The more the visual acuity of ill eyes was decreased, the higher the abnormal rate of EOG in ill eyes was. 14 eyes had the visual acuity less than 0.1, whose EOGs were abnormal. Six eyes had the visual acuity from 0.2 to 0.4, in which the EOGs of 5 eyes were abnormal. Six eyes had the visual acuity more than 0.5, among which the EOGs of 4 eyes were abnormal. Based on the above observations, it may be considered that the circulatory disturbance resulting from RVO damages not only the internal layer but also the external layer of the retina. We suggest that EOG is a useful method for distinguishing lesions caused by RVO and may reflect the functional condition of the outer layer of the retina.

Adult↗
PubMed1993

Hemodynamic and nonhemodynamic mechanisms of experimental pulmonary edema in rats and the effects of anisodamine and tetramethylpyrazine--estimation of blood gas analysis, RBC superoxide dismutase and prostaglandin E2 in plasma and bronchoalveolar lavage (Part 3).

Anisodamine (ADM, 654-2, 30 mg/kg) and tetramethylpyrazine (TMP, 120 mg/kg) have shown an apparent preventive effect on pulmonary edema (PE). In this study, the nonhemodynamic mechanism was studied: The dynamic changes of PaO2, O2Sat, PaCO2, and blood pH were measured, and RBC superoxide dismutase (SOD) and plasma and bronchoalveolar lavage (BAL) PGE2 levels were estimated. It was concluded that ADM and TMP exerted inhibitory effects on the hypoxic state. The ability of ADM and TMP to adjust RBC SOD and PGE2 levels may be one of the preventive mechanisms of the drugs.

Animals↗
PubMed1992

Protective effects of amiloride on the ischemic reperfused rat heart. Relation to mitochondrial function.

We examined the effect of amiloride on mechanical, electrical and mitochondrial function as well as ultrastructural integrity, in isolated rat hearts subjected to 30 min low-flow ischemia and 30 min reperfusion. In control hearts, ischemia produced a rapid loss of contractility and a concomitant elevation in resting tension which were associated with a 100% incidence in arrhythmic activity. Reperfusion produced a 22 and 54% recovery in force and rate of force (dF/dt) development, respectively. In control hearts the incidence of arrhythmias was 100% within 5 min of reperfusion which then declined to 50% by 30 min. Ultrastructural defects in these hearts were restricted primarily to mitochondrial damage. Amiloride significantly attenuated the elevation in resting tension at the end of ischemia. Postischemic recovery was significantly increased to 38 and 86% for force and dF/dt, respectively and the incidence of arrhythmias was reduced to 30%. No ultrastructural defects were ever observed in amiloride-treated reperfused hearts. Both interfibrillar and subsarcolemmal mitochondria exhibited depressed respiratory function and adenine nucleotide translocase activity. Although virtually all parameters tended to be elevated in mitochondria isolated from amiloride-treated hearts, a significant increase was seen in only one case. Our results therefore demonstrate an ability of amiloride to enhance postischemic contractile recovery and reduce the incidence of arrhythmias, particularly during reperfusion, an effect associated with virtual total prevention of ultrastructural defects. Although the salutary effect was not significantly correlated to improved mitochondrial function, this dissociation may have been due to removal of damaged mitochondria during the isolation process, in view of diminished mitochondrial damage as viewed by transmission electron microscopy.(ABSTRACT TRUNCATED AT 250 WORDS)

Amiloride↗
PubMed1992

Potential cellular mechanisms of hydrogen peroxide-induced cardiac arrhythmias.

The electrophysiologic effects of hydrogen peroxide on the isolated guinea pig right ventricular free wall were studied using simultaneous recordings of action potentials from the epicardium and the endocardium. Exposure to hydrogen peroxide caused a time- and concentration-dependent change in action potential characteristics. Action potential durations at 50 and 90% of repolarization (APD50 and APD90, respectively) were significantly prolonged by hydrogen peroxide in both the epicardium and the endocardium. Although prolongation occurred at lower concentrations (0.5 mM) in the epicardium, increases in APD in response to higher concentrations of hydrogen peroxide (1 or 4 mM) were maintained for a longer period of time in the endocardium. In addition, hydrogen peroxide (1 or 4 mM) caused significant depolarization in the epicardium after 10 min, although this effect was observed only in the endocardium exposed to 4 mM hydrogen peroxide. Ventricular arrhythmias were observed in 5 of 7, 6 of 7, and 7 of 7 preparations exposed to 0.5, 1, and 4 mM hydrogen peroxide, respectively. The most frequently observed electrophysiologic abnormalities were associated with increased automaticity. Coupled beats, including clearly identifiable early and delayed depolarizations, were also observed. Verapamil (2 microM) and amiloride (0.1 mM) reduced both the incidence and the duration of hydrogen peroxide-induced arrhythmias but did not influence the effects on APD. This study is the first demonstration of hydrogen peroxide-mediated transmural dispersion in APD that could play an important role in the development of ventricular arrhythmias. In addition, our results demonstrate that hydrogen peroxide can induce ventricular arrhythmias through several cellular mechanisms, including increased automaticity, coupled beats, and triggered activity.

Action Potentials↗
PubMed1991

Protective effects of D,L-carnitine against arrhythmias induced by lysophosphatidylcholine or reperfusion.

Electrophysiological effects of lysophosphatidylcholine (50 or 100 microM) and D,L-carnitine (100 microM) were studied under control conditions and in response to simulated ischaemia and reperfusion using the superfused right ventricular free wall preparation from the guinea pig heart. Lysophosphatidylcholine, 100 microM, induced a significant depolarization of the maximum diastolic potential (MDP) in the epicardium, as well as the development of ventricular premature beats, salvos and ventricular tachycardia. Both coupled beats and abnormal automaticity were observed in lysophosphatidylcholine (100 microM)-treated preparations. Carnitine (100 microM) alone had no effect on preparations superfused with normal Tyrode solution. However, it delayed the time to onset and reduced the cumulative duration of lysophosphatidylcholine-induced arrhythmias (P less than 0.05). The incidence of lysophosphatidylcholine-induced abnormal automaticity and salvos was also significantly decreased in the presence of carnitine. Twenty minutes of simulated ischaemia caused depolarization of MDP as well as prolongation followed by block of transmural conduction. Lysophosphatidylcholine (100 microM) did not alter this response however, carnitine significantly reduced ischaemia-induced depolarization in the epicardium. All control preparations developed arrhythmic activity during 30 min of reperfusion. Carnitine accelerated recovery of MDP in the epicardium upon reperfusion, prolonged the time to onset of arrhythmic activity and reduced both its cumulative duration and incidence. In contrast, reperfusion in the presence of lysophosphatidylcholine (100 microM) significantly increased the incidence of arrhythmic activity. Carnitine exerted only minimal antiarrhythmic action when preparations were exposed to reperfusion in the presence of lysophosphatidylcholine. In conclusion, this study demonstrates that carnitine can modify various cellular mechanisms of arrhythmia induced by lysophosphatidylcholine or by reperfusion but is much less effective when lysophosphatidylcholine and reperfusion are combined.

Action Potentials↗