Biomedical subjects

D Q Liu

Publications and source records attributed to D Q Liu.

36 records · Page 2Linked to original sources

PubMed1992

[Alteration in resistance of Plasmodium falciparum to chloroquine after cessation of chloroquine medication for twelve years].

In view of the fact the resistance of Plasmodium falciparum to chloroquine occurred extensively in Hainan, a decision was made in 1979 that the use of chloroquine should be quit in the whole province. A longitudinal survey on chloroquine-sensitivity of P. falciparum was carried out during 1981-1991 to observe the variation in resistance of the parasite after the cessation of the chloroquine medication for every 2-3 years. A tendency of progressive decline of resistance was revealed. By using in vitro test, the rate of chloroquine-resistant P. falciparum dropped from 97.9% in 1981 to 60.9% in 1991 (P < 0.001). The mean dosage of chloroquine for complete inhibition of schizont formation declined from 10.46 pmol/microliters in 1981 to 3.02 pmol/microliters in 1991 (P < 0.001). The percentage of population requiring larger dosage (6.4 pmol/microliters to completely inhibit schizont formation declined from 83.3% in 1981 to 17.4% in 1991 (P < 0.001); whereas those requiring small dosage (1.6 pmol/microliters), increased from 4.2% in 1981 to 60.8% in 1991 (P < 0.001). In in vivo test, the rate of chloroquine-resistant P. falciparum decreased from 84.2% in 1981 to 40% in 1991 (P < 0.001). The proportion of RII plus RIII cases of the total resistant cases dropped from 59.4% in 1981 to 37.5% in 1991 (0.02 > P > 0.01).

Animals↗

PubMed1992

[Sensitivity in vitro of Plasmodium falciparum to chloroquine, pyronaridine, artesunate and piperaquine in south Yunnan].

The sensitivity of P. falciparum to chloroquine, pyronaridine, artesunate and piperaquine (CQ, PD, AT, PQ) was assayed using in vitro microtechnique in south Yunnan in 1990. The resistance rates were 98.7% (75/76), 27.6% (16/58), 13.8% (9/65) and 97.7% (43/44) respectively, and ID50 were 125.0, 19.0, 4.7 and 243.3 nmol/L, respectively. The resistance rate against CQ showed no change as compared to the rates against CQ 5 and 9 years ago; but the ID50 was lower. CQ-resistant P. falciparum showed a marked cross-resistance to PQ, but not to PD and AT. AT-resistant P. falciparum exhibited cross-resistance to the above-mentioned three drugs. PD-resistant P. falciparum showed no cross resistance to AT, but showed cross resistance to CQ and PQ. In comparison with chloroquine-coated plates, the plates coated with pyronaridine, artesunate or piperaquine gave similar results as the former, which were shown by the rise in schizont inhibition rates along with the rise in drug concentration. It indicates that pyronaridine-, artesunate-, and piperaquine-coated plates can be used in the assay of sensitivity of P. falciparum to the three drugs.

Animals↗

PubMed1992

[Comparison of antiarrhythmic effects of IHC-72 (an iodonium-72), lidocaine and verapamil].

The antiarrhythmic actions of 3,6-dimethylamino-dibenzopyridonium edetate (IHC-72), lidocaine (Lid) and verapamil (Ver) on several models Were compared at equitoxic doses (equal fraction of LD50). The action of IHC-72 against aconitine induced arrhythmia was similar to that of Lid but stronger than that of Ver in anesthetized rats. The effect of IHC-72 on ouabain induced arrhythmia was also similar to that of Lid, but weaker than that of Ver in anesthetized guinea pigs. The activity of IHC-72 to raise electrical ventricular fibrillation thresholds (VFT) was weaker than that of Lid and Ver. The effects of IHC-72 in decreasing the incidence of ventricular premature beat(VP B), ventricular tachycardia (VT), ventricular fibrillation (VF) and shortening the duration of VT yielded by reperfusion were similar to those of Lid anf Ver in vivo.

Aconitine↗

PubMed1991

[Effects of furyl-dihydropyridines I on lipid peroxides of ischemic myocardium and ATPases activity of erythrocyte membranes in rats].

Acute myocardial ischemia and reperfusion in rats increased glutamic oxalacetic transaminase (GOT), non-esterified fatty acid (FFA), malondialdehyde (MDA) content. Furyl-dihydropyridines I 10 mg.kg-1 decreased the release of GOT, FFA, MDA of ischemic myocardium, and prevent ischemia-reperfusion arrhythmia. Furyl-dihydropyridines I increased Na, K-ATPase activity and N-acethylneuraminic acid (NANA) content of erythrocyte membranes, inhibited Ca-ATPase activity of erythrocyte membranes in rats. The results suggested that the mechanism of protecting the ischemic-reperfused myocardium might be associated with the inhibition of cellular lipid peroxidation and Ca-ATPase activity of cell membranes.

Animals↗

PubMed1991

Prevention of global myocardial reperfusion injury on isolated rabbit hearts with furyl-dihydropyridines I.

In the isolated rabbit heart of recirculating nonpulsatile perfusion circuit, furyl-dihydropyridines I 20 mumol.L-1 greatly reduced the leakage of myocardial enzymes and the concentration of malondialdehyde (MDA) in plasma, decreased the myocardial calcium and sodium contents, maintained normal coronary vascular resistance and prevented reperfusion arrhythmias of global postischemic reperfusion hearts. Its mechanism of protecting the ischemic-reperfused myocardium might be associated with the diminution of calcium influx of myocardial cells and cellular lipid peroxidation induced by oxygen free radicals.

Animals↗

PubMed1991

[Changes in atrial natriuretic peptide and vasopressin during the pressor response to central osmotic stimulation].

In order to study the mechanism of pressor response to central osmotic stimulation, rats were administered with hypertonic artificial cerebrospinal fluid (ACSF) intracerebroventricularly. Carotid arterial pressure and heart rate were recorded. Ten minutes after administration, blood samples, hypothalamus and hypophysis were taken for the determination of atrial natriuretic peptide (ANP) and vasopressin (AVP) by radioimmunoassay. The results showed that after central administration of hypertonic ACSF, the plasma level of AVP increased significantly with no apparent change in ANP. In hypothalamus and hypophysis, the content of ANP was increased while that of AVP decreased.

Animals↗

PubMed1991

[Protective effects of furyl-dihydropyridine I on ischemic myocardium in isolated rabbit hearts].

A recirculating nonpulsatile perfusion circuit was used in isolated rabbit hearts. Furyl-dihydropyridine I (2,6-dimethyl-4-furyl-1,4-dihydropyridine-3, 5-dicarboxylate) 20 mumol/L was shown to inhibit the release of creatine phosphokinase (CPK) and alpha-hydroxybutyrate dehydrogenase (HBD) from myocardium, decrease myocardial calcium and sodium contents by 5.3 +/- 1.1 mumol/g dry weight (P less than 0.01, n = 6) and 1.50 +/- 0.17 mmol/g dry weight (P less than 0.05, n = 6) from 8.3 +/- 1.1 mumol/g dry weight and 1.96 +/- 0.32 mmol/g dry weight respectively. It was also found to reduce coronary resistance and increase coronary flow of the ischemic myocardium, and prevent ischemic arrhythmia, thereby limit myocardial injury during regional ischemia in isolated rabbit hearts.

Animals↗

PubMed1989

[Effects of bis(dimethyl amino)-diphenyl methane (BDDM) on action potentials in guinea pig papillary muscle].

The effects of BDDM on action potentials and slow response action potentials in guinea pig papillary muscle were investigated by microelectrode technique. BDDM prolonged action potentials duration at 30, 50, 90, and 100% repolarization (APD30, APD50, APD90, APD100) and prolonged the effective refractory period (ERP), so ERP/APD value became greater. BDDM (51.6 mumol/L) decreased the APA, Vmax and prolonged APD50, APD90. In barium-induced ventricular autorhythmicity, BDDM suppressed the maximal diastolic potential (MDP), APA and reduced the rate of spontaneous rhythm. The results suggest that BDDM may unspecifically inhibit the currents of Ca2+, K+, and Na+.

Action Potentials↗

PubMed1989

[A handy medium for in vitro assessment of sensitivity of Plasmodium falciparum to chloroquine and mefloquine in the field].

The use of liquid RPMI 1640 medium (added NaHCO3 and serum) in sealed ampoule for in vitro assessment of sensitivity of Plasmodium falciparum to chloroquine and meflopuine in the field was very successful. On chloroquine plates with WHO supplied medium, 9 of 13 isolates were interpretable (successful rate 69.2%), the maturation rate from ring-forms to schizonts was 53.3%, the average number of nuclei per schizont 5.1. With lyophilized medium the successful rate was 100%, the maturation rate 65.9%, the average number of nuclei per schizont 7.4, while with medium in sealed ampoule, the corresponding figures were 92.3%, 65.1% and 7.3 respectively. On mefloquine plates with WHO supplied medium, 7 of 11 isolates were interpretable (63.6%). In control wells, 52.3% of schizonts matured, the number of nuclei per schizont was 5.1. With lyophilized medium the successful rate was 100%, the maturation rate 61.9%, the number of nuclei was 8.1, while those with liquid medium in sealed ampoule were 100%, 59.8% and 7.5 respectively. The results showed that the liquid medium in sealed ampoules stored within 56 days at 4 degrees C could still support the growth of Plasmodium falciparum, its supporting effect being better than that of WHO standard medium, but similar to lyophilized medium. The liquid medium in sealed ampoule had the advantages of easy carrying time-saving and more applicability under field conditions.

Animals↗

PubMed1988