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Biomedical subjects

H G Li

Publications and source records attributed to H G Li.

27 records · Page 2Linked to original sources
PubMed1993

Defibrillation shocks produce different effects on Purkinje fibers and ventricular muscle: implications for successful defibrillation, refibrillation and postshock arrhythmia.

OBJECTIVES: To understand the mechanisms of postdefibrillation arrhythmias and failed defibrillation, we studied the cellular effects of high voltage shocks on different cardiomyocytes in the dog. BACKGROUND: The causes of postdefibrillation arrhythmias and unsuccessful defibrillation are not clear. METHODS: High voltage shocks with voltage differentials of 9.3 to 97.6 V/cm were delivered to isolated canine papillary muscles with attached Purkinje fibers. Transmembrane potentials were recorded simultaneously from the Purkinje fiber and the ventricular muscle using standard microelectrode techniques. RESULTS: After delivery of high voltage shocks, significant depolarization and rapid firing were observed in Purkinje fibers. The maximal rate of the rapid firing in the Purkinje fibers correlated with shock intensity (r = 0.69, p < 0.05). In contrast, in ventricular muscle, only slight depolarization and a transient refractory state were observed after the shock. The incidence of the refractory state was correlated with both the shock intensity and the rate of the rapid firing in the Purkinje fiber (r = 0.89 and 0.74, p < 0.01 and 0.05, respectively). Propranolol at a concentration sufficient for complete beta-blockade (1 mg/liter) did not change the tissue response to shocks but suppressed or abolished the shock-induced rapid firing of Purkinje fibers at a higher concentration (3 mg/liter). Blockade of the slow calcium channel with verapamil (400 micrograms/dl) did not alter the responsiveness of the preparation to shocks. CONCLUSION: These results indicate that high voltage shocks induce different responses in Purkinje fibers and ventricular muscle. The shock-induced rapid firing in the Purkinje fiber may contribute to postshock arrhythmias and possibly refibrillation in some cases. The shock-induced transient refractory state in the ventricular muscle may prevent the ventricle from responding to the rapid firing and thus may decrease the incidence of postshock arrhythmias.

Action Potentials↗
PubMed1993

Elimination of slow pathway conduction: an accurate indicator of clinical success after radiofrequency atrioventricular node modification.

OBJECTIVES: The purpose of this study was to determine the optimal end point of radiofrequency atrioventricular (AV) node modification using anatomically guided slow pathway approaches in patients with AV node reentrant tachycardia. BACKGROUND: The optimal end point for AV node modification using radiofrequency energy is uncertain, although elimination of inducible AV node reentrant tachycardia has been used. METHODS: We followed up 51 consecutive patients (40 women, 11 men, mean age +/- SD 41 +/- 16 years) with symptomatic AV node reentrant tachycardia for 12 +/- 6 months (range 4 to 24) after radiofrequency AV node modification using an anatomically guided slow pathway approach. Inducible AV node reentrant tachycardia was eliminated in all patients, whereas residual slow pathway conduction persisted in 12 patients (24%) after ablation. One study was complicated by complete AV block and two patients were lost to follow-up (one with and one without residual slow pathway conduction). RESULTS: Clinical recurrence of AV node reentrant tachycardia was documented in seven patients (14%) 3 days to 3 months (median 1 month) after ablation. The recurrence rate was significantly higher in patients with than in those without residual slow pathway conduction (6 [55%] of 11 vs. 1 [3%] of 37, p < 0.01). The recurrence rate was not different between patients with only residual slow pathway conduction and those with residual slow pathway conduction and inducible single echo cycles (three [60%] of five in both groups, p = NS). The number of radiofrequency energy applications was not significantly different between those without and those with recurrence (20 +/- 17 vs. 16 +/- 9, p = NS). Junctional tachycardia during application of radiofrequency energy tended to be more frequently observed in those with a successful outcome (77% vs. 57%, p > 0.05). Of the 22 patients who underwent modification before 1992, residual slow pathway conduction was present in 9 (41%) of 22 patients. Atrioventricular node reentrant tachycardia recurred in five (56%) of these nine patients. A greater effort made in 1992 to eliminate slow pathway conduction in 29 patients resulted in residual slow pathway conduction in only 3 (11%) with recurrence in 2 (4%). CONCLUSIONS: Complete elimination of slow pathway conduction is feasible in the majority of patients. Elimination of slow pathway conduction is highly predictive of long-term success after AV node modification using an anatomically guided approach.

Adult↗
PubMed1993

Arrhythmogenic effects of catecholamines are decreased in heart failure induced by rapid pacing in dogs.

Increased circulating catecholamines are considered to be arrhythmogenic in heart failure. It is unclear whether increased circulating catecholamines contribute directly to ventricular arrhythmias or are only markers of the severity of heart failure. The present study determined the sensitivity of the failing heart to the arrhythmogenic effect of exogenous norepinephrine in a rapid pacing-induced model of heart failure in dogs (240 beats for 4 wk, n = 14). A similarly operated, non-paced group served as controls (n = 9). Cardiac sensitivity to the arrhythmogenic effect of catecholamines was determined by measuring the minimal dose of exogenous norepinephrine that induced ventricular tachycardia (arrhythmogenic threshold dose, ATD). ATD significantly increased after development of heart failure in heart-failure group (1.62 +/- 0.32 microgram/kg at baseline vs. 16.65 +/- 3.48 micrograms/kg at restudy, P < 0.01), whereas no significant change was noted in the control group (1.08 +/- 0.36 microgram/kg at baseline vs. 2.53 +/- 0.36 micrograms/kg at restudy, P > 0.10). Action potential duration was unchanged by superfusion with 10(-7) M isoproterenol in both ventricular muscles (230.2 +/- 6.1 vs. 229.7 +/- 5.3 ms, P = NS) and Purkinje fibers (273.2 +/- 6.5 vs. 283.8 +/- 4.2 ms, P = NS) from the failing hearts, although isoproterenol induced a shortening in the control group (204.8 +/- 0.9 vs. 181.3 +/- 1.6 ms in ventricular muscles, P < 0.01; 313.8 +/- 6.5 vs. 279.5 +/- 5.7 ms in Purkinje fibers, P < 0.01). We conclude that the failing heart has a decreased sensitivity to the arrhythmogenic effect of catecholamines.

Action Potentials↗
PubMed1993

[Detection of RB gene in osteosarcoma by PCR].

We have established a stable PCR system and studied the structural anomalies of RB gene by it in osteosarcoma, previous studies have proved that 13-17 exons of RB gene are the deletion hotpoints. We designed a pair of perimers, RB1, RB2 stretching across 14-16 exons and studied 10 cases of osteosarcoma. No structural anomaly was found in the leucocyte. Two cases (20%) showed no PCR product. This result demonstrates for the first time the deletion of RB gene is present in Chinese osteosarcoma patients.

Base Sequence↗
PubMed1993

Association between HLA antigens and families with psoriasis vulgaris.

This paper typed HLA-A, B, C and DR antigens in patients with psoriasis vulgaris and healthy persons in 12 families. The phenotype frequencies of HLA-A1, B13, B17, Cw4 and Cw6 in the patients were higher than those in the controls. The analysis of haplotype segregation showed that HLA haplotypes in families with more psoriatic cases were marked deviation from random distribution. One or two HLA haplotypes sharing among affected siblings occurred more frequently than expected. The result of Lods score for six families showed that there was a close linkage between the gene of psoriasis vulgaris and HLA antigens. The gene of psoriasis was coincided with the recessive hereditary mode.

Family Health↗
PubMed1992

Electrophysiologic substrate associated with pacing-induced heart failure in dogs: potential value of programmed stimulation in predicting sudden death.

To investigate the possible mechanisms of sudden death and the potential role of electrophysiologic testing in congestive heart failure, this study evaluated the electrophysiologic substrate in a model of heart failure induced by rapid pacing. Seventeen mongrel dogs underwent cardiac pacing at 220 to 240 beats/min for 5 weeks (paced group) and 11 other dogs served as a sham-operated control group. Rapid pacing of the right ventricle produced clinical and hemodynamic features of congestive heart failure. Dogs in the paced group had prolonged cardiac conduction time as reflected by longer epicardial activation time (36.1 +/- 2.4 vs. 30.8 +/- 0.8 ms, p less than 0.05). The ventricular effective refractory period was significantly prolonged after the development of heart failure (141 +/- 4 vs. 177 +/- 5 ms, p less than 0.01, at a basic pacing cycle length of 300 ms), whereas no significant change was found in the control group (140 +/- 4 vs. 145 +/- 4 ms, p = NS). The prolongation of the ventricular effective refractory period correlated with an increase in left ventricular end-diastolic pressure (r = 0.55, p less than 0.001) and the ventricular effective refractory period correlated inversely with cardiac index (r = -0.49, p less than 0.025). The rest membrane potential of ventricular muscle was less negative in the paced group compared with the control group (-80.7 +/- 2.2 vs. -85.6 +/- 2.2 mV, p less than 0.05). Intracellularly recorded action potential duration of ventricular muscle was longer in the paced than in the control group (236 +/- 9.8 vs. 198.9 +/- 2.6 ms, p less than 0.01), action potential duration at 90% repolarization).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Defibrillation shocks increase myocardial pacing threshold: an intracellular microelectrode study.

Defibrillation is known to cause inability to pace the heart acutely, but the mechanism is unknown. This study used microelectrode techniques to directly evaluate the effect of defibrillation shocks on the pacing threshold and membrane potentials from superfused guinea pig papillary muscles. Failure of pacing stimuli to induce action potentials (pacing failure) followed shocks of 50-200 V/cm, with pacing failure duration correlated with shock intensity. Increasing pacing strength from one to three times diastolic threshold decreased the incidence and duration of pacing failure. Decreased extracellular calcium concentration and verapamil added to the superfusate increased the duration of pacing failure. Membrane potential depolarization occurred after shock, but pacing failure did not correlate with depolarization magnitude. We conclude that defibrillation shocks directly cause shock intensity-dependent increase of myocardial pacing threshold. The pacing threshold of the myocardium can be increased after defibrillation shock independent of hypoxia or shock-induced depolarization and may involve membrane changes in calcium handling.

Action Potentials↗
PubMed1987

DNA fragments of Bombyx mori nuclear polyhedrosis virus containing the promoters active in prokaryotes.

Using a promoter probe plasmid in E. coli called pHE5, eight different HindIII and one SalI DNA fragments of Bombyx mori nuclear polyhedrosis virus, directing the expression of the tetracycline resistance gene, have been cloned and isolated. The tetracycline resistance levels of the strains containing the recombinant plasmids were measured. Among them, the highest level of the resistance to tetracycline was 30 micrograms/ml. Part of the nucleotide sequence of a DNA fragment was determined. A sequence similar to the E. coli promoter was found.

Animals↗