PubMed Health⌕ Search

Biomedical subjects

C H Jiang

Publications and source records attributed to C H Jiang.

9 recordsLinked to original sources
PubMed1998

Modulation of the micturition reflex pathway by intravesical electrical stimulation: an experimental study in the rat.

Intravesical electrical stimulation (IVES) is used clinically to improve bladder evacuation in patients with inadequate micturition contractions. The procedure involves field stimulation of Adelta bladder mechanoreceptor afferents resulting in a prolonged enhancement of the micturition reflex. The aim of the present experimental study in the rat was to identify the site for this neuromodulation, whether it was due to sensitization of bladder mechanoreceptors, to enhancement of transmission in the central micturition reflex pathway, or to improved effectiveness of the peripheral motor system of the bladder. The experiments were performed on female rats, anesthetized by alpha-chloralose. Multi-unit afferent or efferent activity was recorded from bladder pelvic nerve branches during repeated cystometries before and after IVES. The specific antagonist CPPene was used to block central glutaminergic receptors of NMDA type. Micturition threshold volume decreased significantly after IVES. The afferent threshold volume, peak response, and pressure sensitivity were unchanged as were the peak efferent activity and bladder contractility. There was no efferent activity until just before the micturition contraction. The IVES-induced decrease in micturition threshold was blocked by prior administration of the NMDA (N-methyl-D-aspartic acid) antagonist CPPene (3-(2-carboxypiperazin-4-yl)-1-propenyl-1-phosphonic acid). The findings indicate that the IVES-induced modulation of the micturition reflex is due to an enhanced excitatory synaptic transmission in the central micturition reflex pathway. The observed modulation may account for the clinical beneficial effect of IVES treatment.

Animals↗
PubMed1998

Prolonged increase in micturition threshold volume by anogenital afferent stimulation in the rat.

OBJECTIVE: To investigate whether anogenital afferent stimulation induces a prolonged increase in the micturition threshold volume of anaesthetized rats. MATERIALS AND METHODS: Thirteen female rats, anaesthetized by alpha-chloralose and paralysed by pancuronium bromide were used for the experiments. The micturition threshold volume was determined by repeated cystometry. In two experiments, afferent activity was recorded from the exposed pudendal nerve; vaginal and anal afferents were stimulated electrically by ring electrodes. In one experiment, the dorsal clitoris nerves were exposed bilaterally and mounted for electrical stimulation. The afferents were stimulated continuously for 5 min at 10 Hz, using unipolar cathodic pulses of 0.5 ms duration with an amplitude of 10 mA (or 0.8 mA for the dorsal clitoral nerves). RESULTS: Anogenital stimulation for 5 min induced a significant and prolonged increase in the micturition threshold volume (from a median value of 0.35 mL before to 0.45 mL after stimulation; P < 0.01). The increase in threshold volume was maintained for about 40 min after the end of stimulation. There was no obvious difference in effect between the stimulation sites nor with direct dorsal clitoral nerve stimulation. Neither the micturition threshold pressure nor the maximal contraction pressure were altered by stimulation. No tonic afferent after-discharge could be detected in the pudendal nerve recordings. CONCLUSIONS: Artificial electrical stimulation of anogenital afferents induced a prolonged increase in the micturition threshold volume of anaesthetized rats. The change presumably involved the modulation of the synaptic transmission in the central micturition reflex pathway. It is proposed that the observed change represents the first step in the curative 're-education' process induced in patients with urge incontinence by electrical stimulation of anovaginal afferents.

Anal Canal↗
PubMed1997

No correlation between side-chain of propranolol oxidation and S-mephenytoin 4'-hydroxylase activity.

AIM: To determine if any correlation between the side-chain oxidative capacity for propranolol and S-mephenytoin 4'-hydroxylase (cytochrome P-450 2C19, CYP2C19) activity in healthy Chinese of Han nationality. METHODS: S-mephenytoin oxidative metabolite 4'-hydroxymephenytoin (4'OH-M), S- and R-mephenytoin, and naphthoxyl-actic acid (NLA) excreted in urine, and propranolol in plasma were measured after 14 healthy extensive metabolizers of S-mephenytoin oxidation were given a single oral dose of racemic mephenytoin 100 mg and racemic propranolol 80 mg, respectively. S/R-mephenytoin in urine was determined by chiral capillary gas chromatography with nitrogen-phosphorus detection, 4'-OH-M in urine by reversed-phase liquid chromatography (RPLC) with ultraviolet detection, and plasma propranolol or urinary NLA by the RPLC with fluorescence detection. RESULTS: No significant correlations were found between the partial metabolic clearance (Clm) of propranolol to NLA and 8 h urinary S/R ratio of mephenytoin (rs = -0.0484; P = 0.8695), nor between the Clm and log10 of 8 h urinary excretion of 4'-OH-M (rs = -0.1077; P = 0.7140). CONCLUSIONS: CYP2C19 is not a principal P-450 isozyme responsible for the in vivo side-chain oxidation of propranolol in the Chinese.

Aryl Hydrocarbon Hydroxylases↗
PubMed1997

Differences in the incidence of the CYP2C19 polymorphism affecting the S-mephenytoin phenotype in Chinese Han and Bai populations and identification of a new rare CYP2C19 mutant allele.

The incidence of the S-mephenytoin polymorphism was compared in two Chinese ethnic groups, Han (n = 101) and Bai (n = 202) by phenotype and genotype analysis. The frequency of poor metabolizers (PMs) in Han vs. Bai subjects was 19.8% vs. 13.4%. Han subjects had a higher frequency of the mutant CYP2C19m1 allele (0.366 vs. 0.257, P < .01) and a lower frequency of the wild-type allele (0.559 vs. 0.688, P < .01) than Bai subjects, which is consistent with the difference in the frequencies of PMs between the two ethnic groups. This results in a lower percentage of homozygous wild-type extensive metabolizers of mephenytoin (EMs) in Han subjects than in Bai subjects (40% vs. 59%, P = .005). Therefore, Han subjects may be more susceptible than Bai subjects to the drugs metabolized by the CYP2C19 enzyme. Ratios of urinary S/R-mephenytoin in homozygous EMs were lower than those of heterozygous EMs for both Han and Bai subjects, which shows a gene-dosage effect. Genotype analysis identified all but one PM as homozygous or heterozygous for the two known mutant CYP2C19m1 and/or CYP2C19m2 alleles. A single Bai PM outlier was shown to be heterozygous for CYP2C19m1 and a new mutant CYP2C19 allele containing a single amino acid change of Arg433 --> Trp433. A genotyping test demonstrated that only this one individual carried this rare allele (frequency of 0.0025 in Bai subjects).

Alleles↗
PubMed1996

Intravesical electrical stimulation induces a prolonged decrease in micturition threshold volume in the rat.

PURPOSE: Intravesical electrical stimulation (IVES) has been used clinically to treat patients with voiding disorders. The aim of the present experimental study was to obtain objective evidence of a modulation of the micturition reflex by intravesical electrical stimulation (IVES). MATERIALS AND METHODS: Forty-one female rats, anesthetized by alpha-chloralose were used for the experiments. Intravesical electrical stimulation was given by a catheter electrode in the bladder (5 minutes of continuous stimulation at 20 Hz, 7 to 11 mA). The effect was evaluated by the change in cystometric micturition threshold volume. RESULTS: The threshold volume of the micturition reflex decreased significantly to 82% of controls after IVES (p<0.001; n=31). The effect was reversible and lasted for about 1 hour. The decrease was prevented by a transient blockade of the bladder nerves during IVES. CONCLUSIONS: Intravesical electrical stimulation induced a prolonged modulation of the micturition reflex in anesthetized rats. The effect was due to activation of bladder mechanoreceptor afferents and remained long after the period of stimulation. It is proposed that the modulation was due to a prolonged enhancement of excitatory synaptic transmission in the central micturition reflex pathway. Such a modulation may underlie the curative effect of IVES in certain voiding disorders.

Animals↗