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PubMed1978

[Effect of selective application of sodium picrate to the hypogastric ganglion in the hypogastric nerve-vas deferens preparation of the guinea pig (author's transl)].

Effect of sodium picrate (picric acid-Na; PA) on the hypogastric ganglion in the hypogastric nerve-vas deferens preparation of the guinea pig was studied and the results are as follows: PA or acetylcholine (ACh) at doses (g/ml) of 10(-5) approximately 10(-4) applied to the ganglion increased the height of the response (R-NS) of the vas deferens to the hypogastric nerve stimulation. Neither drug restored R-NS blocked by hexamethonium 3 X 10(-5). Effects of PA and ACh on R-NS were potentiated by neostigmine 10(-7) and the potentiation was considerably greater for ACh than for PA. Effects of PA on R-NS were not influenced by pretreatment with atropine. Both PA and ACh recovered R-NS which was partially reduced by hemicholinium-3 (HC-3), although the recovery of R-NS by PA was rapidly abolished more than that by ACh when these drugs were repeatedly applied in the presence of HC-3 3 X 10(-5). PA markedly recovered the R-NS reduced by morphine 10(-4) and ACh slightly restored that R-NS. These results suggest that the site of action of PA on the hypogastric ganglion of the guinea pig is different from that of ACh and the effect of PA on R-NS may be due to the acceleration of ACh-release from preganglionic nerve endings.

Acetylcholine↗
PubMed1986

[Effects of oxybutynin hydrochloride on the urinary bladder and urethra in in situ preparations].

Effects of oxybutynin on the urinary bladder and urethra were studied in comparison with atropine and flavoxate in cats and rabbits. Oxybutynin at 10 mg/kg, i.v., significantly inhibited the bladder contractions induced by electrical stimulation of the peripheral end in pelvic nerve. Oxybutynin was about one half the potency of atropine. On the contrary, 10 mg/kg of flavoxate, i.v., showed both effects of potentiation and inhibition. The bladder contractions induced by acetylcholine (ACh) and AHR-602 were markedly inhibited by oxybutynin and atropine. Oxybutynin was about one-fifteenth the potency of atropine. DMPP-induced contractions were inhibited by oxybutynin and atropine in a high dose, but oxybutynin was about two-fifths the potency of atropine. In addition, 3 mg/kg of oxybutynin, i.v., inhibited the contraction induced by hypogastric nerve stimulation, but 10 mg/kg of oxybutynin, i.v., significantly inhibited this contraction following initial potentiation. Oxybutynin showed an inhibitory effect on spontaneous rhythmical contraction, bladder tone and pelvic nerve discharge, similar to the effects of atropine. On the contrary, flavoxate potentiated this contraction and increased the bladder tone and pelvic and hypogastric nerve discharge. Urethra contractions induced by norepinephrine, ACh and hypogastric nerve stimulation were inhibited by oxybutynin, but not markedly. Oxybutynin and atropine dose-dependently increased the infusion volume, bladder volume capacity and micturition threshold pressure in the cystometrogram in rabbits. Flavoxate also increased them. From these results, it si suggested that oxybutynin is therapeutically a useful agent for pollakisurea nervosa.

Animals↗
PubMed1975

Junction potentials in response to ortho- and anti-dromic stimulation of hypogastric nerve in mouse vas deferens.

The interaction of the junction potentials in response to ortho- and antidromic hypogastric nerve stimulation in mouse vas deferens was studied, using an extracellular recording method. Ortho-dromic repetitive hypogastric nerve stimulation (10 Hz, 5 min) simultaneously depressed the amplitude of the junction potentials in response to both ortho- and anti-dromic hypogastric nerve stimulation (post-te-tanic depression). No time-lag in recovery from the post-tetanic depression was observed between the junction potentials recorded from two separate electrodes, indicating that the proximodistal axonal flow of available transmitter was not involved in the recovery process. Double shocks, with intervals from 10 msec to 1 sec, were applied to the hypogastric nerve. The junction potentials in response to ortho- and ortho-dromic or anti- and anti-dromic double shock were markedly facilitated. On the contrary, the junction potentials in response to ortho- and anti-dromic double shocks were not facilited. The findings indicate that facilitation of the junction potentials is produced by the impulses propagated in the same direction along the terminal axon and also that the origin of the facilitation may be at a pre-junctional site.

Animals↗
PubMed1990

Effects of various drugs on bladder function in conscious restrained-denervated rats placed in a restraining cage and produced by transection of the hypogastric nerve.

We evaluated the effects of various intravenously administered drugs, which had been shown to influence bladder function in anesthetized and/or conscious rats, on the cystometrogram in conscious restrained-denervated rats (produced by transection of the hypogastric nerve) placed in a restraining cage in comparison to those in conscious restrained-intact rats (with the hypogastric nerve intact) placed in a restraining cage. The bladder capacity in the restrained-denervated rats was smaller than that in restrained-intact rats and did not change when they were transferred to a wide cage, but the bladder capacity of the restrained-intact rats decreased following transfer to the wide cage. Therefore, the activity of the hypogastric nerve in conscious rats appears to be stimulated by restraint. Atropine suppressed the amplitude of the micturition contraction (time to micturition in the cystometrogram). In the restrained-denervated rats, thiopental and indomethacin increased the bladder capacity at almost the same doses as those in restrained-intact rats, but it took a higher dose of morphine to increase the bladder capacity than in restrained-intact rats. These findings suggest that cystometrography in restrained-denervated rats is a useful method for evaluating the effect of a newly developed agent on bladder function without any influence from the hypogastric nerve.

Animals↗
PubMed1989

TRH pharmacokinetics and nerve stimulation evoked prostatic fluid secretion during TRH infusion in the dog.

The pharmacokinetics of TRH have been determined in man and the rat as well as other species whose serum contains TRH degrading enzymes, TRH pharmacokinetics have not been determined in the dog. This species is unusual in that its serum contains little or no TRH degrading activity. TRH pharmacokinetics were determined from measurements of plasma TRH concentrations during and following a 1-h infusion of TRH, 20 micrograms.kg-1.min-1, into dogs bearing prostatic urethral cannula. During TRH administration prostatic fluid secretion was evoked by hypogastric nerve stimulation and the content of TRH immunoreactive material in prostatic fluid was determined. Prostatic fluid was also collected after hypogastric nerve stimulation in dogs that did not receive TRH infusion. The TRH plasma profile in TRH-infused dogs exhibited two-compartment characteristics with an initial half-time of 10.4 +/- 5.4 (mean +/- SD) min, a terminal half-time of 69.4 +/- 24 min, and a metabolic clearance rate of 7.64 +/- 4.48 ml.min-1.kg-1. These findings suggest that the half-time of TRH is longer, and its metabolic clearance rate is less, in the dog than in humans or rats. TRH administration was not associated with altered nerve induced prostatic fluid secretion. Prostatic fluid samples contained TRH immunoreactive material regardless of whether they were collected after epithelial cell stimulation with pilocarpine, or after hypogastric nerve stimulation. In contrast to previous results with vasoactive intestinal peptide, TRH does not acutely alter prostatic fluid secretion. As has been reported for prostatic tissue extracts, immunoreactive material is present in prostatic fluid and appears to arise from epithelial cells.

Animals↗
PubMed1984

[Innervation of the rat urinary bladder. I. The morphological changes of intrinsic nerves of the urinary bladder after pelvic ganglionectomy].

The dual autonomic innervation of the urinary bladder of the female rat was studied using histochemical and light and electron microscopic methods. The bladder body in the normal state had a rich supply of cholinergic nerve fibers with a uniformly reticular pattern, but it was sparsely supplied with adrenergic nerves mainly associated with the blood vessels rather than the detrusor muscles. Seven days after the unilateral extirpation of the pelvic ganglion, most cholinergic and adrenergic fibers on the ipsilateral side of the bladder body disappeared markedly with the use of enzymatic and fluorescent histochemical techniques. The acetylcholinesterase activity of cholinergic fibers and the intensity of fluorescence of adrenergic fibers were somewhat restored 14 days after the operation. Seventy days postoperatively, it was found that the former had recovered in the relatively fine nerve fibers, while the latter had been almost completely restored, compared with the normal adrenergic innervation of the bladder body.

Adrenergic Fibers↗
PubMed2004

SEP-diagnosed neuropathy of the lateral cutaneous branch of the iliohypogastric nerve: case report.

The article pertains to the uncommon clinical case of a patient with a proximal neuropathy of the lower extremity. It outlines the electrophysiological evaluation and reviews the medical literature. The electrophysiologic test that most accurately revealed the neuropathy was the segmental somatosensory evoked potential (SEP) of the lateral cutaneous branch of the iliohypogastric nerve. It showed well-defined and replicable cortical waveforms following the excitation of the lateral cutaneous branch of the iliohypogastric nerve in the asymptomatic lower extremity, but failed to present somatosensory evoked potentials arising from the excitation of the contralateral nerve in the symptomatic lower extremity. We did not find any previous reports diagnosing that particular pathology by the use of segmental SEP. In conclusion, it is important to remember that the accurate diagnosis of patients complaining of pain and dysesthesia in the proximal part of the lower extremities can possibly be achieved through the use of electrophysiologic tests such as the segmental SEP.

Adult↗
PubMed2006

Role of peripheral innervation in p-chloroamphetamine-induced ejaculation in anesthetized rats.

The occurrence of ejaculation, which consists of 2 distinct phases (emission and expulsion), requires a tight coordination of peripheral autonomic and somatic nerves. However, some aspects of the mechanism of ejaculation are not clearly defined. To clarify this issue, we used the p-chloroamphetamine (PCA)-induced ejaculation model in anesthetized rats and investigated the effects of selective peripheral nerves lesions on seminal vesicle and bulbospongiosus (BS) muscle activities as representing physiological markers of emission and expulsion phases, respectively. In intact rats, ejaculation induced with PCA (intraperitoneal 5 mg/kg) correlated with coordinated increases in seminal vesicle pressure (SVP) and BS electromyographic activity. PCA-induced ejaculation was still observed in rats with bilateral lesion of hypogastric nerves (HNx), lumbar paravertebral sympathetic chain (LSCx), or dorsal nerves of the penis (DNPx). Conversely, bilateral section of pelvic nerves (PNx) or L6-S1 dorsal roots (DRx) abolished PCA-induced ejaculation. The amplitude of SVP increases induced by PCA was reduced in PNx, HNx, and LSCx rats, whereas it was unchanged in DRx and DNPx rats. The time interval between SVP increases and BS muscle contractions induced by PCA was comparable in the different neural lesion groups. In conclusion, PCA initiates both emission and expulsion independently from each other. In this model, afferents conveyed by the pelvic nerves appear to be unnecessary for occurrence of BS muscle contractions but are essential for a complete ejaculatory response.

Animals↗
PubMed1974

Effects of cocaine on a hypogastric nerve-vas deferens preparation of the guinea pig.

Effects of cocaine on a hypogastric nerve-vas deferens preparation of the guinea pig, in vitro, were investigated with the microelectrode and the double sucrose gap methods. 1) Cocaine, at a concentration of more than 3 X 10 minus-5 M, depolarized the membrane and enhanced the electrical activity of the postjunctional membrane. These effects were, however, not due to accumulated noradrenaline near the postjunctional membrane. 2) The electrical resistance of the postjunctional membrane was slightly increased by treatment with cocaine (3 X 10 minus-5M) but the length constant of the tissue was almost unaffected. The electrical threshold to evoke a spike from the postjunctional membrane was lowered. 3) Cocaine (3 X 10 minus-5M) did not change the amplitude and frequency of the miniature excitatory junction potentials but it markedly suppressed the amplitude of the excitatory junction potentials evoked by hypogastric nerve stimulation. Cocaine prolonged the falling phase of the excitatory junction potentials. 4) The inhibitory action of cocaine on the junction potential evoked by nerve stimulation was not specific for the adrenergic fiber. Cocaine also suppressed the amplitude of the non-adrenergic inhibitory junction potential evoked in the taenia coli by field stimulation. 5) Exogeneously applied noradrenaline enhanced the electrical and mechanical activities of the postjunctional organ but suppressed the amplitude of the excitatory junction potential. This effect of noradrenaline was still observed on pretreatment with cocaine. 6) In the presence of cocaine, the dose-response curves plotted from the mechanical activity induced by excess [K]o or by noradrenaline shifted to the left and the maximum responses evoked by either treatment were enhanced. 7) From the present experiments, it was concluded that supersensitivity induced by cocaine or cocaine potentiation of the mechanical response may be mainly due to direct action on the smooth muscle tissue rather than to inhibition of noradrenaline re-uptake into the nerve terminals.

Animals↗