PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “HYPOGASTRIC PLEXUS”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 577 records · Page 32Linked to original sources

The effects of iproniazid and reserpine on the accumulation of granular vesicles and noradrenaline in constricted adrenergic nerves.

1. The accumulation of granular vesicles proximal to a constriction applied to hypogastric nerves has been investigated with the electron microscope in cats treated with reserpine and/or iproniazid.2. The ultrastructural changes have been correlated with the accumulation of noradrenaline at the same site in similarly treated animals.3. The findings give further support to the view that granular vesicles constitute a major storage site for intraneuronal noradrenaline.

Animals↗

Pharmacological studies on the hypogastric ganglion of the rat and guinea-pig.

1. Preparations were developed whereby the hypogastric ganglion of the rat or guinea-pig was perfused through its vasculature with saline solutions. Drugs were injected into the perfusion stream, and their effects were indicated by contractions of the vas deferens. The base of this organ could be ligated to prevent the drugs reaching the smooth muscle via the blood vessels. For comparison, experiments were also performed on fully isolated preparations of the rat and guinea-pig hypogastric nerve-vas deferens, where the vas deferens was held in an inner bath, so that drugs added to the outer bath could act only on the ganglion. Attempts were made to demonstrate non-nicotinic receptors in these preparations.2. It was shown that the perfused hypogastric ganglion of the guinea-pig would respond repeatedly to several nicotinic stimulants, though autodesensitization eventually occurred. The fully isolated preparation behaved similarly, but desensitized much more rapidly. In contrast, the rat ganglion, either perfused or fully isolated, was remarkably insensitive to nicotinic stimulant drugs.3. Neither species responded well to non-nicotinic stimulants; that from the guinea-pig gave small contractions to methacholine in about 33% of cases, but did not respond to (4-m-chlorophenyl-carbamoyloxy)-2-butynyl trimethylammonium chloride (McN-A-343). With the rat, the situation was opposite.4. The guinea-pig ganglion did not become more sensitive to non-nicotinic stimulants after some treatments known to sensitize the cat superior cervical ganglion. These include preganglionic tetanization, chronic decentralization, and removal of all potassium. Sensitization did occur, however, in the presence of physostigmine, after tachyphylaxis to dimethyl phenyl piperazinium iodide (DMPP) had developed, and when the preparation was perfused with a suspension of washed erythrocytes.5. It is concluded that the responses of sympathetic ganglia vary from one species to another, and according to whether the organs are perfused or fully isolated.

Animals↗

The role of the hypogastric nerve in bladder and urethral activity of the dog.

1. Stimulation of the hypogastric nerves increased the pressure in both the bladder and urethra of anaesthetized female dogs. 2. The responses were reduced but not abolished by the alpha-adrenoceptor antagonist phentolamine, whereas the beta-adrenoceptor antagonist propranolol was either without effect or increased the responses. Atropine, methysergide and hexamethonium were without effect. 3. Close arterial injection of phenylephrine increased and isoprenaline decreased urethral pressure but both produced only a slight increase in bladder pressure. 4. Hypogastric nerve stimulation reduced subsequent responses of the bladder and urethra to pelvic nerve stimulation or to close arterial injection of acetylcholine. Isoprenaline, but not phenylephrine, also had an inhibitory action and 5-hydroxytryptamine enhanced the responses. 5. In the presence of hexamethonium the inhibitory action of isoprenaline still occurred but 5-hydroxytryptamine no longer enhanced the responses, suggesting that 5-hydroxytryptamine acts on the ganglia and isoprenaline acts, at least partially, on smooth muscle. 6. These results suggest that the role of the hypogastric nerves may be to modify inputs to the bladder and urethra as well as to act directly on the smooth muscle.

Acetylcholine↗

The effects of the calcium ionophore, A23187, on the axoplasmic transport of dopamine beta-hydroxylase.

1 The effects of the ionophore, A23187, on the intra-axonal transport of dopamine beta-hydroxylase (DBH) were investigated in the cat hypogastric nerve-inferior mesenteric ganglion preparation by monitoring, in vitro, the enzyme accumulation above a ligature, 2 to 2.5 cm distal to the ganglion. 2 DBH accumulation in the proximal segment immediately above the ligature (P1) increased linearly up to 6 h, during incubation in normal Krebs solution at 37 degrees C. The ionophore, A23187, interfered with the enzyme accumulation, but did not modify the previously accumulated DBH activity present in P1. 3 The blocking effects of A23187 on DBH transport were greatly impaired in the absence of extracellular calcium ions; an excess of calcium in the bathing solution (7.5 mM) itself blocked the enzyme transport by 50%. 4 A23187 did not significantly modify the levels of adenosine triphosphate (ATP) in the segments P1 and P2 of the nerve proximal to the ligature. 5 Nerves incubated in an A23187-containing medium showed many mitochondria of normal shape and fine structure; however, typical microtubules or filaments were not seen in these preparations. 6 The results suggest that the ionophore A23187, by considerably raising the axoplasmic ionized calcium levels, interferes with the assembling of microtubules. In this manner, the ionophore would inhibit the transport of adrenergic vesicles and therefore of DBH along the axon. The results also provide additional evidence in favour of the view that for the transport system to work adequately, it is necessary to maintain the intra-axoplasmic ionized calcium concentration between certain critical levels.

Adenosine Triphosphate↗

Orthograde and retrograde axonal transport of calmodulin in a cat noradrenergic neurone.

Subcellular distribution studies of calmodulin in cat sympathetic ganglia demonstrated that about 90% of the protein remained in the 27,000 g supernatant, suggesting that it is a cytosolic protein. Only 4.5% was recovered in the microsomal fraction pellet. The inferior mesenteric ganglia contained 93.3 +/- 3 ng calmodulin per ganglion, and segments of unligated cat hypogastric nerves had 6.53 +/- 0.32 ng per 5 mm segment. When the nerve was ligated in the middle and left in the cat for 1-6 days, substantial amounts of calmodulin accumulated in segments of nerve immediately proximal (P1) and distal (D1) to the ligature. The amounts found in P1 amounted to 15.3, 20, 30.4 and 39.4 ng calmodulin per 5 mm segment 1, 2, 3 and 6 days after ligation, respectively. The average rate of transport was 5.5 mm per day, which corresponds to a slow component b of axonal transport (SCb). The accumulation of calmodulin in D1 was also increased with the time of ligation. After 1, 2, 3 and 6 days, the amounts of the protein found in D1 were 14.4, 17.7, 19 and 21 ng per 5 mm segment, respectively. The calculated mean rate for the retrograde transport was 3.9 mm per day. Decentralization of the inferior mesenteric ganglia did not affect the rate of accumulation of calmodulin or the basal amounts found in ganglia and nerves. Local injection inhibited the orthograde, but not the retrograde axonal transport of the protein. It is concluded that calmodulin undergoes a process of slow orthograde axonal transport probably incorporated into the axoplasmic matrix of a network of actin microfilaments. The protein is also transported in a retrograde manner.

Animals↗

Effects of calcium channel antagonists on action potential conduction and transmitter release in the guinea-pig vas deferens.

The effects of the Ca2+ channel antagonists amlodipine, cobalt, diltiazem, nifedipine and verapamil and the local anaesthetic lignocaine were investigated on action potential conduction in and on evoked transmitter release from sympathetic nerves in the guinea-pig isolated vas deferens. Transmitter release was investigated by measurement of evoked (trains of pulses at 1 and 2 Hz, 0.1-0.5 ms supramaximal voltage) excitatory junction potentials (e.j.ps) using microelectrodes; tension was recorded simultaneously; tritium [3H] overflow from vasa preincubated (37 degrees C, 30 min) in Krebs solution containing either [3H]-noradrenaline (NA, 25 microCi ml-1, 2 X 10(-6) M NA) or [3H]-adenosine (50 microCi ml-1, 1 X 10(-6) M adenosine). Amlodipine (0.5-2 X 10(-4) M), verapamil (0.5-2 X 10(-4) M), diltiazem (1-8 X 10(-4) M), lignocaine (0.1-2 X 10(-3) M) and cobalt (2-6 X 10(-2) M) in descending order of potency, but not nifedipine (1-5 X 10(-3) M), increased the latency and inhibited, then abolished, the amplitude and number of action potentials in a concentration-dependent manner. Amlodipine (0.5-1 X 10(-4) M), verapamil (1-2 X 10(-4) M), diltiazem (1-5 X 10(-4) M) and cobalt (1 X 10(-3) M), in descending order of potency, but not nifedipine (5 X 10(-4) M), inhibited then abolished evoked e.j.ps in a concentration-dependent manner. Cobalt inhibited e.j.ps at a lower concentration than that (2-6 X 10(-2) M) required to block action potential conduction. In unstimulated tissues, the resting [3H] overflow following preincubation with [3H]-NA consisted largely of 4-hydroxy 3-methoxymandelic acid (VMA), 4-hydroxy 3-methoxy phenylglycol (MOPEG), 3,4 dihydroxyphenylglycol (DOPEG) and NA; stimulated tissues (300 pulses at 20 Hz, 0.5 ms supramaximal voltage) released mainly NA. Verapamil (0.1-1 X 10(-4) M), amlodipine (0.05-1 X 10(-4) M) and nifedipine (1-5 X 10(-4) M), but not cobalt (2 X 10(-3) M), increased, significantly, the resting overflow of 3H comprising mainly DOPEG. Cobalt (2 X 10(-3) M) inhibited, significantly, the stimulation-evoked overflow of 3H. Verapamil (1 X 10(-4) M) had little effect on the resting overflow of 3H following preincubation with [3H]-adenosine. Diltiazem (5 X 10(-4) M) and cobalt (2 X 10(-3) M) both inhibited evoked 3H overflow. Nifedipine (5 X 10(-4) M) was ineffective. 6 The effectiveness of Ca2+ channel antagonists at pre- and postjunctional sites differ; the results are discussed in terms of the selectivity of these drugs for each site and their differential effects on transmitter release.

Action Potentials↗

Spinal 5-HT2 receptor-mediated facilitation of pudendal nerve reflexes in the anaesthetized cat.

1. 5-Hydroxytryptamine (5-HT) is intimately associated with central sympathetic and somatic control of the lower urinary tract. The sympathetic and somatic innervation of the lower urinary tract is conveyed through efferent axons of the hypogastric and pudendal nerves, respectively. 2. The present study examined the effects of 2,5-dimethoxy-4-iodophenylisopropylamine (DOI), a 5-HT2 receptor subtype-selective agonist, on evoked potentials recorded from the central ends of the hypogastric and pudendal nerves in response to electrical stimulation of afferent fibres in the pelvic and pudendal nerves, respectively. Various spinalization paradigms were employed to localize the site of action. All cats were pretreated with xylamidine (1 mg kg-1), a peripherally-restricted 5-HT2 receptor antagonist. 3. In acute spinal cats, DOI (0.01-3 mg kg-1, i.v.) reliably produced dose-dependent increases in the pudendal nerve reflex (to 228 +/- 31% of control). These increases were reversed by the 5-HT2 receptor-selective antagonist, LY53857 (0.3-3 mg kg-1, i.v.). On the other hand, in spinally-intact cats, DOI produced no significant changes in the pudendal reflex. However, within minutes of spinalization of DOI-pretreated cats, a marked increase (to 221 +/- 16% of control) in the pudendal reflex was observed which could be reversed by LY53857. No significant effects were observed on hypogastric reflexes in either acute spinal or spinally-intact cats following DOI administration. No effects were seen in either spinally-intact or acute spinal animals when LY53857 was administered as the initial drug. 4. These results indicate that activation of spinal 5-HT2 receptors facilitates pudendal reflexes. In spinally-intact cats, it is hypothesized that DOI activates supraspinal pathways that mediate inhibition of the pudendal reflexes and counteracts the facilitatory effects of spinal 5-HT2 receptor activation.

Amphetamines↗

Effect of opiates on transmitter release from visualized hypogastric boutons innervating the rat pelvic ganglia.

1. The effect of opiates on neurotransmission between visualized hypogastric nerve boutons and postganglionic cell bodies has been examined using extracellular recording of nerve bouton impulses (NBIs) and excitatory postsynaptic currents (e.p.s.cs). 2. Morphine (10 to 40 microM) did not affect neurotransmission in the ganglia. Dynorphin-A (4 microM) and U50488H (1 microM) decreased quantal transmitter release and naloxone (10 microM) reversed these effects. 3. Morphine (10 microM), dynorphin-A (4 microM) and U50488H (1 microM) did not affect either the time course or consistency with which the NBI was recorded. 4. Dynorphin-A (1 to 4 microM) and U50488H (1 microM) decreased the average amplitude of e.p.s.cs by increasing the number of failures to release quanta from single or small groups of 2 to 4 boutons during continuous nerve stimulation at 0.1 Hz. 5. The decrease in quantal release induced by dynorphin-A and U50488H in 0.2 to 0.5 mM [Ca2+]zero was readily reversed by increasing the extracellular calcium ion concentration to 1 mM. 6. It was concluded that kappa-opioid receptors are located on the boutons of the hypogastric nerve and when activated by kappa-opioid receptor agonists reduce quantal release without affecting the NBI.

Animals↗

Spinal cord stimulation is an effective treatment for the chronic intractable visceral pelvic pain.

OBJECTIVE: Recent studies have demonstrated significant involvement of dorsal column pathways in transmission of visceral pelvic pain. Spinal cord stimulation (SCS) suppresses visceral response to colon distension in an animal model and therefore may be an effective therapy for chronic pelvic pain of visceral origin. We are reporting on the value of neurostimulation for chronic visceral pelvic pain in six female patients with the diagnosis of long-standing pelvic pain (history of endometriosis, multiple surgical explorations, and dyspareunia). DESIGN AND SETTINGS: Case-series report. All patients received repeated hypogastric blocks (in an average of 5.3 blocks) with a significant pain relief for a period ranging from 1 to 6 weeks. Three received neurolytic hypogastric block with the pain relief of 3, 8, and 12 months, respectively. Following psychological evaluation and clearance by our Multidisciplinary Committee on Implantable Devices, they all underwent SCS trial for 7-14 days. All patients received SCS systems with dual leads (Compact or Quad leads, Medtronic Inc., Minneapolis, MN, USA). RESULTS: The average follow-up was 30.6 months. Median visual analog scale pain score decreased from 8 to 3. All patients had more than 50% of the pain relief. Pain Disability Index changed from an average of 57.7 +/- 12 to 19.5 +/- 7. Opiate use decreased from an average 22.5 mg to 6.6 mg of morphine sulfate milligram equivalents per day. CONCLUSION: It appears that SCS may have a significant therapeutic potential for treatment of visceral pelvic pain.

Adult↗

Recent neuroanatomical studies on the neurovascular bundle of the prostate and cavernosal nerves: clinical reflections on radical prostatectomy.

The neurovascular bundle of the prostate and cavernosal nerves have been used to describe the same structure ever since the publication of the first studies on the neuroanatomy of the lower urogenital tract of men, studies that were prompted by postoperative complications arising from radical prostatectomy. In urological surgery every effort is made to preserve or restore the neurovascular bundle of the prostate to avoid erectile dysfunction (ED). However, the postoperative potency rates are yet to be satisfactory despite all advancements in radical prostatectomy technique. As the technology associated with urological surgery develops and topographical studies on neuroanatomy are cultivated, new observations seriously challenge the classical teachings on the topography of the neurovascular bundle of the prostate and the cavernosal nerves. The present review revisits the classical and most recent data on the topographical anatomy of the neurovascular bundle of the prostate and cavernosal nerves and their implications on radical prostatectomy techniques.

Erectile Dysfunction↗

Choline acetyltransferase activity in the denervated urinary bladder of the rat.

After extirpation of the pelvic ganglia the choline acetyltransferase activity decreased markedly indicating that most of the postganglionic cholinergic neurones of the bladder take this route. A small decrease in the activity of this enzyme was found after section of the hypogastric nerve, showing that these nerves contribute to some extent to the cholinergic innervation. The residual enzyme activity found after a combination of the two surgical procedures suggests that neurones relay distal to the level of the section of the hypogastric nerves and pass outside the pelvic ganglia and (or) that neurones pass the pelvic ganglia and relay distal to them. Electrical stimualtion of the hypogastric nerves after extirpation of the pelvic ganglia and the use of blocking drugs showed on the existence of cholinergic neurones passing outside the pelvic ganglia, some of them relaying distal to the point of stimulation.

Animals↗