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Prospective randomized double-blind trial of neurolytic coeliac plexus block in patients with pancreatic cancer.

BACKGROUND: In a randomized double-blind study the efficacy of neurolytic coeliac plexus block (NCPB) was compared with pharmacological therapy in the treatment of pain from pancreatic cancer. METHODS: Twenty-four patients were divided into two groups: 12 patients underwent NCPB (group 1) and 12 were treated with pharmacological therapy (group 2). Immediate and long-term efficacy, mean analgesic consumption, mortality and morbidity were evaluated at follow-up. Statistical analysis was performed with the unpaired t test, Mann-Whitney U test and Fisher's exact test. RESULTS: Immediately after the block, patients in group 1 reported significant pain relief compared with those in group 2 (P < 0.05), but long-term results did not differ between the groups. Mean analgesic consumption was lower in group 1. There were no deaths. Complications related to NCPB were transient diarrhoea and hypotension (P not significant between groups). Drug-related adverse effects were constipation (five of 12 patients in group 1 versus 12 of 12 in group 2), nausea and/or vomiting (four of 12 patients in group 1 versus 12 of 12 in group 2) (P < 0.05), one gastric ulcer and one gluteal abscess in group 2. CONCLUSION: NCPB was associated with a reduction in analgesic drug administration and drug-related adverse effects, representing an effective tool in the treatment of pancreatic cancer pain.

Adult↗

Reflex pathways in the abdominal prevertebral ganglia: evidence for a colo-colonic inhibitory reflex.

1. In vitro experiments were performed on preparations consisting of prevertebral ganglia attached to the entire colon of guinea-pigs. The colon was divided into an orad and a caudad segment and intraluminal pressure was recorded from the terminal end of each segment. Intracellular recordings were simultaneously obtained from neurones in the coeliac plexus. 2. The source of mechanosensory input from the colon paralleled the responses to mesenteric nerve stimulation. That is, section of the mesenteric nerve that contributed the strongest synaptic input to a neurone eliminated most of the mechanosensory input to that neurone. 3. The origin of the mechanosensory input to some neurones could be localized as coming from either the orad or caudad segment of the colon. In the coeliac ganglia 68% of the neurones tested responded primarily to orad distension and 37% to caudad distension. In the superior mesenteric ganglion 57% responded to orad distension and 43% to caudad distension. 4. Repetitive stimulation of the mesenteric nerve trunks arising from the prevertebral ganglia inhibited contractions differentially in the orad and caudad segments. The inferior coeliac nerves inhibited primarily the orad segments of colon and the lumbar colonic nerves inhibited primarily the caudad segments of colon. Stimulation of the superior coeliac nerves did not alter the motility of either segment. 5. When one of the colonic segments was distended, contractions in the other colonic segment were inhibited in 71% of the distensions. This inhibition operated in both directions: either orad inhibiting caudad or vice versa. 6. Cutting the intermesenteric nerve which communicates between the orad and caudad prevertebral ganglia eliminated the inhibitory reflex. 7. These experiments provide evidence for a colo-colonic inhibitory reflex mediated through pathways in the prevertebral ganglia.

Afferent Pathways↗

Distribution of enteric nerve cells that project to the coeliac ganglion of the guinea-pig.

The digestive tract of the guinea-pig, from the esophagus to the rectum, was examined in detail to determine the distribution and relative abundances of neurons in these organs that project to the coeliac ganglion and the routes by which their axons reach the ganglion. A retrogradely transported neuronal marker, Fast Blue, was injected into the coeliac ganglion. The esophagus, stomach, gallbladder, pancreas, duodenum, small intestine, caecum, proximal colon, distal colon and rectum were analysed for labelled neurons. Retrogradely labelled neurons were found only in the myenteric plexus of these organs, and in the pancreas. No labelled neurons were found in the gallbladder or the fundus of the stomach, or in the submucous plexus of any region. A small number of labelled neurons was found in the gastric antrum. An increasing density of labelled neurons was found along the duodenum. Similarly, an increasing density of labelled neurons was found from proximal to distal along the jejuno-ileum. However, the greatest densities of labelled neurons were in the large intestine. Many labelled neurons were found in the caecum, including a high density underneath its taeniae. An increasing density of labelled neurons was found along the length of the proximal colon, and labelled neurons were found in the distal colon and rectum. In total, more labelled cell bodies occurred in the large intestine than in the small intestine. The routes taken by the axons of viscerofugal neurons were ascertained by lesioning the nerve bundles which accompany vessels supplying regions of the digestive tract. Viscerofugal neurons of the caecum project to the coeliac ganglion via the ileocaeco-colic nerves; neurons in the proximal colon project to the ganglion via the right colic nerves, and neurons in the distal colon project to the ganglion via the mid colic and intermesenteric nerves. Neurons in the rectum project to the coeliac ganglion via the intermesenteric nerves. These nerves (except for the intermesenterics) all join nerve bundles from the small intestine that follow the superior mesenteric artery. All viscerofugal neurons of the caecum were calbindin-immunoreactive (calb-IR) and 94% were immunoreactive for vasoactive intestinal peptide (VIP-IR). In the proximal colon, 49% of labelled neurons were calb-IR and 85% were VIP-IR. In the distal colon, 80% of labelled neurons were calb-IR and 71% were VIP-IR.

Animals↗

Diagnostic, prognostic, and therapeutic nerve blocks.

During the past three quarters of a century, nerve blocks have been used with varying success as a primary treatment technique for patients with acute and chronic pain. However, practicing dolorologists soon realized that, in certain individuals, anesthetic blocking of noxious, peripheral afferent sensations did not always amelliorate pain complaints and at times even exaggerated them. The recent advent of the multidisciplinary approach to the management of pain, including neurosurgical procedures, new drugs, electrical stimulation and psychosocial intervention, has helped to clarify the indications for, limitations of, and disadvantages of the use of nerve blocks. The purpose of this article is to place nerve blocks in proper perspective and to define their role among the many methods currently available for the evaluation and control of severe pain.

Ammonium Sulfate↗

Glutenin is involved in the gluten-driven mucosal T cell response.

Gluten ingestion causes coeliac disease in susceptible individuals. Gluten is a heterogeneous mixture of glutenin and gliadin, the latter of which is considered responsible for disease induction. By combining high-performance liquid chromatography purification steps of gluten with a T cell bioassay and mass spectral analyses, we have identified a glutenin peptide (glt04 707-742) that activates T cells from the small intestine of a coeliac disease patient and results in the secretion of large amounts of IFN-gamma. The minimal T cell stimulatory core of the peptide (residues 724-734) is repetitively present in glutenin molecules. Moreover, it was observed that a large number of naturally occurring variants of this peptide are recognized by the T cells. These data suggest that the large heterogeneity of glutenin proteins dramatically increases the number of available T cell epitopes. Together, the results provide new insight into the nature of the gluten antigens that lead to coeliac disease and suggest that glutenin, next to gliadin-derived antigens, may be involved in the disease process.

Amino Acid Sequence↗

Neurochemical differentiation of functionally distinct populations of autonomic neurons.

The coeliac ganglion of guinea pigs displays a unique topographical arrangement of neurochemically and functionally distinct populations of sympathetic neurons. The authors used multiple-labeling immunohistochemistry to investigate the neurochemical differentiation of these neurons during embryonic and fetal development. Sympathoadrenal precursors, located on either side of the abdominal aorta, were intensely immunoreactive for tyrosine hydroxylase (TH-IR), neurofilament, and the human natural killer 1 antibody at midembryonic stages (Carnegie stages 16-19). During late embryonic stages (stages 20-23), a single bilobed ganglion had formed. At this time, neuropeptide Y immunoreactivity (NPY-IR) was widely expressed in sympathetic neurons (with moderate TH-IR) and chromaffin cells (with intense TH-IR). The onset of somatostatin (Som-IR) expression followed that of NPY-IR and was restricted to sympathetic neurons. However, at late embryonic stages, most TH-IR neurons with Som-IR also expressed NPY-IR (a combination of peptides not found in the mature coeliac ganglion). Between late embryonic stages and the end of the early fetal period, there was a significant increase in the proportion of neurons in lateral regions that had both NPY-IR and TH-IR. At the same time, there was an increase in the proportion of neurons in medial regions that had both Som-IR and TH-IR. Neurons expressing both Som-IR and TH-IR were rarely observed in lateral regions of the coeliac ganglion. Thus, a clear topography within the coeliac ganglion is established during late embryonic and early fetal stages of development and reflects that found in the mature animal by the end of the early fetal period.

Adrenal Glands↗

Coeliac artery compression syndrome: the effect of decompression.

The effects of operation to decompress the coeliac artery were evaluated in 11 consecutive patients with coeliac artery compression syndrome. Immediately after the operation all patients were free of symptoms. Three months later three of the 11 had recurrent abdominal pain. Long-term follow-up between 15 and 23 years, obtained by questionnaire, was available for eight patients. All eight had return of symptoms similar to those before surgery. These unsatisfactory results suggest that operation should not be undertaken in patients with vague upper abdominal complaints and compression of the coeliac artery by the median arcuate ligament, who do not otherwise have pathological conditions which might explain their symptoms.

Adolescent↗

Effects of celiacectomy and stellatectomy on gastric mucosal innervation and acid secretion in the dog.

The effect of surgical excision of the celiac and superior mesenteric ganglia and the stellate ganglia, respectively, on gastric acid secretion and adrenergic innervation of gastric mucosa was studied in five dogs. After removal of the abdominal ganglia, there was a significant increase in acid secretion while there was a marked decrease in the number of adrenergic nerve terminals in the mucosa. When, addition, the stellate ganglia were excised, acid secretion increased slightly in two dogs, while little change in mucosal innervation was noted. These data suggest that the adrenergic innervation of the stomach has an inhibitory role in the control of acid secretion in the dog. Vagal adrenergic nerve fibers seem to be of limited importance in gastric acid production.

Adrenergic Fibers↗

Anatomy and blood supply of the coeliac-superior mesenteric ganglion complex of the rat.

The anatomy of the coeliac-superior mesenteric ganglion (CSMG) complex of 28 female Wistar rats was studied by serial paraffin sections and found to be consistent in composition and in relations. The CSMG comprises tow suprarenal ganglia in continuity with the major splanchnic nerves, these continuing as splanchnic trunks into paired coeliac ganglia. The left coeliac ganglion is larger than the right as it has a superior mesenteric component related to the artery of that name. Lastly, intermesenteric ganglia are related to the renal and ovarian arteries and to the origin of the intermesenteric nerves. Ink injections and microvascular casts indicate that the main extrinsic blood supply to the CSMG is derived from the inferior phrenic artery, a branch of which enters the complex at the suprarenal ganglia and supplies the CSMG via the splanchnic trunks. Also, recurrent branches of the ovarian arteries enter the intermesenteric nerves to supply the complex at its caudal pole. A few small arteries not associated with nerves and probably derived from lumbar arteries also supply the CSMG complex. The two major post-ganglionic nerve trunks have an abundant vasculature in continuity with that of the CSMG but whose origin and direction of blood flow has yet to be determined.

Animals↗

Ultrastructure and distribution of somatostatin-like immunoreactive neurons and nerve fibres in the coeliac ganglion of cats.

Somatostatin-like immunoreactivity was localized in nerve cell bodies and nerve terminals in the cat coeliac ganglion. Two types of somatostatin-immunoreactive cell bodies were revealed, the first being large (diameter 35 microns), numerous and weakly labelled, whereas the second was considerably smaller (diameter 10.4 microns), sparsely distributed and heavily stained. The immunoreactive nerve terminals were in synaptic contact with many immunonegative large neurons and dendrites. However, in a few cases, somatostatin-immunoreactive nerve terminals could also be observed on the surface of lightly stained neurons. Transection of vagal or mesenteric nerves failed to affect the distribution or density of somatostatin-like immunoreactive nerve terminals. These results demonstrate the existence of a synaptic input to the principal neurons of the coeliac ganglion of the cat by somatostatin-containing nerve terminals and suggest that this peptide may act as a neuromodulator or neurotransmitter. It is proposed that somatostatin-positive neurons provide intrinsic projections to other somatostatin-positive and to somatostatin-negative neurons throughout the coeliac ganglion, thereby creating a complex interneuronal system.

Animals↗