Feline Pylorus Research Articles

Unique distribution of interstitial cells of Cajal in the feline pylorus

The feline gastrointestinal (GI) tract is an important model for GI physiology but no immunohistochemical assessment of interstitial cells of Cajal (ICC) has been performed because of the lack of suitable antibodies. The aim of the present study was to investigate the various types of ICC and associated nerve structures in the pyloric sphincter region, by using immunohistochemistry and electron microscopy to complement functional studies. In the sphincter, ICC associated with Auerbach's plexus (ICC-AP) were markedly decreased within a region of 6-8 mm in length, thereby forming an interruption in this network of ICC-AP, which is otherwise continuous from corpus to distal ileum. In contrast, intramuscular ICC (ICC-IM) were abundant within the pylorus, especially at the inner edge of the circular muscle adjacent to the submucosa. Similar distribution patterns of nerves positive for vesicular acetylcholine transporter (VAChT), nitric oxide synthase (NOS) and substance P (SP) were encountered. Quantification showed a significantly higher number of ICC-IM and the various types of nerves in the pylorus compared with the circular muscle layers in the adjacent antrum and duodenum. Electron-microscopic studies demonstrated that ICC-IM were closely associated with enteric nerves through synapse-like junctions and with smooth muscle cells through gap junctions. Thus, for the first time, immunohistochemical studies have been successful in documenting the unique distribution of ICC in the feline pylorus. A lack of ICC-AP guarantees the distinct properties of antral and duodenal pacemaker activities. ICC-IM are associated with enteric nerves, which are concentrated in the inner portion of the circular muscle layer, being part of a unique innervation pattern of the sphincter.

Nitric oxide synthase-containing nerve elements in the pylorus of the cat

Combined nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) histochemistry, nitric oxide synthase (NOS) and vasoactive intestinal polypeptide (VIP) immunocytochemistry were used to study the distribution of NOS- and VIP-containing nerve elements in the feline pylorus. A large number of stained multipolar neurons was found in the myenteric plexus. However, some NADPH-d and NOS positive neurons were also observed in the submucous plexus and in the internal part of muscular layer. A few stained perikarya were found in the tunica mucosa, in a very close situation to the blood vessels. A large number of thin varicose fibres, with intense reaction for all markers were seen around or in close contact with the unstained perikarya to the blood vessels and some of them around the pyloric glands. The density of NOS and NADPH-d positive nerve elements was much higher than that of VIP-immunoreactive (IR) nerve elements. Our results suggest that nitric oxide (NO) might act as a regulatory neurotransmitter of the pyloric sphincter, blood flow and secretion in this region.

Mechanics and neuropeptide responses of feline pylorus and gastric muscle in vitro

Mechanical properties and neuropeptide responses were compared for feline pyloric and gastric muscle under isometric conditions in vitro. Total tension in antral circular muscle (0.699 +/- 0.003 kg/cm2) was less than in corpus circular (1.597 +/- 0.007 kg/cm2) or longitudinal muscle from the lesser and greater curvatures (1.256 +/- 0.009 and 1.253 +/- 0.007 kg/cm2, n greater than or equal to 55, P less than 0.05). The components of tension at optimal length were similar for all gastric muscles (P greater than 0.1). The pylorus maintained less total tension (0.335 +/- 0.003 kg/cm2) and a greater component of resting tension (75.6%) than gastric muscle (P less than 0.01). Substance P, cholecystokinin-8 (CCK-8), and neurotensin varied in potency and efficacy in circular muscle of the antrum, corpus, and inferior portion of the pyloric ring. Longitudinal muscle and the superior portion of pylorus responded poorly if at all to neuropeptides. Substance P- but not CCK-8- or neurotensin-induced contractions of gastric muscle were reduced by tetrodotoxin (TTX) and atropine (P less than 0.05). Substance P-induced pyloric contractions were TTX sensitive (P less than 0.05) but were unaffected by atropine. We concluded that 1) length-tension properties of gastric muscle are similar and distinct from the pylorus and that 2) neuropeptide efficacy varies regionally within the feline stomach and within the pylorus.

Properties of the feline pyloric sphincter in vitro

The purpose of this study was to determine the intrinsic functions of the feline pylorus in vitro. The myoelectric and pressure characteristics of the intact pylorus, antrum, and duodenum, free of extrinsic hormonal or neural influences, were studied in an in vitro bath that allowed separation of the bathing medium surrounding the different bowel segments. Basal recordings revealed a zone of tonic high pressure of 28.4 ± 3.5 mmHg (mean ± SEM) at the pylorus. The basal slow wave frequencies in the pylorus and duodenum were 2.8 ± 1.4 and 12.6 ± 0.6 cycles/min, respectively. Spontaneous action potential-associated phasic contractions of the pylorus were noted in 38% of preparations. Enteric nerve stimulation with direct electric current (10 Hz, 1 ms, 10–50 V) applied proximal to the pylorus gave relaxation of the pylorus at the lower voltages and rebound excitation at higher voltages. Electrical stimulation distal to the pylorus yielded phasic contractile pyloric response during the entire stimulus. The duodenal instillation of 0.5 N HCl produced action potential-associated phasic contractions of the pylorus and duodenum but not the antrum. Pyloric responses to electrical stimulation or acidification were abolished by tetrodotoxin (10−5 M). Bethanechol (10−6 M) or substance P (10−7 M) produced a contractile response at the site of stimulation but this response was not transmitted to include adjacent bowel segments. These studies suggest that the pyloric sphincter with its intrinsic reflex properties can be studied in vitro.

Is 5-HT a Mediator in the Motor Control of the Feline Pylorus?

Since serotonin (5-HT) is a potent spasmogen of pyloric smooth muscle in vivo, and since it is released on electrical stimulation of extrinsic nerves to the gut, the amine may mediate the excitatory motor responses elicited by vagal or splanchnic stimulation. In this study in cats intra-arterial administration of 5-HT to the stomach evoked a dose-dependent pyloric contraction, which was efficiently antagonized by Ketanserin, a peripheral 5-HT2 receptor antagonist. Such treatment did not affect the vagally or splanchnically induced pyloric motor responses, whereas the blood pressure reaction on splanchnic stimulation was greatly reduced. Therefore, 5-HT does not seem to be essential for the extrinsic neural control of pyloric motility. On the other hand, by means of immunocytochemistry, using a 5-HT antiserum, varicose nerve fibres with tryptamine-like immunofluorescence were demonstrated not only in the myenteric plexus and circular muscle layer but also in vascular nerve terminals of the feline pylorus. The function of these tryptamine-containing nerves is still unclear.

Evidence for an opiate-mediated pyloric sphincter reflex.

The purpose of this study was to determine the mechanism by which the feline pylorus contracts in response to duodenal acidification. Simultaneous intraluminal pressures and serosal electrical activity were recorded from the antrum, pylorus, and duodenum of the anesthetized cat. The pylorus demonstrated a narrow zone of tonically increased pressure. Duodenal but not antral acidification increased the frequency and amplitude of phasic spike-associated pyloric contractions (P less than 0.001). This response was antagonized by tetrodotoxin, intraluminal (ethyl aminobenzoate), or naloxone. Bilateral cervical vagotomy, atropine, phentolamine, propranolol, cinanserine, diphenhydramine, or cimetidine had no effect on the pyloric response to duodenal acidification. Duodenal spike activity was also increased by duodenal acidification but was antagonized by atropine and not by naloxone. Leucine- or methionine-enkephalin intra-arterially produced dose-dependent increases in phasic pyloric contractions. The EDmax for leucin-enkephalin was 1.0 microgram/kg. The enkephalins inhibited duodenal spike activity in a dose-dependent fashion. These studies suggest that the pyloric spike-associated, high-amplitude phasic contractions in response to duodenal acidification involve local neural pathways that may be mediated through an opioid peptide. The pyloric response to duodenal acidification is distinguished from that of the duodenum, which is cholinergic.

Involvement of intrinsic and extrinsic substance P neurons in the motor control of the feline pylorus

Involvement of intrinsic and extrinsic substance P neurons in the motor control of the feline pylorus

Evidence for a non-classical splanchnic neural control of the feline pylorus.

Electrical stimulation of the divided splanchnic nerves proximal to the celiac ganglion in chloralosed cats induced a dilation of the pylorus in the majority of animals. However, in some cats a pure contractile motor response or a biphasic motor response (contraction followed by dilation) was elicited suggesting that the splanchnic nerves convey excitatory fibres to the pylorus as well. The pyloric and gastric contraction at such stimulation was sensitive to atropine, while the pyloric dilation was not sensitive to cholinergic, adrenergic or ganglionic blocking agents in contrast to the adrenergic gastric dilation. Since the splanchnic nerve and the pyloric wall contain numerous neuropeptides, these substances might be involved in a nonclassical neurotransmission of the splanchnic motor responses of the pylorus.

The involvement of substance P in the vagal control of the feline pylorus.

The involvement of substance P in the vagal control of the feline pylorus.

Atropine sensitive contractile motor effects of substance P on the feline pylorus and stomach in vivo.

Atropine sensitive contractile motor effects of substance P on the feline pylorus and stomach in vivo.

The transmission mechanism of the vagal control of the feline pylorus.

Gastric motility and pyloric contractility were studied in laparotomized cats under chloralose anaesthesia by recording the intragastric volume and changes in an applied constant transpyloric flow of body-warm saline. Unilateralefferent electrical stimulation of the cervical vagi resulted in a prompt gastric contraction and a delayed pyloric contraction. In one third of the animals abiphasic pyloric motor response, consisting of a short period of increased flow preceding the longlasting decrease or cessation of the flow was observed. Afteratropine (0.2 mg/kg b.w.) the vagal nerve stimulation resulted in agastric relaxation, while the biphasic pyloric motor response was even more pronounced, with a significantly longer latency of the contractile phase. Addition ofguanethidine (2 mg/kg b.w.) did not affect these motor responses. Afterhexamethonium (25 mg/kg i.v. and 50±10 mg per kg i.a. b.w.) the stimulation procedure still resulted in a slight gastric relaxation, while the pyloric contraction was effectively blocked. However, the relaxatory phase required theaddition of atropine to become antagonized indicating separate transmission mechanisms for the relaxatory and contractile components of the pyloric motor response at efferent vagal stimulation.

Evidence for vagal enkephalinergic neural control of the feline pylorus and stomach

The atropine- and guanethidine-resistant contraction of the cat pyloric sphincter induced by efferent stimulation of the cervical vagi, was studied with a new method for measuring transpyloric flow. The pyloric contraction was blocked in a dose-dependent manner by the opiate antagonist naloxone infused intraarterially to the pyloric region. Local intraarterial injection of morphine or enkephalinamide elicited a pyloric and gastric contraction. Leuand met-enkephalin intraarterially elicited a pyloric contraction and a gastric relaxation. These effects could be prevented or reversed by naloxone. Immunohistochemical studies revealed a particularly rich enkephalinergic innervation of the pylorus with dense networks of varicose nerve fibers with enkephalin-like immunoreactivity both in the circular smooth muscle layer and in the myenteric plexus. Furthermore, many cell bodies of the myenteric plexus with enkephalin-like material were demonstrated. The corpus-antrum was sparsely innervated by enkephalin-like nerves to the circular muscle layer and only few immunoreactive cell bodies were observed in the myenteric plexus. These results together suggest a vagal control of the feline pylorus and stomach mediated via enkephalinergic neurons.

The peptidergic neural control of the feline pylorus.

By immunohistochemistry the three neuropeptides enkephalin, substance P, and VIP were all localized to numerous nerve fibers in the smooth muscle layer and the myenteric plexus of the feline pylorus. The motor activity of the pylorus was studied by recording changes in the volume flow of body-warm saline through the sphincter at constant perfusion pressure in anesthetized cats. Efferent electric stimulation of the cervical vagi (8 V; 5 ms; 8 Hz) elicited a noncholinergic, nonadrenergic pyloric contraction, which was blocked by infusion of the opiate receptor antagonist naloxone. The peptides were injected into a regional gastric artery to the pylorus antrum. Enkephalin and substance P in micronanomolar doses resulted in a prompt contraction of 3 - 5 min duration. Equimolar doses of naloxone blocked the enkephalin-induced contraction, and atropine blocked the SP contraction. On the other hand, VIP caused a prompt dilatation, which could not be blocked in this study. Altogether the findings suggest a peptidergic motor control of the feline pylorus using several transmission mechanisms.

The vagal control of the feline pyloric sphincter.

In acute experiments on cats in chloralose anesthesia the effects of efferent and afferent electrical stimulation of the cervical vagi on an applied constant flow of saline through the feline pylorus was studied. The motor activity of the stomach was recorded simultaneously with a volume recording technique. Efferent cervical vagal stimulation caused a decrease in the transpyloric flow and an increased gastric motor activity. In a few animals the decreased transsphincteric flow was preceded by a short period of increased flow. When the transpyloric flow was reduced by splanchnic nerve stimulation or a noradrenaline infusion, vagal nerve stimulation induced an increased flow through the pylorus indicating the presence of relaxatory fibres to the pylorus within the vagi. Electrical stimulation of the central end of the ipsilateral vagal nerve in the neck, with the contralateral vagal verve left intact, resulted in a decreased transpyloric flow and relaxation of the stomach. This response could be induced with or without intact splanchnic nerves, and disappeared when the intact contralateral vagus was cut. It is concluded that the vagi mediate both excitatory and inhibitory fibres to the pyloric sphincter in the cat. A vago-vagal excitatory reflex to the pylorus can be elicited by afferent vagal nerve stimulation together with a vago-vagal relaxatory response of the stomach.

On the VIP‐ergic innervation of the feline pylorus

Acta Physiologica ScandinavicaVolume 107, Issue 2 p. 185-187 On the VIP-ergic innervation of the feline pylorus R. EDIN, R. EDIN Institute of Neurobiology and the Department of Surgery III, University of Göteborg, the Department of Histology, Karolinska Institutet, Stockholm, Sweden, and the Department of Clinical Chemistry, Bispebjerg Hospital, Copenhagen, DenmarkSearch for more papers by this authorJ. M. LUNDBERG, J. M. LUNDBERG Institute of Neurobiology and the Department of Surgery III, University of Göteborg, the Department of Histology, Karolinska Institutet, Stockholm, Sweden, and the Department of Clinical Chemistry, Bispebjerg Hospital, Copenhagen, DenmarkSearch for more papers by this authorH. AHLMAN, H. AHLMAN Institute of Neurobiology and the Department of Surgery III, University of Göteborg, the Department of Histology, Karolinska Institutet, Stockholm, Sweden, and the Department of Clinical Chemistry, Bispebjerg Hospital, Copenhagen, DenmarkSearch for more papers by this authorA. DAHLSTRÖM, A. DAHLSTRÖM Institute of Neurobiology and the Department of Surgery III, University of Göteborg, the Department of Histology, Karolinska Institutet, Stockholm, Sweden, and the Department of Clinical Chemistry, Bispebjerg Hospital, Copenhagen, DenmarkSearch for more papers by this authorJ. FAHRENKRUG, J. FAHRENKRUG Institute of Neurobiology and the Department of Surgery III, University of Göteborg, the Department of Histology, Karolinska Institutet, Stockholm, Sweden, and the Department of Clinical Chemistry, Bispebjerg Hospital, Copenhagen, DenmarkSearch for more papers by this authorT. HÖKFELT, T. HÖKFELT Institute of Neurobiology and the Department of Surgery III, University of Göteborg, the Department of Histology, Karolinska Institutet, Stockholm, Sweden, and the Department of Clinical Chemistry, Bispebjerg Hospital, Copenhagen, DenmarkSearch for more papers by this authorJ. KEWENTER, J. KEWENTER Institute of Neurobiology and the Department of Surgery III, University of Göteborg, the Department of Histology, Karolinska Institutet, Stockholm, Sweden, and the Department of Clinical Chemistry, Bispebjerg Hospital, Copenhagen, DenmarkSearch for more papers by this author R. EDIN, R. EDIN Institute of Neurobiology and the Department of Surgery III, University of Göteborg, the Department of Histology, Karolinska Institutet, Stockholm, Sweden, and the Department of Clinical Chemistry, Bispebjerg Hospital, Copenhagen, DenmarkSearch for more papers by this authorJ. M. LUNDBERG, J. M. LUNDBERG Institute of Neurobiology and the Department of Surgery III, University of Göteborg, the Department of Histology, Karolinska Institutet, Stockholm, Sweden, and the Department of Clinical Chemistry, Bispebjerg Hospital, Copenhagen, DenmarkSearch for more papers by this authorH. AHLMAN, H. AHLMAN Institute of Neurobiology and the Department of Surgery III, University of Göteborg, the Department of Histology, Karolinska Institutet, Stockholm, Sweden, and the Department of Clinical Chemistry, Bispebjerg Hospital, Copenhagen, DenmarkSearch for more papers by this authorA. DAHLSTRÖM, A. DAHLSTRÖM Institute of Neurobiology and the Department of Surgery III, University of Göteborg, the Department of Histology, Karolinska Institutet, Stockholm, Sweden, and the Department of Clinical Chemistry, Bispebjerg Hospital, Copenhagen, DenmarkSearch for more papers by this authorJ. FAHRENKRUG, J. FAHRENKRUG Institute of Neurobiology and the Department of Surgery III, University of Göteborg, the Department of Histology, Karolinska Institutet, Stockholm, Sweden, and the Department of Clinical Chemistry, Bispebjerg Hospital, Copenhagen, DenmarkSearch for more papers by this authorT. HÖKFELT, T. HÖKFELT Institute of Neurobiology and the Department of Surgery III, University of Göteborg, the Department of Histology, Karolinska Institutet, Stockholm, Sweden, and the Department of Clinical Chemistry, Bispebjerg Hospital, Copenhagen, DenmarkSearch for more papers by this authorJ. KEWENTER, J. KEWENTER Institute of Neurobiology and the Department of Surgery III, University of Göteborg, the Department of Histology, Karolinska Institutet, Stockholm, Sweden, and the Department of Clinical Chemistry, Bispebjerg Hospital, Copenhagen, DenmarkSearch for more papers by this author First published: October 1979 https://doi.org/10.1111/j.1748-1716.1979.tb06461.xCitations: 27AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Citing Literature Volume107, Issue2October 1979Pages 185-187 RelatedInformation