On the gastrocecal inhibitory reflex in the rat

In rats anesthetized with urethane, the effects of distention of the stomach upon cecal motility and neural mechanisms which generate this effect were studied. Cecal motility was inhibited which generate this effect were studied. Cecal motility was inhibited when the pars glandularis of the stomach was distended by pressure ranging from 25 to 30 cm H2O. This inhibitory reflex was not affected by bilateral cervical vagotomy, but completely abolished following bilateral severance of the greater splanchnic nerves or after intravenous administration of guanethidine. After transection of the spinal cord at the level of the 5th thoracic segment the inhibitory reflex remained intact, but was abolished following pithing of the 6th thoracic segment and below. It may be concluded that the afferent and efferent path of the gastrocecal inhibitory reflex mainly pass through the greater splanchnic nerves and the reflex center is located in thoracic segments caudal to the 6th thoracic segment.     

Afferent electrical stimulation of mesenteric nerves inhibits duodenal HCO3- secretion via a spinal reflex activation of the splanchnic nerves in the rat

The experiments were performed on male Sprague-Dawley rats anaesthetized with chloralose. Duodenal HCO3- secretion was measured in situ by pH-stat titration. The nerves bundles surrounding two randomly chosen mesenteric vessels were electrically stimulated (3 Hz, supramaximal intensity) in the afferent direction. This was done in order to mimic the intestino-intestinal spinal reflex activation of the splanchnic sympathetic fibres. The procedure reduced duodenal HCO3- secretion by 20% together with an increase in mean arterial pressure and heart rate. Duodenal HCO3- secretion decreased similarly in control rats and in those subjected to a cervical cord transection, whereas animals with bilaterally cut splanchnic nerves did not respond to such mesenteric nerve stimulation. Pharmacological pretreatment with guanethidine or yohimbine, but not prazosin, inhibited the reduction in duodenal HCO3- secretion. Thus the data suggest that electrical stimulation of mesenteric afferent nerves inhibits duodenal HCO3- secretion via a spinal reflex activation of splanchnic sympathetic nerve fibres to the duodenum, and that the response is mediated via alpha 2 adrenoceptors.     

Afferent vagal control of fluid absorption in the feline jejunum

The aim of the study was to test experimentally whether vagal afferent pathways are involved in the reflex regulation of jejunal fluid absorption. Acute bilateral cervical vagotomy led to an increase in net jejunal fluid absorption rate, an effect which was abolished by previous division of the splanchnic nerves. Selective division of the right cardiac branch of the vagal nerve induced an increase in fluid absorption similar to that elicited by truncal cervical vagotomy. Afferent stimulation of the right cardiac nerve at frequencies within the physiological firing range for unmyelinated C-fibre afferents induced an inhibition of net fluid absorption. Based on these findings, we propose a reflex pathway containing a non-myelinated vagal afferent branch originating from cardiopulmonary receptor endings, and an efferent sympathetic branch reaching the jejunum via the splanchnic nerves. Such a pathway might be of physiological importance in extracellular volume control by regulating the rate of fluid transport across the intestinal mucosa.     

Sympatho-adrenergic inhibition of vagally induced gastric motility and gastroduodenal HCO-3 secretion in the cat

Chloralosed cats were acutely vagotomized and their adrenal glands were ligated. The gastric lumen was perfused with isotonic NaCl and gastric motility was recorded as change in hydrostatic pressure within the perfusion circuit. Gastric secretions of H+ and HCO3- were calculated from continuous measurements of pH and pCO2 in the perfusate. Mucosal HCO3- secretion in the distal duodenum was titrated in situ by pH-stat equipment. The experiments were divided into three different groups dependent on the state of sympathetic splanchnic nervous supply: intact; cut on a preganglionic level; blocked with the adrenolytic agent guanethidine. Basal levels for gastric motility, gastric H+ and HCO3- secretions and duodenal HCO3- secretion were more or less similar in all groups. Gastric motility, gastric HCO3- and duodenal HCO3- secretory responses to bilateral vagal stimulation were significantly enhanced in splanchnicotomized or guanethidine-treated animals as compared to controls with intact sympathetic supply. However, no clear differences in gastric H+ secretory responses to vagal stimulation were demonstrated between animals with an intact or disrupted sympathetic innervation. These results suggest a sympatho-adrenergic inhibitory action on vagally induced mucosa-protective HCO3- secretion in the stomach and the duodenum. Furthermore, vagal stimulation in animals with intact splanchnic nerves induced a guanethidine-resistant delayed increase in duodenal HCO3- secretion. The nature of this response was not further analysed.     

Afferent electrical stimulation of mesenteric nerves inhibits duodenal HCO3 secretion via a spinal reflex activation of the splanchnic nerves in the rat

The experiments were performed on male Sprague-Dawley rats anaesthetized with chloralose. Duodenal HGO^- ₃ secretion was measured in situ by pH-stat titration. The nerves bundles surrounding two randomly chosen mesenteric vessels were electrically stimulated (3 Hz, supramaximal intensity) in the afferent direction. This was done in order to mimic the intestino-intestinal spinal reflex activation of the splanchnic sympathetic fibres. The procedure reduced duodenal HCO^- ₃ secretion by 20% together with an increase in mean arterial pressure and heart rate. Duodenal HGO^- ₃ secretion decreased similarly in control rats and in those subjected to a cervical cord transection, whereas animals with bilaterally cut splanchnic nerves did not respond to such mesenteric nerve stimulation. Pharmacological pretreatment with guanethidine or yohimbine, but not prazosin, inhibited the reduction in duodenal HCO^- ₃ secretion. Thus the data suggest that electrical stimulation of mesenteric afferent nerves inhibits duodenal HCO^- ₃ secretion via a spinal reflex activation of splanchnic sympathetic nerve fibres to the duodenum, and that the response is mediated via alpha₂ adrenoceptors.     

Effects of caerulein on the gastric motility of rats

The effects of caerulein on gastric motility in urethane-anesthetized rats were studied. Caerulein administered into the lateral cerebral ventricle (i.c.v.) and jugular vein (i.v.) caused predominantly an inhibitory effect on gastric motility but sometimes an excitatory or a biphasic effect. The inhibitory response was reduced after vagotomy and/or splanchnicotomy, or after guanethidine. The remaining inhibitory response was abolished by tetrodotoxin, but was resistant to atropine and guanethidine. The excitatory response was abolished by atropine. Discharges of the gastric branch of the vagus nerve were decreased by i.v. injection of caerulein but increased by i.c.v. injection, whereas those of the splanchnic nerve were increased by both i.v. and i.c.v. injection. These results suggest that caerulein causes an inhibition of gastric motility by centrally stimulating vagal non-adrenergic inhibitory nerves and splanchnic adrenergic nerves and inhibiting vagal cholinergic nerves, and by peripherally stimulating non-adrenergic inhibitory neurons of the myenteric plexus. This peptide causes an excitation by stimulating cholinergic neurons of the myenteric plexus.     

Vago-vagal Gastro-gastric Relaxation in the Cat

In anesthetized cats electric afferent stimulation of nerve branches emanating from the gastric corpus region promptly elicited reflex gastric relaxation. The response was not blocked by atropine, guanethidine or cervical spinal cord transection but was abolished by cervical vagotomy, showing that the vagal “relaxatory” fibres to the stomach mediate this reflex effect. Transient distension of the stomach produced a long-lasting gastric relaxation with similar characteristics as that obtained by the mentioned afferent electric stimulation. By vagal blockade in atropinized cats it was shown that the vagal nerves exerted no or only slight relaxatory effects if the stomach was only slightly filled, hut then had a profound relaxatory effect when the stomach was moderately or greatly filled. It is concluded that a vago-vagal gastro-gastric relaxatory reflex exists where the vagal non-adrenergic relaxatory fibres serve as the efferent link. The reflex can be activated from gastric mechanoreceptors responding to distension and is suggested to be involved in the regulation of receptive relaxation in gastric filling.     

Reflux mechanisms involved in cardiac arrhythmias induced by hypothalamic stimulation

Electrical stimulation of widespread areas in the CNS has been shown to cause cardiac arrhythmias, which occur most frequently after cessation of stimulation. To determine the reflex and autonomic mechanism responsible for the poststimulation arrhythmias, we anesthetized cats with chloralose, and recorded arterial pressure, ECG, and cardiac vagal nerve activity. Stimulation of the hypothalamus consistently caused increases in blood pressure and heart rate during stimulation and caused arrhythmias, accompanied by vagal hyperactivity, immediately following stimulation. The arrhythmias were mediated solely by the vagus nerves because vagotomy or propantheline administration prevented them, whereas propranolol did not. Administration of either phentolamine or spinal cord transection prevented both the rise in blood pressure during stimulation and the poststimulation arrhythmias, but sectioning the carotid sinus and aortic depressor nerves had no preventative effect. However, when this denervation was combined with sectioning of vagal afferents, bursts of vagal activity (used as an index of cardiac rhythm disturbances) were prevented in three of six animals. Subsequent administration of phentolamine prevented the bursts in the remaining animals. It is concluded that poststimulation arrhythmias are elicited by the rise in blood pressure occurring during stimulation causing a sudden surge in parasympathetic outflow to the heart. The reflexogenic areas involved appear to be stretch receptors innervated by afferent vagal fibers.     

Effects of splanchnic nerve stimulation and of clonidine on gastric and duodenal HCO3- secretion in the anaesthetized cat

Experiments were performed on chloralose-anaesthetized cats with ligated adrenals. The vagal and splanchnic nerves were cut and arranged for peripheral electric stimulation. The gastric lumen was perfused with isotonic saline and gastric H+ and HCO3- secretions were calculated from pH/pCO2 measurements in the perfusate. Gastric motility was recorded as changes in hydrostatic pressure in the perfusion circuit. Mucosal HCO3- secretion into the duodenum was monitored in situ by pH-stat titration. Vagal stimulation (10 Hz for 10 min) increased gastric and duodenal HCO3- secretions, as well as gastric motor activity and H+ secretion. Splanchnic nerve stimulation (10 Hz for 10 min) did not affect gastric H+ and HCO3- secretions, but tended to decrease gastric motor tone and basal duodenal HCO3- secretion. Splanchnic nerve stimulation simultaneously with vagal stimulation inhibited gastric contractions and the rise in gastric H+ and duodenal HCO3- secretions observed in response to vagal stimulation alone, but had little effect on the rise in gastric HCO3- secretion. However, such vago-splanchnic stimulation in the presence of the alpha 2-adrenoceptor blocker yohimbine induced gastric contractions, H+ secretory and duodenal HCO3- secretory responses with magnitudes similar to those induced by vagal stimulation alone, whereas the gastric HCO3- secretory response was larger than by vagal stimulation alone. The alpha 2-adrenoceptor agonist clonidine (50 micrograms kg-1 h-1, i.v.) inhibited the gastric contractions and increases in gastric and duodenal HCO3- secretion in response to vagal stimulation, but did not influence vagal stimulation of gastric H+ secretion. The results suggest the existence of a peripheral sympatho-inhibitory action on gastric and duodenal HCO3- secretion involving alpha 2-adrenoceptors. Also splanchnic neural stimulatory effects on gastric and duodenal HCO3- secretion may exist.     

Persistence of the cardio-inhibitory response to brain stem ischaemia after destruction of the area postrema and the dorsal vagal nuclei

1. In anaesthetized cats, in which the carotid arterial bifurcation had been denervated and the spinal cord transected at the cervical level, reversible bradycardia mediated by the vagus nerves was elicited by temporary arrest of the cranial circulation. Methoxamine was infused intravenously to maintain peripheral vascular resistance, and artificial ventilation was given to avert systemic asphyxia.2. The bradycardia persisted in cats subjected to one or more of the following acute surgical procedures: left vagotomy, mid-collicular decerebration, decerebellation, bulbar transections at the acoustic striae and inferior fovea, and destruction of the area postrema and the underlying dorsal vagal nuclei. Ischaemia-induced bradycardia was invariably abolished after bilateral vagotomy or the administration of atropine.3. Bradycardia could not be elicited by electrical stimulation of the dorsal vagal nuclei, but was evoked by stimulation of deep structures in the vicinity of the nucleus ambiguus even after destruction of the dorsal vagal nuclei.4. Simultaneous application of ischaemia and electrical stimulation of the medullary cardio-decelerator locus produced convergent occlusion of the vagal response. The effect of ischaemia was inhibited by stimulation of a neighbouring region in the medial reticular formation. These interactions indicate that an interneuronal link is involved in the mechanism of ischaemia-induced bradycardia.5. It is concluded that the cardio-decelerator response to ischaemia is initiated upstream to the primary efferent vagal motor neurones and that the cardio-inhibitory fibres do not originate in the dorsal vagal nuclei.     

Sympatho-adrenergic inhibition of vagaliy induced gastric motility and gastroduodenal HCO3- secretion in the cat

Chloralosed cats were acutely vagotomized and their adrenal glands were ligated. The gastric lumen was perfused with isotonic NaCl and gastric motility was recorded as change in hydrostatic pressure within the perfusion circuit. Gastric secretions of H⁺ HCO₃^- were calculated from continuous measurements of pH and pCO₂ in the perfusate. Mucosal HCO₃^- secretion in the distal duodenum was titrated in situ by pH-stat equipment. The experiments were divided into three different groups dependent on the state of sympathetic splanchnic nervous supply: (1) intact; (2) cut on a preganglionic level; (3) blocked with the adrenolytic agent guanethidine. Basal levels for gastric motility, gastric H⁺ HCO₃^- secretions and duodenal HCO₃^- secretion were more or less similar in all groups. Gastric motility, gastric HCO₃^- duodenal HCO₃^- secretory responses to bilateral vagal stimulation were significantly enhanced in splanchnicotom-ized or guanethidine-treated animals as compared to controls with intact sympathetic supply. However, no clear differences in gastric H⁺ secretory responses to vagal stimulation were demonstrated between animals with an intact or disrupted sympathetic innervation. These results suggest a sympatho-adrenergic inhibitory action on vagaliy induced mucosa-protective HCO₃^- secretion in the stomach and the duodenum. Furthermore, vagal stimulation in animals with intact splanchnic nerves induced a guanethidine-resistant delayed increase in duodenal HCO₃^- secretion. The nature of this response was not further analysed.     

Nervous control of pancreatic exocrine secretion in pigs.

The pancreatic secretion of fluid, bicarbonate and protein in response to electrical stimulation of the vagus and splanchnic nerves, to exogenous and endogenous secretin and to various pharmacological agents was studied in anesthetized young pigs (21 kg). Vagal stimulation increased flow, bicarbonate output and protein output in a frequency dependent manner; the half maximal effective frequency was 2--4 Hz and the maximal effective frequency 12 Hz. The secretory response to vagal stimulation was potentiated by physiological elevations of the arterial concentration of secretin brought about by injection of secretin or by acidification of the duodenal bulb. Simultaneous stimulation of the splanchnic nerves strongly inhibited the response to vagal stimulation; splanchnic nerve stimulation alone had no demonstrable effect. The flow and bicarbonate response to vagal stimulation was unaffected by atropine, but abolished by hexamethonium. Protein output was strongly inhibited by both agents. The response to intraarterial infusion of acetylcholine resembled that elicited by vagal stimulation but it was smaller and it was completely abolished by atropine and unaffected by hexamethonium. Alpha- and beta-adrenergic blockade stimulated rather than inhibited the secretory response to vagal stimulation. The portal vein plasma concentration of secretin was not affected by vagal stimulation. The results indicate that the protein response, and the flow and bicarbonate response to vagal stimulation are not brought about by the same mechanism. An increased release of secretin is not involved. Peptidergic (VIP-containing) nerves may contribute.     

Nervous control of pancreatic exocrine secretion in pigs

The pancreatic secretion of fluid, bicarbonate and protein in response to electrical stimulation of the vagus and splanchnic nerves, to exogenous and endogenous secretin and to various pharmacological agents was studied in anesthetized young pigs (21 kg). Vagal stimulation increased flow, bicarbonate output and protein output in a frequency dependent manner; the half maximal effective frequency was 2–4 Hz and the maximal effective frequency 12 Hz. The secretory response to vagal stimulation was potentiated by physiological elevations of the arterial concentration of secretin brought about by injection of secretin or by acidification of the duodenal bulb. Simultaneous stimulation of the splanchnic nerves strongly inhibited the response to vagal stimulation; splanchnic nerve stimulation alone had no demonstrable effect. The flow and bicarbonate response to vagal stimulation was unaffected by atropine, but abolished by hexa-methonium. Protein output was strongly inhibited by both agents. The response to intraarterial infusion of acetylcholine resembled that elicited by vagal stimulation but it was smaller and it was completely abolished by atropine and unaffected by hexamethonium. Alpha- and beta-adrenergic blockade stimulated rather than inhibited the secretory response to vagal stimulation. The portal vein plasma concentration of secretin was not affected by vagal stimulation. The results indicate that the protein response, and the flow and bicarbonate response to vagal stimulation are not brought about by the same mechanism. An increased release of secretin is not involved. Peptidergic (VIP-containing) nerves may contribute.     

The effect of intracisternal injection of thyrotropin-releasing hormone on gastric and duodenal motility in the urethane-anaesthetized rat.

Intracisternal injection of thyrotropin-releasing hormone (TRH; 1-3 micrograms) caused an increase in gastric motility and usually an inhibition of duodenal motility. These effects were abolished by vagotomy and atropine. No inhibition was seen even after tone and motility had been restored to a point at which vagal stimulation could evoke profound inhibition of gastric and duodenal motility. It is concluded that TRH is a specific activator of enteric excitatory pathways and that duodenal inhibition seen in control animals is a consequence of gastro-duodenal inhibitory reflexes.     

Neural Mechanisms Involved in the Noxious Physical Stress-Induced Inhibition of Ovarian Estradiol Secretion

Stress is known to change the secretion of ovarian steroid hormones via the hypothalamic–pituitary–ovarian (HPO) axis. Noxious physical stress can cause reflex responses in visceral function via autonomic nerves. This article reviews our recent animal studies on neural mechanisms involved in ovarian estradiol secretion induced by noxious physical stress stimulation. In anesthetized rats, noxious physical stress (pinching the hindpaw or electrical stimulation of the tibial nerve) decreased ovarian estradiol secretion. These noxious stress-induced ovarian hormonal responses were observed after decerebration but were abolished after spinal transection. Electrical stimulation of the ovarian sympathetic nerves (superior ovarian nerves: SON) decreased ovarian estradiol secretion. The reduced secretion of ovarian estradiol induced by hindpaw pinching was abolished by bilateral severance of the SON. Efferent activity of the SON was increased following hindpaw pinching. Thus, the inhibition of ovarian estradiol secretion during noxious physical stress was mainly integrated in the brainstem, and this inhibitory response was due to reflex activation of sympathetic nerves to the ovary. In rats, the sympathetic inhibitory regulation of ovarian estradiol secretion was pronounced when the HPO axis was inhibited by chronic estradiol treatment. Considering the female life cycle, extensive physical stress may inhibit ovarian function, especially before puberty and during old ages when the HPO axis is inactive. Anat Rec, 302:904–911, 2019. © 2019 Wiley Periodicals, Inc.     

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.     

Responses of adrenal sympathetic nerve activity and catecholamine secretion to cutaneous stimulation in anesthetized rats

Reflex effects of cutaneous mechanical stimulation on adrenal sympathetic efferent nerve activity and secretion rates of the adrenal medullary hormones (epinephrine and norepinephrine) were studied in anesthetized rats. Noxious pinching stimulation of the lower chest or hindpaw skin for 3 min produced proportional reflex increases in both the nerve activity and secretion rates of epinephrine and norepinephrine from the adrenal medulla in animals with an intact central nervous system. However, lower chest stimulation elicited a longer lasting response than hindpaw stimulation, 7-17 min vs 1 min after cessation of the stimulation, respectively. After spinal transection at the C1-2 level, only lower chest stimulation was capable of producing a reflex response, lasting 1 min after cessation of the stimulation. Contrary to the responses elicited by pinching, non-noxious brushing stimulation of the lower chest or hindlimb skin for 3 min in animals with an intact central nervous system produced proportional reflex decreases in nerve activity and epinephrine and norepinephrine secretion rates during the stimulation period only. Some slight increases in both nerve activity and secretion rates, lasting several minutes, followed cessation of the stimulation. However, in spinalized animals, non-noxious lower chest or hindlimb stimulation produced opposite effects, increasing both the nerve activity and secretion rates of epinephrine and norepinephrine. In spinalized animals lower chest brushing stimulation elicited a much stronger response than hindlimb brushing stimulation. It was concluded that; (1) the secretion of adrenal medullary hormones can be controlled reflexly by mechanical cutaneous stimulation through the central nervous system via adrenal sympathetic efferent nerves; (2) the excitatory effect of the cutaneo-adrenal medullary reflexes was independent of noxious or non-noxious stimulation at the spinal level, whereas in rats with an intact central nervous system the effect was either excitatory or inhibitory in response to noxious or non-noxious stimulation, respectively; (3) there is a marked segmental organization of this reflex at the spinal level which is modified into a generalized response through supraspinal central structures.     

The Vagal Control of the Ileo-Cecal Sphincter in the Cat

In acute experiments on chloralosed cats the effect of efferent cervical vagal stimulation on a flow through the ileo-cecal sphincter (ICS) was studied. The motor activity of the jejunum, ileum and large intestine adjacent to the sphincter was recorded simultaneously. Vagal stimulation caused a decrease in the transsphincteric flow and increased motor activity in the ileum. Increased motor activity in the proximal colon was recorded only occasionally. When the vagal nerves were stimulated during continuous splanchnic stimulation the transsphincteric flow was decreased although the tone and motility of the ileum was supposed. Furthermore, guanethidine (1–3 mg/kg b.w.) blocked or suppressed the effect of vagal stimulation on the transsphincteric flow while the excitatory response of the proximal colon was greatly enhanced. This indicates that the reduction of the transsphincteric flow following vagal stimulation was at least partly due to a direct effect of the vagal nerves on the sphincteric muscle and not to a squeezing effect of that part of the colonic wall that surrounds the sphincter. Atropine (0.1 and 1 mg/kg b.w.) blocked all responses to vagal stimulation. Thus, both guanethidine and atropine blocked the vagally induced contraction of the ICS. Relaxation of the ICS was never obtained by vagal stimulation even when the tone of the sphincter had been increased by infusion of noradrenaline.     

The effect of cecal volume change on gastric motility in rats

The effect of a change in cecal volume on gastric motility was studied in 24 h fasted rats anesthetized with urethane (0.8 g/kg, i.p.). A cecal volume increase from 1 to 10 ml (in 1 ml steps) produced a decrease in the basal tone of the stomach. The maximal inhibitory response was produced with an 8 to 10-ml increase in cecal volume. The gastric inhibitory response continued as long as the increased cecal volume was maintained. It was abolished by a combination of a splanchnicotomy and vagotomy, or only a splanchnicotomy in a few cases. The inhibition of gastric motility by increasing the cecal volume also occurred after severance of dorsal roots between T8 and L4 and gastric branches of vagus nerves. It is suggested that an increase in cecal volume induces gastric relaxation mainly via the splanchnico-splanchnic pathway and partly via the vago-vagal and vago-splanchnic pathways. Therefore, retardation in transit of the gastric contents in germ free rats having an enlarged cecum may be attributed to an enhancement of the ceco-gastric inhibitory reflex. The ceco-gastric inhibitory response mediated by the splanchnic pathway was abolished by guanethidine (3-5 mg/kg, i.v.), but the response mediated by the vagal pathway was resistant to guanethidine as well as to atropine (0.2 mg/kg, i.v.). This result indicates that splanchnic postganglionic efferents are adrenergic, while vagal postganglionic efferents are non-adrenergic and non-cholinergic.     

Sympathetic activity in the recto-rectal reflex of the guinea pig

In the guinea pig, defecation is controlled by the myenteric plexus, whose activity is modulated by the sacral spinal and supraspinal centers. The purpose of this study is to clarify the control of defecation reflex by sympathetic nerves. The propulsive contractions of the rectum produced by rectal distension (recto-rectal excitatory reflex response) were abolished after transection of the Th 13 and/or the L 4 segment. This response was reproduced again after removal of the lumbar segments (L1-4), division of the lumbar dorsal roots (L1-4), the lumbar splanchnic nerves or lumbar colonic nerves (LCN). The frequency of efferent discharges of LCN was increased slightly by rectal distension and remarkably increased after Th 13 and/or L 4 transection. Thus, there occurs during the recto-rectal reflex not only mucosal intrinsic reflex and sacral excitatory reflex via the pelvic nerves but also a lumbar inhibitory reflex via the colonic nerves, whose center may be located in the upper lumbar segments.But, the activity of the inhibitory center was depressed by the supraspinal center, so that an excitatory reflex is produced more dominantly than an inhibitory one in normal animals. All these extrinsic reflexes coordinate the activity of the myenteric plexus in defecation reflex.