A mechanism of excessive accumulation of abomasal gas in vagotomized cattle determined using fluoroscopy.

To better understand the mechanism of excessive gas accumulation in the abomasum in bovine abomasal displacement, we performed gastric fluoroscopy in vagotomized cattle. Fifteen 6-month-old Holstein steers were divided into three groups: a non-vagotomized control group (Group C; n=5), a ventral thoraco-vagotomized group (Group V; n=5), and a dorsal and ventral thoraco-vagotomized group (Group DV; n=5). These groups were examined by fluoroscopy before and during a 5-week observation period after surgery. In Group C, no change was observed throughout the observation period. In Group DV, immediately after surgery, reticuloruminal motility was completely absent and ruminal distention was seen. Two weeks after surgery, abnormal reticulum motility and increased gas accumulation in the abomasal body were noted. Abomasal dilatation was also observed. In Group V, 1 week after surgery, gas inflow into the abomasum and relatively normal reticulum motility were observed along with a rapid increase in abomasal gas. Abomasal dilatation was also observed. In addition, left-displaced abomasum occurred in one of the steers in this group. From these results, we concluded that one of the mechanisms of excessive gas accumulation in the abomasum is reticulum-mediated gas inflow from the rumen combined with vagotomy-induced hypomotility.

Vagal and splanchnic afferent nerves are not essential for anorexia associated with abomasal parasitism in sheep.

Heavy burdens of the abomasal nematode, Ostertagia (Telodorsagia) circumcincta, in growing lambs result in a reduction in liveweight gain due largely to a drop in voluntary feed intake. The present study investigated: (1) the role of subdiaphragmatic vagal and non-vagal visceral afferent nerves in mediating a reduction in voluntary feed intake, using subdiaphragmatic vagal deafferentation (vagotomy) either alone or in combination with coeliac-superior mesenteric ganglionectomy (vagotomy and sympathectomy); and (2) the association between appetite, abomasal pH, selected blood values (amidated gastrin (G-17-amide), glycine-extended gastrin (G-17-Gly), pepsinogen and leptin) and worm burden, in sheep experimentally infected with 100,000 O. circumcincta infective larvae per os. Neither vagotomy alone nor vagotomy and sympathectomy in combination adversely affected the establishment or course of development of the parasite burden, when compared with a control group subject to sham surgery. Furthermore, neither surgical procedure prevented the drop in appetite seen 5-10 days post-infection, although combined vagotomy and sympathectomy did reduce voluntary feed intake prior to the start of the study. Ostertagia infection resulted in a significant increase in abomasal pH in all three groups, which was accompanied by an increase in blood G-17-amide and in G-17-Gly, the latter reported for the first time in parasitized ruminants. There were no significant differences in blood leptin, also reported for the first time in parasitized sheep, either between groups or in comparison with pre-infection levels, though weak negative correlations were established between blood leptin and appetite from day 5 to the end of the study in all three groups and a positive correlation with blood G-17-amide in the control group over the same period. These data suggest that neither intact subdiaphragmatic vagal afferent nerves or coeliac-superior mesenteric ganglion fibres, nor changes in circulating gastrin and leptin concentrations play a major role in mediating the hypophagic effects of O. circumcincta in parasitized sheep.

The use of power spectral analysis to determine cardiorespiratory control in the short-horned sculpin Myoxocephalus scorpius.

Anaesthesia and minor surgery to place electrocardiogram recording electrodes in the short-horned sculpin caused a decrease in mean normal beat (R-R) interval and heart rate variability (HRV), measured as the standard deviation in the R-R interval (SDRR). Mean R-R interval increased to a steady state value (1.9+/-2.9 s) 72 h post-surgery, but SDRR took 120 h to stabilise (0.56+/-0.09 s). Power spectral analysis applied to recordings of instantaneous heart rate showed no spectral peaks immediately after surgery, with the development of twin peaks (at 0.02 and 0.05 Hz) that also became stable 120 h post surgery. Bilateral cardiac vagotomy abolished the variability in beat-to-beat interval, and both the high and low frequency peaks, suggesting that much of the regulation of heart rate and HRV in sculpin was under parasympathetic, cholinergic control that was withdrawn as a result of surgical and handling stress. Rate of oxygen consumption and heart rate (f(H)) were monitored simultaneously and showed a good correlation with both mean R-R interval (r(2)=-0.89) and SDRR (r(2)=0.93), although a more significant (ANCOVA, P=0.02) covariance existed between the post-surgical decrease in and increase in SDRR. These data suggest that sculpin use f(H) as a way of moderating oxygen consumption, fine-tuned on a beat-to-beat basis by cholinergic control. We conclude that power spectral analysis is a useful method of determining HRV in fish, and that HRV is a more sensitive measure of recovery from disturbance than f(H) alone.

An immunohistochemical study of endocrine cells in the abomasum of vagotomized calf.

The effect of thoraco-vagotomy on the distribution and frequency of chromogranin-, serotonin-, somatostatin- and gastrin-immunoreactive cells in the abomasum of the calf were investigated by immunohistochemistry. Calves were vagotomized at 1 week old and sampled 2 and 4 weeks later. The endocrine cells generally decreased in number in vagotomized calves as compared to non-operated control calves. However, the detailed responses of endocrine cells to vagotomy varied depending on the endocrine cell type, region of gastric mucosa, and period after vagotomy. The present result suggests that the vagus nerve has an influence on the intrinsic regulatory system by endocrine cell control in the ruminant abomasum.

The effects of vagotomy on the abomasum in calves: radiography and protein gene product 9.5 immunohistochemistry.

Abomasal disorders of calves with total vagotomy, operated on at 1 week old, were investigated with radiography and protein gene product (PGP) 9.5 immunohistochemistry. Radiographic findings indicated abomasal atony with dilatation in all calves 2 weeks after vagotomy, while 4 weeks after vagotomy abomasal dilatation was detected in 2 calves and another 2 calves showed dilatation and impaction. The densities of PGP 9.5-immunoreactive nerves in the tunica muscularis decreased significantly in the corpus region of the greater curvature 2 weeks after vagotomy and in the pyloric region of the lesser curvature 4 weeks after vagotomy, and it was at its lowest 4 weeks after vagotomy in all regions examined. In conclusion, abomasal dilatation and/or impaction in vagotomized calves confirmed by radiography were related with a decreased frequency of nerves in the tunica muscularis of the abomasum.

A juxtaposition between A-cells and D-cells in the chicken pancreatic islets following vagotomy.

Conventional electron microscopy and enzyme-cytochemistry were applied to elucidate the juxtaposition between the pancreatic D-cell and A-cell, 1-2 weeks after abdominal vagotomy in chickens. A pancreatic D-cell frequently encircled an A-cell. Around this juxtaposition, several D-cells, characterized by the occurrence of peculiar dense bodies, formed a cluster. Both the D-cell and the A-cell juxtaposed with each other and had an irregularly shaped nucleus with several indentations. Exocytosis of secretory granules from D-cells encircling an A-cell was often observed in the capillary side, but no release of secretory granules from A-cells was detected, except on the capillary side. A few large dense bodies, resembling a multivesicular body, were observed in the A-cell cytoplasm, showed positive acid-phosphatase activity, and contained remnants of several types of cell organelles. They thus seemed to be secondary lysosomes. It is possible that the juxtaposition between the A-cell and the D-cell may be morphological evidence of the inhibitory action on the A-cell by the D-cell.

Regression of hypertrophic osteopathy following removal of intrathoracic neoplasia derived from vagus nerve in a dog.

Surgical removal of an intrathoracic tumor derived from a vagus nerve was undergone in a dog with hypertrophic osteopathy. The tumor was pathologically diagnosed as malignant schwanoma. Soft tissue swelling, lameness, and itchiness in four limbs disappeared within 7 days after surgery. The proliferated periosteal osteophytes of the four limbs was progressively reduced with time by follow-up radiography on the 58th day after surgery. On the 710th day after surgery, these osteophytes were greatly decreased as osteopathy, malignant schwanoma.

Oesophageal compliance in naturally occurring canine megaoesophagus.

The passive biomechanical property of oesophageal compliance (OC) was measured in 8 naturally occurring cases of canine megaoesophagus, 8 matched control and 7 vagotomised control dogs. Of the 8 dogs with megaoesophagus, 6 had congenital idiopathic megaoesophagus and 2 had secondary megaoesophagus attributable to generalised skeletal muscle disease. Stepwise distension of the whole oesophagus was employed for measurement of OC at the 4.0 and 8.0 mL/kg injected volume steps within the control volume range (0 to 12.0 mL/kg). At both injected volume steps OC was higher in megaoesophagus dogs than in either matched control or vagotomised control dogs (P < 0.01 in both cases), and no significant difference was observed in OC between matched control and vagotomised control dogs. No correlation was demonstrated between OC and the estimated duration of clinical signs of dogs with megaoesophagus. These findings suggest that in most cases of canine megaoesophagus the viscoelastic properties of the oesophageal wall are significantly altered, that in such cases the disorder is unlikely to be purely dynamic and that processes other than the duration of oesophageal dilatation are responsible for the alteration in oesophageal wall biomechanical properties. The relevance of these findings to current concepts on pathophysiological mechanisms underlying the evolution and resolution of various forms of canine megaoesophagus is discussed.

Desheathing the nodose ganglion is not a reliable method of de-efferentation in the ferret.

The present study reports the results of physiological and anatomical experiments in which the purpose was to determine whether desheathing the nodose ganglion is a reliable method of vagal de-efferentation in the ferret. In physiological studies, the effects of electrically stimulating the treated and untreated vagal nerves on cardiovascular and intestinal responses were examined and compared with previously obtained data after left supranodose vagotomy. The anatomical studies illustrated the effects of desheathing the left nodose ganglion on the transport of horseradish peroxidase (HRP) within a thoracic vagal communicating branch. These data were compared to data from control animals and animals that had undergone left supranodose vagotomy. The results demonstrated that severing the fascicles overlying the left nodose ganglion and allowing the nerve fibers to degenerate, caused no reduction in labeled efferent cell bodies in the left dorsal motor nucleus of the vagus as compared to controls. However, after left supranodose vagotomy there were no efferent cell bodies labeled in the left dorsal motor nucleus of the vagus. Following degeneration of the fascicles, electrical stimulation of the peripheral cut end of this nerve did not abolish the efferent responses in 7 out of 9 animals studied, whereas supranodose vagotomy abolished the responses in all animals. These findings demonstrate that desheathing the nodose ganglion and thereby removing the nerve bundles overlying the nodose ganglion is not a guaranteed method of destroying the efferent fibers in the vagus nerve of the ferret. Supranodose vagotomy, therefore, is a more reliable method of de-efferentation in this species.

Eructation of gas through the gastroesophageal sphincter before and after truncal vagotomy in dogs.

The function of the gastroesophageal sphincter (GES) to eructate gas before and after vagotomy was investigated in conscious, fed dogs. Gastric and GES pressures were measured in 5 dogs, using a perfused 4-lumen catheter with a Dent sleeve. To induce eructation, nitrogen gas was insufflated (440 ml/min) into the stomach through 1 channel of the catheter. After base-line studies were completed on each dog, bilateral truncal vagotomy was performed 5 cm cranial to the diaphragm. Mean (+/- SE) GES pressure was 51.5 +/- 1 mm of Hg before vagotomy and 28 +/- 1.7 mm of Hg after vagotomy (P less than 0.001). Mean gastric contraction rates were the same, 4.91 +/- 0.11/min and 4.78 +/- 0.06/min in dogs before and after vagotomy, respectively. During insufflation, gastric pressures increased to 11.8 +/- 0.7 mm of Hg before eructation in dogs before vagotomy and to 18.4 +/- 0.8 mm of Hg in dogs after vagotomy (P less than 0.001). Eructation occurred at intervals of 1.79 +/- 0.09 minutes before vagotomy and 5.71 +/- 0.41 minutes after vagotomy (P less than 0.001). Atropine resulted in an interval of 1.98 +/- 0.18 minutes before vagotomy. Eructation was not seen in 2 dogs after vagotomy and was sometimes not seen in the 3 others. Gastroesophageal sphincter pressure in dogs before vagotomy began to decrease 4.5 +/- 0.2 s before the GES-pressure gradient disappeared, and GES pressure remained there for 5.3 +/- 0.3 s before the gradient began to return.(ABSTRACT TRUNCATED AT 250 WORDS)

[Total vagal deafferentation and gastric emptying in swine]. / Déafférentation vagale totale et évacuation gastrique chez le porc.

50-kg pigs fed a purified wheat starch and casein diet were fitted with a gastric cannula. Gastric emptying was studied by checking the residual gastric contents at 30 min and 1, 2, 4 and 7 hrs after feeding. Five of the 25 pigs were used as controls; 5 were submitted to total vagal deafferentation including removal of the left nodose ganglion, right truncal vagotomy at the diaphragm and resection of the interconnecting branches between the two vagi on their intrathoracic course; 5 were submitted to total contralateral vagal deafferentation; 5 only underwent left truncal vagotomy and resection of the connectives; 5 were submitted to the contralateral operation. Total vagal deafferentation, suppressing bilateral afferences originating below the diaphragm, resulted in much higher residual gastric contents at all times studied after the meal. Significant gastric retention was also observed after unilateral truncal vagotomy as compared to the controls. Nevertheless, this retention was significantly lower than after total deafferentation. The reduced emptying rate after total vagal deafferentation was a result of the loss of all afferences, while the simultaneous reduction of efferences was of little importance. The mechanisms responsible for gastric retention have been discussed in relation with the sustained antral hyperactivity previously found in deafferented pigs and with the various controls of gastric emptying. Several factors may be involved, including both motor and secretory changes. The prolonged postprandial activity of the gastric antrum seemed to be a consequence of gastric retention.

Arrhythmogenicity of dopamine, dobutamine, and epinephrine in thiamylal-halothane anesthetized dogs.

The arrhythmogenicity of epinephrine, dopamine, and dobutamine, administered by constant-rate infusion, was determined in vagotomized and nonvagotomized thiamylal-halothane anesthetized dogs. Electrocardiograms and atrioventricular bundle electrograms revealed the development of atrial, junctional, and ventricular arrhythmias. The 3 drugs produced atrial arrhythmias at dosages smaller than those required to produce ventricular arrhythmias. The mean dosages (microgram/kg-1/min-1) required to produce ventricular arrhythmias on duplicate trials in vagotomized dogs were for epinephrine, 0.6 +/- 0.2; dopamine, 22.8 +/- 14.8; and dobutamine, 11.6 +/- 5.2. The corresponding doses for nonvagotomized dogs were for epinephrine, 0.8 +/- 0.3; dopamine, 35.3 +/- 13.5; and dobutamine, 21.9 +/- 13.9. Most ventricular arrhythmias originated from a single focus in the left ventricle. Heart rate and blood pressure were significantly increased immediately before ventricular arrhythmia appeared. We conclude that epinephrine, dopamine, and dobutamine are capable of producing cardiac arrhythmias in vagotomized and nonvagotomized thiamylal-halothane anesthetized dogs and that bilateral vagotomy decreases the dosage of epinephrine, dopamine, and dobutamine required to produce cardiac arrhythmias.

Effect of vagotomy on respiratory mechanics and gas exchange in the neonatal calf.

The effect of vagotomy on the mechanical and gas exchange properties of the respiratory system was determined in 7 healthy, anesthetized neonatal Holstein calves. A pressure-compensated volume displacement plethysmograph measured the quasi-static pressure-volume (PV) characteristics of the lungs and thoracic cage. Functional residual capacity (FRC) was determined by He equilibration. Lung and chest wall compliances per kilogram of body weight were 2.25 +/- 0.19 ml/cm of H2O/kg and 8.85 +/- 2.44 ml/cm of H2O/kg, respectively. Total lung capacity (TLC) averaged 78.3 +/- 13 ml/kg and FRC was 51 +/- 5% of TLC. The lung PV curve deviated from single exponential behavior below 75% of TLC, indicating airway closure at large lung volumes. Residual volume, which averaged 28.1 +/- 6.0% of TLC, appeared to be determined by airway closure because the thoracic cage was compliant between FRC and residual volume. Vagotomy had no effect on the lung and thoracic cage PV curves, lung volumes, or the alveolar-arterial oxygen difference, but it decreased pulmonary resistance and increased respiratory system conductance and the dead space/tidal volume ratio, indicating dilation of large conducting airways. The calf appears similar to other neonates, in that the thoracic cage is compliant and airway closure occurs at large lung volumes. Both of these factors may predispose the calf to atelectasis.

3-methylindole-induced pulmonary toxicosis in ponies.

In unanesthetized ponies, arterial blood gas tensions, pulmonary mechanics, and lung volumes were determined before and 24 to 48 hours after oral administration of 500 ml of corn oil or 100 mg of 3-methylindole (3MI)/kg of body weight in 500 ml of corn oil. In the latter group, variables were also measured after bilateral cervical vagotomy. Respiratory rate and minute ventilation were increased by 3MI treatment and decreased after vagotomy, suggesting that the tachypnea induced by 3MI was vagally mediated. The arterial O2 tension (PaO2) was unaffected but arterial CO2 tension (PaCO2) decreased below base line after 3 MI and vagotomy. Specific respiratory conductance and dynamic compliance wee decreased by 3MI. Specific conductance increased again after vagotomy. Functional residual capacity, which increased after 3MI, was unaffected by vagotomy. Total lung capacity and quasistatic compliance were unaffected by either treatment. Minimal volume was larger in 3MI-treated ponies than in untreated ponies. Decreased dynamic compliance and specific respiratory conductance and increased functional residual capacity and minimal volume are all compatible with small airway obstruction produced by the necrotizing bronchiolitis and bronchiolar obstruction observed histologically in 3MI-treated ponies.

Mouth breathing in chickens under rebreathing conditions, cervical vagotomy of heat load.

By recording the lower beak movement, open-mouth breathing was monitored in adult hens restrained in a supine position with the cannulated trachea under rebreathing conditions, bilateral cervical vagotomy or heat load. Tidal volume and respiratory carbon-dioxide and oxygen contents were recorded simultaneously. The beak movement can be a significant indication of hypercapnia and/or increase in respiratory CO2 content, but not of hypoxia or decrease in respiratory O2 content. Vagotomy causes big oscillatory movements of the beak, which do not mainly depend on hypercapnic hypoxia induced by the vagotomy. If the dysfunction of the vagus is aggravated progressively, it will be unable for the pattern and amplitude of beak movement to be any differential indication of this dysfunction from hypercapnia and/or increase in respiratory CO2 content seen at respiratory failure. Two patterns of beak movement are noticed. One appears at an early stage of beak movement and at a certain direct level superimposed with or without small beak-oscillation. The other indicates a bigger oscillatory beak movement than the former. This oscillatory movement is synchronous with the inspiration after vagotomy and hypercapnia. This is the case with hyperthermia at a remarkably high breathing frequency. The amplitude of beak movement is not always proportional to the tidal volume. The onset and end of inspiration cannot precisely be indicated by those of a beak movement.

Unusual response of anaesthetised pigs to asphyxia.

The effects of vagosympathectomy, asphyxia, hypoxia and hypercapnia on the breathing of anaesthetised pigs are described. Vagosympathectomy caused changes in cardiovascular variables and in the pattern of breathing characteristic of the loss of stretch receptor activity. After vagosympathectomy the linear relationship between tI and tE was abolished. Hypoxia in intact animals produced changes in minute ventilation by peripheral chemoreceptor drive. When this drive was removed by vagosympathectomy the central depressing effects of hypoxia were revealed as a slowing of breathing and reduction in minute volume. The central depressing effect of hypoxia on respiration was very potent in the pig and very clearly seen in asphyxia. Vagosympathectomy caused a reduction in frequency of breathing and respiratory arrest occurred when a dead space of only moderate size was used. Breathing slowed from the moment of connection of the dead space to produce respiratory arrest within 2 min. The pig lung has been considered similar to the human lung on morphometric and physiological grounds but these results show that there are very important species differences in response to asphyxia.