Vagally Denervated Research Articles

Hypoxemia and low Crs in vagally denervated lambs result from reduced lung volume and not pulmonary edema.

Vagal denervation performed in the intrathoracic region in newborn lambs leads to hypoxemia and decreased respiratory system compliance (Crs), which could result from atelectasis and/or pulmonary edema. The objective of the present study was to quantify the relative roles of alveolar derecruitment and pulmonary edema as underlying cause(s) of respiratory failure. Vagal denervation was performed in the intrathoracic region and below the recurrent laryngeal nerves in six newborn lambs within 24 h of birth, whereas six were sham operated. Pre- and postinflation Crs was measured to investigate the presence of alveolar derecruitment. Pulmonary edema was assessed with lung wet-dry-to-wet and lung tissue wet-to-dry ratios, total protein, and FITC-BSA recovery in lung tissue and bronchoalveolar lavage. Compared with that in the sham-operated animals, Crs was significantly lower in vagally denervated animals. However, postinflation, pulmonary system compliance obtained by quasi-static lung inflation and deflation to 30 cmH2O showed no significant difference between the sham-operated and denervated lambs. The lung wet-dry-to-wet and lung tissue wet-to-dry ratios, total protein, and FITC-BSA recovery in lung tissue and bronchoalveolar lavage were similar in denervated and sham-operated groups. We provide evidence that reduced lung volume and not pulmonary edema is associated with intrathoracic vagal denervation and is the likely underlying mechanism for hypoxemia and low Crs.

Effects of vagal denervation on cardiorespiratory and behavioral responses in the newborn lamb.

Recently, Wong et al. (Wong KA, Bano A, Rigaux A, Wang B, Bharadwaj B, Schurch S, Green F, Remmers JE, and Hasan SU, J Appl Physiol 85: 849-859, 1998) demonstrated that fetal lambs that have undergone vagal denervation prenatally do not establish adequate alveolar ventilation shortly after birth. In their study, however, vagal denervation was performed prenatally and the deleterious effects of vagal denervation on breathing patterns and gas exchange could have resulted from the prenatal actions of the neurotomy. To quantify the relative roles of pre- vs. postnatal vagal denervation on control of breathing, we studied 14 newborn lambs; 6 were sham operated, and 8 were vagally denervated below the origin of the recurrent laryngeal nerve. Postoperatively, all denervated animals became hypoxemic and seven of eight succumbed to respiratory failure. In vagally denervated lambs, expiratory time increased, whereas respiratory rate, minute ventilation, and lung compliance decreased compared with the sham-operated animals. In the early postoperative period, the frequency of augmented breaths was lower but gradually increased over time in the denervated vs. sham-operated group. The dynamic functional residual capacity was significantly higher than the passive functional residual capacity among the sham-operated group compared with the denervated group. No significant differences were observed in the prevalence of various sleep states and in the amount of total phospholipids or large- and small-aggregate surfactants between the two groups. We provide new evidence indicating that intrauterine actions of denervation are not required to explain the effects of vagal denervation on postnatal survival. Our data suggest that vagal input is critical in the maintenance of normal breathing patterns, end-expiratory lung volume, and gas exchange during the early neonatal period.

Gastric pouch acid secretion in response to physiologic digestive function

Objectives. To evaluate acid secretion and histologic features of the gastric segment used for bladder replacement in bladder cancer. Methods. Nine patients were investigated a mean of 36 months after gastric pouch surgery with modified shamfeeding and feeding. We determined urinary acidity, urinary pH, serum gastrin, and serum pancreatic polypeptide values and tried to find a relationship between feeding and acid secretion in the gastric pouch. In 6 patients, biopsy and histopathologic examination were performed. Results. In 8 patients, urinary acidity increased after feeding following the rise of gastrin; in 1 patient no increase of gastrin or acidity was observed. In 7 patients, urinary acidity did not change after modified shamfeeding, indicating vagal denervation after surgery. This group showed a minimal urinary pH of above 4 after feeding. On the other hand, in 2 patients an increased acid secretion was observed after modified shamfeeding, indicating the possible presence of residual vagal innervation. In this group, the acid secretion in the pouch was higher, reaching the minimal pH level earlier after feeding. Histopathologic examination showed no major structural changes of gastric mucosa. Conclusions. Most patients are vagally denervated after gastric pouch surgery, and the gastric segment continues its original gastrointestinal function by a hormonal pathway. Our data indicate, however, that in some patients, the gastric pouch keeps a residual vagal innervation. We therefore suggest that nerve fibers present in the blood supply of the gastric segment be interrupted to avoid the complications associated with increased acid secretion of the gastric pouch.

Selective vagal denervation of the atria eliminates heart rate variability and baroreflex sensitivity while preserving ventricular innervation.

The purpose of this study was to test whether radiofrequency catheter ablation (RFCA) of 3 epicardial fat pads that resulted in efferent vagal denervation of the atria and sinus and atrioventricular nodes also denervated the ventricles. Vagal innervation of the ventricles was determined by measuring prolongation of ventricular effective refractory period induced by bilateral vagal stimulation (20 Hz, 10 V, 4 ms). Changes in heart rate variability (HRV) and baroreflex sensitivity (BRS) were also examined. We found that RFCA of the 3 epicardial fat pads vagally denervated the sinus and AV nodes and atria without affecting vagal innervation of the ventricles, indicating that efferent vagal fibers to the ventricles do not travel through the 3 epicardial fat pads. Parameters of time-domain variables decreased significantly; the total-power, high-frequency, and low-frequency components of frequency-domain variables decreased significantly; and the ratio of the low- and high-frequency components increased significantly after chronic vagal denervation. Vagally modulated sinus arrhythmia and BRS were also eliminated after chronic vagal denervation. These data also indicate that HRV and BRS represent vagal activity at the level of the sinus node and may not accurately reflect efferent vagal activity at the ventricular level. Selective vagal denervation of the sinus and AV nodes and atria decreased HRV and eliminated BRS while preserving ventricular innervation.

Vagal Denervation Decreases the Large Surfactant Aggregates and mRNAs for SP-A and SP-B. 1951

We have previously shown that fetal lambs which have undergone intrathoracic vagal denervation have increased surface tension and develop respiratory failure at birth. However, the mechanism of surfactant dysfunction remains unknown. To quantify the relative roles of surfactant synthesis, release and activity, we studied 15 chronically instrumented unanesthetized newborn lambs; eight of 15 fetuses underwent intrathoracic vagal denervation whereas seven were sham-operated. Each fetus was instrumented to record heart rate, blood pressure, diaphragmatic electromyogram, arterial pH, and blood gas tensions between 131-133 d gestation (term=147±2 d) and studied at 142-143 d after spontaneous vaginal delivery. Various cardiorespiratory variables were recorded immediately after birth and the animals were sacrificed at 1 hr of age. Surfactant associated proteins (SP-A, -B and -C) mRNAs were analyzed in the right middle lobe whereas bronchoalveolar lavage(BAL) was performed on the remaining lungs to determine total and various phospholipid (PL) species, large aggregates (LA), small aggregates (SA) and plasma proteins. Recovery of BAL was similar in both groups (91±1 vrs 90±2%). Total phospholipids were also similar in the sham-operated and vagotomized animals. However, LA (mg/kg) in sham group (23±4.24) were significantly higher than in the vagotomized group (10±1.9; p=0.01). Also, the LA as a percentage of total PL was significantly higher in the sham operated animals (52±6 vrs. 25±8, respectively, p=0.009). The percentage of phosphatidylcholine (n=9) was similar in both groups, however, phosphatidylinositol (PI) was higher (p=0.02) and phosphatidylglycerol (PG) was lower (p=0.05) in the vagotomized group. Northern blot analysis showed decreased mRNA levels of SP-A and SP-B, whereas no significant differences were observed for SP-C. We conclude that vagally denervated animals have an increased proportion of SA, an inactive form of surfactant, decreased LA, and delayed surfactant maturation as indicated by the PI and PG ratios, and decreased expression of surfactant apoproteins mRNAs. These changes in surfactant system may play a role in respiratory failure in vagally denervated newborn lambs.

Efferent vagal innervation of the canine atria and sinus and atrioventricular nodes. The third fat pad.

The purpose of this study was to investigate the functional pathways of efferent vagal innervation to the atrial myocardium and sinus and atrioventricular (AV) nodes. Using vagally induced atrial effective refractory period shortening, slowing of spontaneous sinus rate, and prolongation of AV nodal conduction time as end points of vagal effects, we determined the actions of phenol and epicardial radiofrequency catheter ablation (RFCA) applied to different sites at or near the atrial myocardium to inhibit these responses. We found that efferent vagal fibers to the atria are located both subepicardially and intramurally or subendocardially. Most efferent vagal fibers to the atria appear to travel through a newly described fat pad located between the medial superior vena cava and aortic root (SVC-Ao fat pad), superior to the right pulmonary artery, and then project onto two previously noted fat pads at the inferior vena cava-left atrial junction (IVC-LA fat pad) and the right pulmonary vein-atrial junction (RPV fat pad) and to both atria. A few vagal fibers may bypass the SVC-Ao fat pad and go directly to the IVC-LA or RPV fat pad and then innervate the atrial myocardium. Vagal fibers to the sinus and AV nodes also converge at the SVC-Ao fat pad (a few fibers to the sinus node go directly to the RPV fat pad) before projecting to the RPV and IVC-LA fat pads. Long-term vagal denervation of the atria and sinus and AV nodes can be produced by RFCA of these fat pads and results in vagal denervation supersensitivity. Vagal denervation prevents induction of atrial fibrillation in this model. The newly described SVC-Ao fat pad receives most of the vagal fibers to the atria and sinus and AV nodes. Elimination of the fat pads with RFCA selectively vagally denervated the atria and sinus and AV nodes.

Role of Airway Mechanoreceptors in the Inhibition of Inspiration during Mechanical Ventilation in Humans

The purpose of this study was to demonstrate a neuromechanical inhibitory effect on respiratory muscle activity during mechanical ventilation and to determine whether upper and lower airway receptors provide this inhibitory feedback. Several protocols were completed during mechanical ventilation: (1) positive and negative pressure changes in the upper airway, (2) airway anesthesia to examine the consequences of receptor blockade on respiratory muscle activity, (3) increasing FRC with positive end-expiratory pressure to study the effect of hyperinflation or stretch on respiratory muscle activity, and (4) use of heart-lung transplant patients to determine the effects of vagal denervation on respiratory muscle activity. All subjects were mechanically hyperventilated with positive pressure until inspiratory muscle activity was undetectable and the end-tidal PCO2 decreased to less than 30 mm Hg. End-tidal PCO2 (PETCO2) was increased by either adding CO2 to the inspired gas or decreasing tidal volume (50 ml/min). The PETCO2 where a change in inspiratory muscle activity occurred was taken as the recruitment threshold (PCO2RT). Neuromechanical feedback caused significant inspiratory muscle inhibition during mechanical ventilation, as evidenced by the difference between PCO2RT and PETCO2 during spontaneous eupnea (45 +/- 4 versus 39 +/- 4 mm Hg) and a lower PCO2RT when tidal volume was reduced with a constant frequency and fraction of inspired CO2. Recruitment threshold was unchanged during positive and negative pressure ventilation, during upper and lower airway anesthesia, and in vagally denervated lung transplant patients. These findings demonstrate that neuromechanical feedback causes highly significant inhibition of inspiratory muscle activity during mechanical ventilation; upper and lower airway receptors do not appear to mediate this effect.

Supersensitivity to acetylcholine of canine sinus and AV nodes after parasympathetic denervation.

Supersensitivity of the sinus (SAN) and atrioventricular (AVN) nodes to acetylcholine (ACh) after parasympathetic denervation has not been demonstrated conclusively. In this study, we denervated the SAN and AVN by surgically removing parasympathetic ganglia and painting the area with phenol. Sham dogs underwent thoracotomy without denervation. Four to 9 days later, vagal denervation was proved by supramaximal bilateral vagal stimulation, which prolonged the sinus cycle length (SCL) only 32 +/- 7% (mean +/- SE) and the AVN conduction time (AH interval) 15 +/- 7% in denervated dogs. We tested for supersensitivity by obtaining dose-response curves to ACh (1 ml, 10(-8.0) to 10(-4.0) M in 10(0.5) steps) infused over 15 s into the sinus nodal and posterior septal arteries in open chest-denervated (Den) dogs and in sham-operated (Sham) dogs that were anesthetized with alpha-chloralose. ACh concentration (Log[ACh], M) required to prolong SCL 50, 100, and 300% was -5.7 +/- 0.1, -5.6 +/- 0.1, and -5.4 +/- 0.1 in 10 Sham dogs vs. -6.4 +/- 0.1 (P less than 0.001), -6.3 +/- 0.1 (P less than 0.001) and -6.1 +/- 0.1 (P less than 0.001) in 11 Den dogs. ACh concentration necessary to produce second degree and complete AV block was -5.7 +/- 0.1 and -5.3 +/- 0.1 in 11 Sham dogs vs. -6.3 +/- 0.1 (P less than 0.001) and -5.8 +/- 0.1 (P less than 0.01) in 10 Den dogs. Because significantly lower doses of ACh prolonged SCL or produced AV block in Den compared with Sham dogs, we conclude that dogs with vagally denervated SAN and AVN develop a supersensitive response to ACh.

Factors related to gastric hypersecretion during pregnancy and lactation in rats.

We attempted to elucidate the factors involved in gastric hypersecretion of rats during pregnancy and lactation. Acid secretion in pylorus-ligated and vagally denervated fistula rats stimulated with histamine, tetragastrin, and methacholine increased from midterm pregnancy and persisted during lactation. Pepsin secretion remained unaltered during pregnancy but increased during lactation. Vagal denervation itself abolished this hypersecretion. In late pregnancy, a delayed appearance of maximal acid response to histamine was apparent, as compared to nonpregnant rats, and was abolished by aminoguanidine treatment. There was a delay in the maximal response to tetragastrin but not to methacholine. Serum histamine concentrations were 3-4 times higher in late pregnancy, as compared to nonpregnant, lactating and nonlactating rats. Gastric DNA and protein concentrations were significantly increased in lactating rats with concomitant elevation of food intake and serum gastrin levels. Those changes disappeared in nonlactating rats, and gastric secretion was much the same in the nonpregnant rats. These results indicate that acid hypersecretion during pregnancy was exclusively associated with vagal innervation plus high serum histamine levels, while acid and pepsin hypersecretion in lactating rats were associated with vagal innervation plus hyperplastic gastric mucosa and high serum gastrin levels.

The vagus, the duodenal brake, and gastric emptying.

It has been suggested that an intact vagal supply is essential for the normal function of the recptors in the duodenum and proximal small bowel, which influence the rate of gastric emptying. This paper reports the effect of vagal denervation on gastric emptying and also examines the site and mode of action of receptors in the proximal small bowel. It has been demonstrated in the dog that most, if not all, the receptors controlling gastric emptying lie in the proximal 50 cm of the small bowel. Following truncal vagotomy the emptying time of each instillation increased significantly and the differential rate of emptying of different instillations remained unchanged. The proximal 50 cm of small bowel was capable to differentiating between different instillates even after selective extragastric vagotomy, in which the duodenum was vagally denervated and, therefore, duodenal braking receptors function independently of vagal innervation.

Secretin-Induced Inhibition of Acid Secretion before and after Vagal Denervation of Canine Gastric Pouches

Sjödin, L. & Miura, S. Secretin-induced inhibition of acid secretion before and after vagal denervation of canine gastric pouches. Scand. J. Gastroent. 1974, 9, 185-190.The inhibitory effect of secretin on pentugastrin-stimulated secretion was studied before and after transformation of vagally innervated futidic pouches (Pavlov type) into vagally denervated pouches (Heidenhain type). A high dose of secretin (3.0 U per kg-hr) profoundly inhibited the secretion from both types of pouch, whereas a lower dose of secretin (0.75 U per kg-hr) produced a significant inhibition only in the Heidenhain pouches. Urecholine was shown to reduce the inhibitory effect of secretin on pentagastrin-stimu-lated secretion from vagally denervated pouches. It is suggested that when the fundic mucosa is vagally innervated, endogenous secretin is of little or no importance as an inhibitor of gastric acid secretion under physiological conditions. Pepsin output evoked by combinations of pentagastrin and secretin was low compared with that produced by a single infusion of Urecholine. The physiological significance of the stimulatory effect of secretin on pepsin secretion remains to he established.

Effects of brocresine (NSD-1055) and cycloheximide on amino acid decarboxylase activities in gastric mucosa of normal and vagally denervated rats.

1. Histidine decarboxylase activity of rat stomach fluctuates depending upon the functional state of the stomach. This varying enzyme activity poses special problems in assessing the effectiveness of enzyme inhibitors. After vagal denervation gastric histidine decarboxylase is markedly activated and remains at a high, stable level, which is unaffected by the functional state of the stomach. Thus it appears that vagally denervated rats are well suited for studies on histidine decarboxylase inhibitors.2. In vivo, brocresine (NSD-1055) was found to be a more effective inhibitor of gastric DOPA decarboxylase than of gastric histidine decarboxylase. With the fairly high dose given (200 mg/kg) the inhibition of histidine decarboxylase was at most 75-85% and quite short-lasting. The DOPA decarboxylase activity, which was not affected by vagal denervation, was inhibited more than 95% by brocresine; this inhibition was longer-lasting.3. Cycloheximide, which probably lowers gastric histidine decarboxylase activity by inhibiting enzyme synthesis, was maximally effective at a dose level as low as 1 mg/kg. Gastric DOPA decarboxylase was not inhibited by cycloheximide. Vagotomized rats and control rats responded similarly.4. Combined treatment of vagally denervated rats with brocresine and cycloheximide resulted in a rapid and persistent reduction of the histidine decarboxylase activity. It is concluded that the failure of brocresine alone to induce a lasting inhibition of histidine decarboxylase is due to continuous, rapid synthesis of new enzyme.5. The calculated half-life of gastric histidine decarboxylase was 75 min in vagally denervated rats and 45 min in normal fasted rats. The results suggest that the increased enzyme activity after vagal denervation is caused by an increased rate of enzyme synthesis.

Mechanism of activation of rat stomach histidine decarboxylase after vagal denervation

Vagal denervation causes a powerful activation of histidine decarboxylase in the oxyntic gland area of the rat stomach. It was decided to investigate the mechanism behind the activation following vagotomy and to identify the histamine-forming enzyme. A semi-purified preparation of gastric histidine decarboxylase from vagally denervated rats was found to be identical with the specific histidine decarboxylase previously characterized in extracts of gastric mucosa of normal rats and in tissues of the foetal rat. The pH optimum varied with the substrate concentration: 6.2 with 6 × 10 −3 M histidine, 6.7 with 6 × 10 −4 M histidine. The Michaelis-Menten constant increased with diminishing pH. Gastric histidine decarboxylase in the fasted rat was markedly activated after bilateral, but not after unilateral, vagal denervation. The enzyme activation normally seen in the rat stomach after feeding and after the injection of insulin persisted after unilateral denervation, both in the innervated and the denervated side of the stomach. These findings exclude a direct vagal regulation of the enzyme activity of the histamine-producing cell. Antrectomy abolished the enzyme activation following vagal denervation, suggesting that the enzyme activation is a consequence of enhanced release of some antral hormone, possibly gastrin. The release of gastrin is regulated by a variety of factors, one being the antral pH. Accordingly, perfusion of the stomach with hydrochloric acid markedly reduced the enzyme activity of vagotomized rats, whereas perfusion with phosphate buffer (pH 7.0) resulted in an increase in the enzyme activity of normal, fasted rats. Atropine and propantheline in doses sufficient to inhibit acid secretion activated the enzyme of normal, fasted rats. The enzyme-activating effect of atropine was abolished by antrectomy. Histamine, which stimulated acid secretion in normal rats but not in vagotomized rats, reduced the enzyme activity of normal, fasted rats, but not that of vagotomized rats. Histamine also inhibited the enzyme activation after feeding and after the injection of insulin but not that seen after the injection of pentagastrin. The following conclusion is drawn: All agents (except gastrin itself) and all experimental conditions which increase gastric acid secretion without directly affecting gastrin release, result in a reduction of the histidine decarboxylase activity through acid-induced inhibition of gastrin release. All agents and conditions which inhibit acid secretion but not gastrin release, cause an increase in the enzyme activity through enhanced gastrin release secondary to the elevation of antral pH.

Effect of gastric vagal denervation on inhibition of acid secretion by secretin.

In dogs with vagally innervated gastric pouches and gastric fistulas, acid secretion was stimulated by intravenous administration of Urecholine, 0.025 and 0.1 (mg/kg)/hr; of pentagastrin, 4 (µg/kg)/hr; or by feeding a meal of liver and bone dust, 25 g/kg. Acid secretion elicited by these stimulants was significantly inhibited (P<0.05 to 0.001) by intravenous infusion of secretin, 2 (units/kg)/hr. With Urecholine, 0.1 (mg/kg)/hr, comparable inhibition resulted from endogenous duodenal acidification which was produced by closing the gastric fistula. The pouches were then vagally denervated by cutting the muscular connection, and dividing the septum between pouch and main stomach; all tests were repeated. Vagal denervation decreased the stimulatory potency of feeding and pentagastrin, but increased Urecholine-stimulated acid output. This increased sensitivity of parietal cells to a cholinomimetic stimulus after vagal denervation is an example of Cannon's law of denervation supersensitivity. Inhibition of Urecholine-stimulated secretion by duodenal acidification was not significantly modified by vagal denervation (40% inhibition before, 38% after). Percentage inhibition of acid output by secretin was slightly increased after vagal denervation when the stimulant was Urecholine (42% inhibition before, 52% after) or pentagastrin (63% inhibition before, 73% after), but these changes were not statistically significant. Vagal denervation markedly increased the degree of inhibition of food-stimulated secretion (20% inhibition before, 71% after), suggesting that secretin is primarily an antagonist of gastrin.

The role of endogenous gastrin in the activation of gastric histidine decarboxylase in the rat. Effect of antrectomy and vagal denervation.

The activity of gastruc histidine decarboxylase in normal rats was markedly reduced after prolonged fasting. The reduction was reversed by feeding and by injection of gastrin, insulin (vagal stimulation) or carbachol. Feeding, vagal stimulation or treatment with parasympathomimetics released endogenous gastrin. The role of endogenous gastrin (believed to be located in the antrum) and of the vagus nerve in activating gastric histidine decarboxylase was studied in antrectomized and in vagally denervated rats. Antrectomy reduced the activation of gastric histidine decarboxylase induced by feeding and abolished that induced by the injection of insulin or carbachol (but not that induced by pentagastrin). Antral exclusion, on the other hand, caused a marked enzyme activation. These results indicate the existence of an antral agent (presumably gastrin) which mediated in the process of enzyme activation. The effect of antrectomy on gastric acid secretion was studied in rats fitted with chronic gastric fistulas. Antrectomy depressed basal acid secretion, but did not abolish the effect of insulin hypogylcemia on acid secretion. Vagal denervation (truncal vagotomy or selective vastric vagotomy) in combination with pyloroplasty caused a marked activation of the gastric histidine decarboxylase in fasted rats. This activation was totally abolished by combined vagotomy and antrectomy. Consequently, enzyme activation observed after vagotomy is induced by some agent from the antrum, possibly gastrin. The activation of gastric histidine decarboxylase seen upon truncal vagotomy was abolished not only by antrectomy but also by perfusion of the stomach with dilute hydrochloric acid. It is therefore suggested, that low antral pH inhibits the release of gastrin and that the elevated antral pH caused by vagotomy stimulates its release. In chronic fistula rats, vagotomy caused a profound decreased of acid secretion and inhibited the secretory response to insulin and pentagastrin. The following concept is advanced: The activity of gastric histidine decarboxylase is under the influence of endogenous gastrin. The influence of the vagus nerve on histidine decarboxylase is exerted via the gastrin-containing cell in the antrum and not by direct action on the cell containing the enzyme. The influence of the vagus on the gastrin cell has two facets, possibly constituting the components in a feed-back mechanism: a) vagal stimulation of the gastrin cell releases gastrin; b) vagal stimulation of the parietal cell causes acid hypersecretion, whicc inhibits gastrin release. Activation of gastrin histidine decarboxylase is a consequence of gastrin-induced stimulation of the enzyme-containing cell. Important factors regulating the gastrin release are the vagal activity and the antral pH.

Effect of Vagal Denervation of Pouches on Gastric Secretion in Dogs with Intact or Resected Antrums

Summary Pavlov type pouches in dogs were vagally denervated by transecting the muscular bridge, thus converting them into Heidenhain pouches. The effect of this form of vagal denervation on the secretion of acid and pepsin by the pouches in response to stimulation by histamine, gastrin, Urecholine, or combinations of these stimulants was studied. The studies were performed on two groups of dogs, one with intact, the other with resected antrum. Vagotomy reduced the maximal acid secretion in response to histamine, gastrin, and combinations of histamine or gastrin with Urecholine. The one exception to this statement was in the nonantrectomized dogs stimulated with histamine alone; in this instance the maximal acid secretion in response to histamine was not decreased. Acid secretion in response to submaximal doses of histamine, gastrin, and combinations of histamine or gastrin with Urecholine was significantly reduced by vagotomy in both the antrectomized and nonantrectomized dogs. Acid secretion in response to submaximal doses of Urecholine alone showed some tendency to increase after vagotomy. Vagotomy depressed the secretion of acid in response to gastrin more than in response to histamine. Urecholine produced greater augmentation of the maximal secretion of acid in response to gastrin than to histamine. The effect of vagotomy on the secretion of pepsin cannot be described by any simple generalizations; the nature of the stimulant and its dose and the presence or absence of the antrum were modifying factors. Two observations are noteworthy: 1) in the vagally denervated pouches (antrum intact) doses of gastrin that were maximal or supramaximal for acid secretion stimulated pepsin secretion, and 2) vagal denervation caused unequivocal supersensitivity of the pepsin stimulating action of Urecholine.

Respiratory and circulatory vagal reflexes in rabbits exposed to high explosive shock waves.

Changes in respiration and heart rate were studied in rabbits which were exposed to high explosive shock waves in a detonation chamber after bilateral cervical vagotomy, or after pulmonary vagal denervation with the innervation of the sinoaortic region and heart left intact. The rapid shallow breathing occurring after the detonation in nondenervated animals was almost completely absent after cervical vagotomy or pulmonary vagal denervation. Sometimes an often very long period of apnea preceded the tachypnea after the detonation in the control animals. In the denervated animals, especially in the pulmonary vagally denervated ones, apnea was rare or of only very short duration. The bradycardia that can be prevented by bilateral cervical vagotomy, was not elicited by reflexes from the lungs, as the heart rate was lowered to the same extent in the lung vagus denervated as in the control animals. A cardiac standstill or severe distortions of the ECG waves during the first 1–3 seconds after the detonation were common in the nondenervated and in the lung vagus denervated animals but were rare in animals in which bilateral cervical vagotomy had been made.

THE NERVOUS CONTROL OF RESPIRATION IN KITTENS

ArticleTHE NERVOUS CONTROL OF RESPIRATION IN KITTENSHelen C. Coombs, and F. H. PikeHelen C. CoombsFrom the Department of Physiology, New York Homeopathic Medical College, and Columbia University, and F. H. PikeFrom the Department of Physiology, New York Homeopathic Medical College, and Columbia UniversityPublished Online:01 Dec 1930https://doi.org/10.1152/ajplegacy.1930.95.3.681MoreSectionsPDF (2 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByPostnatal development of right atrial injection of capsaicin-induced apneic response in ratsRurong Wang, and Fadi Xu1 July 2006 | Journal of Applied Physiology, Vol. 101, No. 1Hypoxemia and low Crs in vagally denervated lambs result from reduced lung volume and not pulmonary edemaSalim Lalani, John E. Remmers, Yolanda MacKinnon, Gordon T. Ford, and Shabih U. Hasan1 August 2002 | Journal of Applied Physiology, Vol. 93, No. 2Effects of vagal denervation on cardiorespiratory and behavioral responses in the newborn lambSalim Lalani, John E. Remmers, Francis H. Green, Ashfaq Bukhari, Gordon T. Ford, and Shabih U. Hasan1 November 2001 | Journal of Applied Physiology, Vol. 91, No. 5Pulmonary vagal innervation is required to establish adequate alveolar ventilation in the newborn lambKevin A. Wong, Ather Bano, Anita Rigaux, Bing Wang, Baikhunth Bharadwaj, Samuel Schürch, Francis Green, John E. Remmers, and Shabih U. Hasan1 September 1998 | Journal of Applied Physiology, Vol. 85, No. 3 More from this issue > Volume 95Issue 3December 1930Pages 681-693 Copyright & PermissionsCopyright © 1930 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1930.95.3.681History Received 20 September 1930 Published online 1 December 1930 Published in print 1 December 1930 Metrics