The Effects of Vagotomy on the Abomasum in Calves: Radiography and Protein Gene Product 9.5 Immunohistochemistry.

Abstract

ABSTRACT. 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. KEY WORDS: abomasal disorder, PGP 9.5, vagotomy.J. Vet. Med. Sci. 63(6): 671-674, 2001 Gastric motility is greatly influenced by the vagus nerves whose activity is integrated by gastric centers in the medulla oblongata [6,18]. This innervation is of much greater importance in ruminants than in other species [11]. Since the abomasum retains considerable activity after vagotomy, the importance of its innervation contrasts markedly with that of the forestomach [5]. In the milk-fed calf, the abomasum has a more important role in digestion than the still undeveloped forestomach. The vagus may control abomasal motility through its innervation of the tunica muscularis. Mechanical malfunction of the abomasum in cattle might involve the disorder of vagal innervation through the dorsal and ventral vagal nerves which ramify to the abomasum [2]. Although a vagal nervous dysfunction has been suggested as a possible cause of abomasal disorders [16], vagal nerve injury in the abomasal wall is still uncertain. The distribution of vagal nerve endings in the sheep stomach has been reported after short-term vagotomy [15], however, the long-term effects of vagotomy on the mural innervation of the ruminant stomach have not been described.Radiographic studies of the abomasum of lambs and calves before and after vagotomy were mostly undertaken during motility [17] and abomasal emptying [1]. The former was a short-term investigation while the latter maintained the calf after vagotomy by cannulation feeding into the abomasum. The radiography of the long-term effects of vagotomy on the abomasum maintained with normal feeding has not yet been reported. Furthermore, radiographic findings on the functional state of the abomasum have not yet been compared with the histology of the regulatory systems in the abomasal wall.Protein gene product 9.5 (PGP) is a neuronal soluble protein distributed in the central and peripheral nervous systems of different animals [14,20]. It is useful as a general immunohistochemical marker for nervous elements and for the assessment of neuronal development and the detection of neuronal damage in diseases of the nervo...

A Mechanism of Excessive Accumulation of Abomasal Gas in Vagotomized Cattle Determined using Fluoroscopy

“…[17,24,27,28], and nitroxidergic and vasoactive intestinal peptide-containing nerves in the muscular layer of the abomasum [9,21]. However, none of these factors have been established by experimental work, and the exact mechanism of displacement remains largely unknown.Two pathogenic factors are crucial for the development of DA: abomasal atony with hypomotility is the essential prerequisite [5,8,24], while excessive accumulation of abomasal gas is the absolute requirement [25]. As for the former requirement, Soehartono et al [24] have proposed that decreased intramural innervation of the abomasum due to vagal nerve injury is one of the etiological factors in abomasal atony with hypomotility, based on the radiographic and immunohistochemical findings in calves that underwent total thoraco-vagotomy.…”

“…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. [17,24,27,28], and nitroxidergic and vasoactive intestinal peptide-containing nerves in the muscular layer of the abomasum [9,21]. However, none of these factors have been established by experimental work, and the exact mechanism of displacement remains largely unknown.…”

“…Two pathogenic factors are crucial for the development of DA: abomasal atony with hypomotility is the essential prerequisite [5,8,24], while excessive accumulation of abomasal gas is the absolute requirement [25]. As for the former requirement, Soehartono et al [24] have proposed that decreased intramural innervation of the abomasum due to vagal nerve injury is one of the etiological factors in abomasal atony with hypomotility, based on the radiographic and immunohistochemical findings in calves that underwent total thoraco-vagotomy.…”

“…Its etiology is multifactorial [7], reportedly involving increased levels of volatile fatty acids in the rumen and abomasum [26], hypocalcemia [4,16,20,22], negative energy balance [13 23], metabolic alkalosis [19], prostaglandins [3], vagus nerve injury [17,24,27,28], and nitroxidergic and vasoactive intestinal peptide-containing nerves in the muscular layer of the abomasum [9,21]. However, none of these factors have been established by experimental work, and the exact mechanism of displacement remains largely unknown.…”

“…As for the former requirement, Soehartono et al [24] have proposed that decreased intramural innervation of the abomasum due to vagal nerve injury is one of the etiological factors in abomasal atony with hypomotility, based on the radiographic and immunohistochemical findings in calves that underwent total thoraco-vagotomy. On the other hand, no study has reported the mechanism of abomasal gas accumulation to date.…”