Fibres In Dogs Research Articles

Vasoactive Intestinal Polypeptide (VIP) in the Intestinal Mucosal Nerve Fibers in Dogs with Inflammatory Bowel Disease.

Simple SummaryCanine inflammatory bowel disease (IBD)—a group of gastrointestinal disorders—is a serious problem in veterinary medicine. The etiology of IBD remains unknown, and its diagnosis and effective treatment are difficult. One of the less-known aspects of IBD pathology is the influence of this disease on the enteric nervous system, which is located in the intestinal wall and regulates most of the gastrointestinal functions. Therefore, the aim of the present study was to evaluate the influence of IBD on the intramucosal nerve fibers containing vasoactive intestinal polypeptide (VIP). VIP is one of the most important substances produced by the enteric nervous structures that is involved in many regulatory processes in the gastrointestinal tract. The obtained results show that IBD induces changes in the density of intramucosal VIP-positive nerve fibers in the canine gastrointestinal tract. It suggests that VIP is involved in the pathological processes occurring during this disease. Observed changes may be a result of neuroprotective and/or adaptive processes regulated by VIP, aimed at the homeostasis maintenance in the inflamed gastrointestinal (GI) tract and induced by proinflammatory factors.Canine inflammatory bowel disease (IBD) is a group of enteropathies with nonspecific chronic symptoms and poorly understood etiology. Many aspects connected with IBD are not understood. One of them is the participation of the intestinal nervous system in the development of pathological processes. Thus, this study aimed to demonstrate changes in the density of intramucosal nerve fibers containing vasoactive intestinal polypeptide (VIP)—one of the most important intestinal nervous factors caused by the various stages of IBD development. Mucosal biopsy specimens collected from the duodenum, jejunum and descending colon of healthy dogs and dogs with varied severity of IBD were included in the experiment. The density of VIP-like immunoreactive (VIP-LI) nerves was determined by a single immunofluorescence technique and a semi-quantitative method consisting in VIP-LI fiber counts in the field of view (0.1 mm2). The obtained results indicate that IBD induces changes in the density of mucosal VIP-LI nerve fibers in the canine gastrointestinal tract. The initial decrease is followed by an increase in VIP-like immunoreactivity in successive stages of the disease. These observations show that VIP is a neuronal factor that participates in the pathological processes connected with canine IBD. The observed changes probably result from the neuroprotective and/or adaptive properties of VIP. Protective and adaptive reactions induced by inflammation aim to protect the GI tract against damage by proinflammatory factors and ensure the homeostasis in the enteric nervous system (ENS) under the conditions changed by the disease process.

Immunohistochemical analysis of canine and feline muscle disorders using formalin-fixed, paraffin-embedded tissues.

Histochemical techniques used in examination of muscle biopsies typically require frozen sections. Given that most of the specimens submitted to a veterinary laboratory for diagnosis are formalin-fixed, the choice of staining methods is limited. We aimed to further advance the diagnostic capabilities of pathologists presented with formalin-fixed muscle samples and to describe the differences in immunohistopathologic findings between neurogenic and myogenic muscle disorders. Based on hematoxylin and eosin staining, we defined in dogs the histologic lesions in 4 neurogenic disorders (degenerative myelopathy and polyneuropathy) and 2 myogenic disorders (dystrophin-deficient muscular dystrophy). In cats, we defined the lesions in 2 neurogenic disorders (lymphoma of nerve roots and spinal cords) and 1 myogenic disorder (laminin α2-deficient muscular dystrophy). Immunohistochemistry for slow and fast myosins revealed angular and group atrophy of type 1 and type 2 fibers in dogs and cats, and fiber type grouping in dogs. These immunohistopathologic findings were specific to neurogenic muscle disorders. Immunohistochemistry for nestin and myogenin revealed nestin-positive fibers and myogenin-positive nuclei in dogs and cats. They were not specific, but these fibers in myogenic disorders can be interpreted as regenerating fibers. The immunohistochemical method described herein appears to be useful for discriminating neurogenic and myogenic disorders in formalin-fixed, paraffin-embedded muscle tissue of dogs and cats.

Fermentable soluble fibres spare amino acids in healthy dogs fed a low-protein diet.

BackgroundResearch in cats has shown that increased fermentation-derived propionic acid and its metabolites can be used as alternative substrates for gluconeogenesis, thus sparing amino acids for other purposes. This amino acid sparing effect could be of particular interest in patients with kidney or liver disease, where this could reduce the kidneys’/liver’s burden of N-waste removal. Since dogs are known to have a different metabolism than the obligatory carnivorous cat, the main objective of this study was to assess the possibility of altering amino acid metabolism through intestinal fermentation in healthy dogs. This was studied by supplementing a low-protein diet with fermentable fibres, hereby providing an initial model for future studies in dogs suffering from renal/liver disease.ResultsEight healthy dogs were randomly assigned to one of two treatment groups: sugar beet pulp and guar gum mix (SF: soluble fibre, estimated to mainly stimulate propionic acid production) or cellulose (IF: insoluble fibre). Treatments were incorporated into a low-protein (17 %) extruded dry diet in amounts to obtain similar total dietary fibre (TDF) contents for both diets (9.4 % and 8.2 % for the SF and IF diet, respectively) and were tested in a 4-week crossover feeding trial. Apparent faecal nitrogen digestibility and post-prandial fermentation metabolites in faeces and plasma were evaluated. Dogs fed the SF diet showed significantly higher faecal excretion of acetic and propionic acid, resulting in a higher total SCFA excretion compared to IF. SF affected the three to six-hour postprandial plasma acylcarnitine profile by significantly increasing AUC of acetyl-, propionyl-, butyryl- + isobutyryl-, 3-OH-butyryl-, 3-OH-isovaleryl- and malonyl-L-carnitine. Moreover, the amino acid plasma profile at that time was modified as leucine + isoleucine concentrations were significantly increased by SF, and a similar trend for phenylalanine and tyrosine’s AUC was found.ConclusionThese results indicate that guar gum and sugar beet pulp supplementation diminishes postprandial use of amino acids favoring instead the use of short-chain fatty acids as substrate for the tricarboxylic acid (TCA) cycle. Further research is warranted to investigate the amino acid sparing effect of fermentable fibres in dogs with kidney/liver disease.

Structural arrangement of the cardiac collagen fibers of healthy and diabetic dogs

The heart is composed by a specialized muscle, whose form and function are essentials for an adequate work and shows an amount of connective tissue which support and provide insertion for this muscle, whose collagen fibers are responsible for determination of tissue feature. Our objective was to identify the structural arrangement of the heart collagen fibers in dogs. The hearts of the dogs were submitted to the process of the controlled digestion with NaOH solution and observed by scanning electron microscope. Our results showed that the collagen fibers of the endomysial wall have structural arrangement composed by an irregular network with one layer in normal dogs but in diabetic dogs the network acquires a greater amount of the fibers and layers, looking like a "rug" of fibers modifying the relationships of the stress/strain of the tissue. Ahead of the observed results we are able to conclude that exist increase in the amount and thickness of cardiac collagen fibers, beyond the increase of layers and architectural disarrangement in the endomysial wall in the diabetic dogs.

Assessment of impulse duration thresholds for electrical stimulation of muscles (chronaxy) in dogs

To determine the electrical impulse duration thresholds (chronaxy) for maximal motor contraction of various muscles without stimulation of pain fibers in dogs. 10 healthy adult Beagles. The dogs were used to assess the minimal intensity (rheobase) required to elicit motor contraction of 11 muscles (5 in the forelimb [supraspinatus, infraspinatus, deltoideus, lateral head of the triceps brachii, and extensor carpi radialis], 5 in the hind limb [gluteus medius, biceps femoris, semitendinosus, vastus lateralis, and tibialis cranialis], and the erector spinae). The rheobase was used to determine the chronaxy for each of the 11 muscles in the 10 dogs; chronaxy values were compared with those reported for the corresponding muscles in humans. Compared with values in humans, chronaxy values for stimulation of AA motor fibers in the biceps femoris and semitendinosus muscles and muscles of the more distal portions of limbs were lower in dogs. For the other muscles evaluated, chronaxy values did not differ between dogs and humans. Application of the dog-specific chronaxy values when performing electrical stimulation for strengthening muscles or providing pain relief is likely to minimize the pain perceived during treatment in dogs.

Detection of attenuated wavy fibers in the myocardium of Newfoundlands without clinical or echocardiographic evidence of heart disease.

To determine whether attenuated wavy fibers may be found in the myocardium of Newfoundlands without clinical or echocardiographic evidence of heart disease. 15 Newfoundlands from a kennel with a known predisposition to dilated cardiomyopathy (DCM) and 32 dogs of other breeds that died suddenly or were euthanatized for reasons unrelated to heart disease and did not have gross postmortem evidence of heart disease. Echocardiography was performed on all Newfoundlands on a yearly basis. Necropsy specimens from all dogs were evaluated for attenuated wavy fibers (i.e., myocardial cells <6 microm in diameter with a wavy appearance). None of the Newfoundlands had clinical signs of heart disease, and results of echocardiographic examinations were within reference ranges. Seven Newfoundlands had histologic evidence of attenuated wavy fibers, whereas attenuated wavy fibers were not found in the remaining 8 Newfoundlands or in any of the 32 dogs of other breeds. Findings suggest that attenuated wavy fibers in dogs with a known predisposition for DCM may indicate an early stage of the disease. However, further studies on a larger number of dogs are needed to confirm this hypothesis.

Metabolites of 5-fluorouracil, alpha-fluoro-beta-alanine and fluoroacetic acid, directly injure myelinated fibers in tissue culture.

The neurotoxicity of two 5-fluorouracil (5-FU) derivatives, tegafur (FT) and carmofur (HCFU), which selectively induce leukoencephalopathy involving the cerebral white matter in humans and vacuolation of myelinated fibers in dogs and cats, was examined in vitro. The common metabolites of these drugs, alpha-fluoro-beta-alanine (FBAL) and fluoroacetic acid (FA), were added to the medium of cultured murine cerebellar myelinated fibers. On day 1 of exposure to 7 microM FBAL and FA, which corresponds to their blood concentrations 2 h after oral administration of 10 mg.kg-1 HCFU to dogs that induced central nervous system vacuolation after 30 days, partial splits of the myelinic intraperiod line were observed by electron microscopy. On days 4-7, phase contrast microscopy revealed spindle-shaped swelling and granulation of myelin and electron microscopy demonstrated prominent dissociation of the myelinic intraperiod line with monolocular and multilocular vacuolation. More severe changes, such as myelin loss, were found in cultures exposed to a higher concentration (70 microM) of FBAL and FA, but no remarkable neuronal, astrocytic or oligodendrocytic changes occurred. Quantitative evaluation of myelin injury by electron microscopy revealed significant toxicity of FBAL and FA, at concentrations of 7 and 70 microM, on day 4. However, groups treated with 0.7 microM FBAL and FA, 5-FU (7 microM) and controls exposed to beta-alanine and acetic acid concentrations of 0.7, 7 and 70 microM showed no marked injury. We concluded that these anticancer drug metabolites injure myelin fibers directly, resulting in vacuolation due to myelin splitting and destruction.

Distribution and appearance of elastic fibers in the dermis of clinically normal dogs and dogs with solar dermatitis and other dermatoses

Abstract Objective To determine the distribution and amount of elastic fibers in the dermis of clinically normal dogs and dogs with dermatoses, particularly solar dermatitis. Design Skin specimens from 7 anatomic sites were obtained from 19 clinically normal dogs after euthanasia to evaluate the normal distribution o elastic fibers. Biopsy specimens also were obtained from 34 dogs with dermatoses, including 16 with solar dermatitis. Tissue sections were stained with H&amp;E, Verhoeff-van Gieson, and periodic acid-Schiff. Animals 19 clinically normal dogs and 34 dogs with dermatoses. Procedure Numbers of elastic fibers were graded subjectively. Comparisons between clinically normal dogs and dogs with dermatoses were made. Results Normal elastic fibers were present in low numbers in the dermis of adult dogs, regardless of anatomic site or presence or severity of dermatitis. Condensed elastotic material was visualized in only 2 dogs with solar dermatitis. In both dogs, the elastotic material was Verhoeff-van Gieson and periodic acid-Schiff stain positive but was not visible with H&amp;E stain. The most frequent histopathologic finding in the dermis of dogs with solar dermatitis was superficial dermal fibrosis. Conclusions The dermis of clinically normal dogs does not contain abundant elastic fibers. Alterations of elastic fibers in dogs with solar dermatitis are rare. Superficial dermal fibrosis may be a better indicator of solar damage.

A cytochemical method for the identification of ischemic and necrotic myocardial fibres.

The author studied the nickel-dimethylglioxim reaction in ischemic and necrotic myocardium fibres in dogs, following ligature of the left anterior descending coronary artery. The nickel-dimethylglioxim reaction was positive in ischemic fibers, but not in necrotic ones. The cytochemical reaction, observed in ischemic fibers, was localized in the intracellular compartment and in the mitochondria.

Reflex coronary vasodilation evoked by chemical stimulation of cardiac afferent vagal C fibres in dogs.

1. Veratridine injected into the coronary circulation stimulates afferent vagal endings in the heart to evoke bradycardia and systemic hypotension (Bezold-Jarisch reflex, coronary chemoreflex) and coronary vasodilation. We have examined certain features of the reflex coronary vasodilator response in anaesthetized dogs. 2. When the circumflex coronary artery was perfused at constant pressure (100 mmHg), injection of veratridine (0.3 micrograms kg-1) into the anterior descending artery decreased blood pressure and heart rate, and increased circumflex blood flow by 54%; when heart rate was kept constant, circumflex flow increased by 57%. The increase in circumflex flow was reduced 63% by atropine, and finally abolished by phentolamine. 3. During severe coronary underperfusion (perfusion pressure 45 mmHg), veratridine still increased coronary flow by 35%, an increase amounting to 24-64% of the coronary vascular reserve. Flow increased in all layers of the myocardium, but the relative distribution of flow between subendocardial and subepicardial layers was unaltered. 4. Veratridine stimulates both mechanosensitive and chemosensitive cardiac endings. Stimulating chemosensitive afferents selectively by injecting capsaicin (1.5 micrograms kg-1) into the anterior descending artery decreased blood pressure and heart rate, and increased circumflex flow by 50% (and by 36% when heart rate was kept constant). 5. In ten of fifteen dogs, veratridine and capsaicin still evoked coronary vasodilatation when vagal A fibres were blocked selectively by cooling to 7.5 degrees C, the increase in coronary flow averaging 45% of that at 37 degrees C. All responses were abolished by cooling to 0 degrees C. 6. We conclude that coronary vasodilatation can be evoked by selective stimulation of cardiac chemosensitive vagal C fibres, although the coronary vasodilation of the veratridine-induced Bezold-Jarisch reflex may be due to stimulation of both mechanosensitive and chemosensitive C fibres. We speculate that during periods of coronary underperfusion ischaemic stimulation of chemosensitive vagal C fibres evokes a reflex dilatation of the coronary vascular bed that supplements the dilatation dependent upon autoregulatory mechanisms.

Discharges of bulbar respiratory neurons during rhythmic straining evoked by activation of pelvic afferent fibers in dogs

Each cycle of rhythmic straining evoked through the reflex center in th Kölliker-Fuse nucleus by stimulation of pelvic afferents in decerebrate dogs usually began in early expiration. During the rhythmic straining cycle, postinspiratory discharges of the phrenic nerve increased simultaneously with a burst of discharges of the nerves innervating the rectus abdominis and adductors of the glottis. While about half of the bulbar expiratory units discharged concurrently with the rhythmic straining, almost none of the inspiratory units examined did so. Nearly all expiratory bulbospinal units discharged concurrently, but none of the inspiratory bulbospinal units did so. These results show that expiratory neurons in the caudal bulb relay commands for rhythmic straining from the pontine reflex center to motor neurons of expiratory muscles, but that bulbar inspiratory neurons do not relay the commands to inspiratory motor neurons. Discharges concurrent with rhythmic straining were also evoked in all 4 postinspiratory units of the ventral group. 3 every early onset expiratory units and all 9 inspiratory-expiratory units of the dorsal group. Possible roles played by these respiratory neurons in the organization of rhythmic straining were discussed.

Rapid shallow breathing evoked by selective stimulation of airway C fibres in dogs.

1. We have examined the reflex changes in breathing evoked in anaesthetized dogs by stimulation of the afferent vagal C fibres that supply the intrapulmonary and lower extrapulmonary airways. We stimulated bronchial (intrapulmonary) C fibres selectively by injecting bradykinin into the right bronchial artery (the chest had been opened briefly for insertion of a bronchial arterial catheter).2. Bronchial arterial injection of bradykinin (0.15-1.5 mug in 3-6 sec) usually caused a brief bout of rapid shallow breathing, which was sometimes preceded by apnoea. Infusion of bradykinin (0.2-2.0 mug min(-1) for 2-12 min) caused prolonged rapid shallow breathing, the breathing frequency (f) increasing by 19-102% and tidal volume (V(T)) decreasing by 13-87%; end-tidal P(CO2) decreased by 2-9 mmHg in several experiments. Rapid shallow breathing was also evoked by administration of bradykinin aerosol through a lower tracheal cannula.3. Cutting the vagus nerves or cooling them to 0 degrees C abolished the prolonged rapid shallow breathing evoked by bradykinin, but intermittent disturbances of breathing could still be elicited in some dogs. These residual effects often consisted of irregular spasmodic inspirations, which were abolished by avulsion of the right upper thoracic sympathetic chain.4. Rapid shallow breathing was accompanied by contraction of airway smooth muscle in an innervated segment of the upper trachea; contraction was abolished by cutting or cooling the vagus nerves.5. Arterial blood pressure often decreased briefly when bradykinin was injected into the bronchial artery; changes in pressure were smaller and less frequent when bradykinin was infused slowly, and pressure was usually unaltered when bradykinin was administered as an aerosol. Rapid shallow breathing occurred whether pressure decreased, increased or was unchanged. A number of other observations indicated that the changes in breathing were independent of the changes in blood pressure. Changes in heart rate were complex and appeared to result from the interplay of several reflexes. Marked cardiac slowing was evoked by bradykinin aerosol.6. Bradykinin injected into a bronchial artery is known to stimulate bronchial (intrapulmonary) C fibres. Results of recording afferent vagal impulses in the present study indicated that bradykinin administered as an aerosol stimulated bronchial C fibres and also C fibres with endings in the lower trachea and extrapulmonary bronchi. Irritant and pulmonary stretch receptors were not stimulated unless aerosols were administered repeatedly and in higher concentration. Hence airway C fibres appeared to be responsible for the reflex effects of bradykinin aerosol.7. Bronchial C fibres are stimulated by substances (bradykinin, prostaglandins and histamine) known to be released by the lungs and airways in a variety of pathophysiological circumstances. Results of this and previous studies are compatible with the hypothesis that stimulation of bronchial C fibres plays a major role in evoking the rapid shallow breathing, bronchoconstriction and increased secretion by airway submucosal glands that are part of the pulmonary defence response.

Interaction between mianserin and clonidine at ? 2-Adrenoceptors

The purpose of the present study was to characterize the effects of mianserin at alpha 2-adrenoceptors. Firstly, the action of mianserin on postganglionic sympathetic fibres has been studied using the tachycardia induced by stimulation of the cardiac nerve in dogs. Mianserin increased this tachycardia, but could not prevent the inhibitory effect of clonidine in this model. However, an antagonistic effect of mianserin against clonidine was observed when animals were pretreated with desipramine. Secondly, mianserin antagonized the inhibitory effect of clonidine on the electrically stimulated guinea-pig ileum. In high concentrations, mianserin reduced both electrically and acetylcholine induced contractions. Thirdly, mianserin antagonised the sleep induced by clonidine in chickens. These results are consistent with alpha 2-adrenoceptor blocking properties of mianserin in peripheral noradrenergic fibres in dogs, in cholinergic fibres in guinea-pig ileum and in the central nervous system in chickens.

Fiber orientation in hypertrophied canine left ventricle

Myocardial fiber orientation was examined in transmural specimens obtained at the maximum diameter of the left ventricle from five dogs with pressure-overload hypertrophy produced by aortic stenosis, six dogs with volume-overload hypertrophy due to an arteriovenous fistula, and six exercise-hypertrophied greyhounds trained for racing. Hearts arrested in diastole were fixed in situ while the operating end-diastolic pressure was maintained. Fiber orientation changed smoothly from about +60 degrees (with respect to the equator) at the endocardium to about -69 degrees at the epicardium. The majority of fibers near the midwall were oriented circumferentially. These findings are quite similar to those previously reported for normal dogs. In comparison to normals, the left ventricles from dogs with pressure-overload had an increase in longitudinally oriented fibers, i.e. fiber angles between -67.5 degrees and -90 degrees and between +67.5 degrees and +90 degrees; these fibers comprised 10.4 +/- 1.8% of the total fibers in dogs with aortic stenosis vs. 2.9 +/- 1.8% of total fibers in normal dogs (P less than 0.001). Neither the dogs with volume-overload hypertrophy nor exercise-trained animals were significantly different from normals.

Spinal root pathway of the adrenal medullary secretory nerve fibers in the dog.

In dogs anesthetized with sodium pentobarbital, adrenal venous blood was collected and analyzed for adrenaline and noradrenaline fluorometrically. Electrical stimulation of the ventral spinal root from the fifth thoracic (T5) to the first lumbar (L1) segments produced a significant increase in adrenal medullary secretion. On the contrary, stimulation of the dorsal spinal root had no effect on adrenal medullary secretion. Unilateral section of the ventral spinal roots from T5 to L1 abolished an increased adrenal medullary secretion of the ipsilateral adrenal gland in response to insulin-induced hypoglycemia. Section of the dorsal spinal roots had no effect. It is concluded that the adrenal medullary secretory nerve fibers in dogs pass through the ventral spinal roots at the levels of T5-L1.