Gerentological studies on the gross and histomorphology of the vesicular gland of gaddi goat (Copra hircus) / Estudios gerontológicos en anatomía e histomorfología de la glándula vesicular de cabra gaddi (Cabra hircus)

The study was conducted on the vesicular glands of 30 entire pure male Gaddi goats from birth to 5yrs and 6 months of age, divided into three equal size groups of 10 animals in each viz; Pre-pubertal (lday old to <18 months of age), Pubertal (18 months to < 5years of age) and Post-pubertal (>5 years) age groups. In new born kid the glands were small, white cord like. It became "?" shaped at 6 months and "S" shaped at 12 months of age. A significant growth in size and weight of gland occurred at 6 month, then up to 12 month and beyond it grew slowly. The secretory acini of the lobules were lined by pseudostratified ciliated columnar epithelium which contained A-tall columnar, B-basal and C-narrow columnar type of cells. The number per unit area and size of the gland increased with age significantly from birth in the prepubertal animals and up to puberty. In post-pubertal animals it did not grow significantly, rather the connective tissue elements were increased in the capsule (adventitia). The intralobular connective tissue however, decreased at the expense of growth of acini at all ages.

Se realizó un estudio de las glándulas vesiculares de 30 cabras Gaddi, macho, totalmente puras desde el nacimiento hasta los 5 años y 6 meses de edad, divididas en tres grupos de 10 animales cada uno, pre-puberal (día 1 de edad a <18 meses de edad), pubertad (18 meses a <5 años de edad) y post-puberal (> 5 años). En el recién nacido las glándulas eran pequeñas, como un cordón blanco. Se presentó en forma de "?" a los 6 meses y de "S" a los 12 meses de edad. Un importante crecimiento en tamaño y peso de la glándula se produjo a los 6 meses, luego de 12 meses y más, creció lentamente. Los acinos secretores de los lóbulos se alinearon como epitelio columnar ciliado pseudoestratificado, los cuales contienen células de tipo A-columnar alto, B-basal y C-columnar estrecho. El número por unidad de área y el tamaño de la glándula aumentó significativamente con la edad desde su nacimiento en los animales prepuberes y hasta la pubertad. En animales post-puberales no creció significativamente, y los elementos del tejido conectivo se incrementaron en la cápsula (adventicia). Sin embargo, el tejido conectivo intralobular, disminuyó a expensas del crecimiento de los acinos, en todas las edades.

Gallbladder neuron count in cholelithiasis patients with and without Chagas disease

Various investigators agree that the incidence of cholelithiasis is greater in patients with Chagas disease. The most plausible explanation for this is based on the parasympathetic denervation that occurs over the whole digestive tract due to Chagas disease. In order to analyze the occurrence of this alteration, gallbladder neuron counts were performed on cholelithiasis patients with and without Chagas disease who were being treated at the Department of Digestive Surgery, Universidade Federal do Triângulo Mineiro, Uberaba, Brazil. In the present study, a notable reduction in the number of neurons in the gallbladder wall was observed in Chagas patients, in comparison with non-Chagas subjects.

Vários autores concordam que a incidência de colelitíase encontra-se elevada nos pacientes portadores de doença de Chagas. A explicação mais plausível para este fato baseia-se na desnervação parassimpática existente em todo o tubo digestivo na doença de Chagas. No intuito de analisar a ocorrência desta alteração, foi realizada contagem neuronal da vesícula biliar de pacientes chagásicos e não chagásicos, portadores de colelitíase, tratados na Disciplina de Cirurgia do Aparelho Digestivo, Universidade Federal do Triângulo Mineiro, Uberaba, Brasil. No presente estudo, observou-se uma redução expressiva do número de neurônios na parede da vesícula biliar dos pacientes chagásicos quando comparado com os não chagásicos.

Diabetic autonomic neuropathy causing gall bladder dysfunction.

OBJECTIVE: The objective of the study was to study gall bladder volume in fasting and 45 minutes post-prandial, by real time ultrasound in healthy controls and diabetic patients with and without autonomic neuropathy and to compare them. METHOD: Age, Sex and body mass index (BMI) matched 50 healthy subjects and 10 patients with insulin dependent diabetes mellitus and 40 patients with noninsulin dependent diabetes mellitus were evaluated according to National diabetes Data Group of National Institute of Health (1979) criteria: 1. Fasting (overnight) venous plasma glucose concentration of > 140 mg/dl on two separate occasions. 2. Following ingestion of 75 gms of glucose, venous plasma glucose concentration of > 200 mg/dl at second hour and at one other occasion during two hour test. Autonomic neuropathy was assessed by the presence of symptoms like dysphagia, abdominal fullness, nausea, vomiting, diarrhea +/- nocturnal, faecal incontinence or constipation, dysuria, urinary incontinence, the gustatory sweating, impotence etc. and were confirmed by standing test for orthostatic hypotension, hand grip test, Valsalva test and deep breaths test. RESULT: The study showed that: 1. Patients of diabetes mellitus had statistically significant larger fasting gall bladder volumes and these values were highly significant amongst patients with autonomic neuropathy. 2. Patients of diabetes mellitus and statistically significant larger post fatty meal gall bladder volume and these values were highly significant in patients with autonomic neuropathy. CONCLUSIONS: We therefore conclude that impaired gall bladder contraction was found amongst patients of diabetes mellitus with autonomic neuropathy. The mechanism responsible for cholecystoparesis is attributed to vagal neuropathy. Incomplete gall bladder emptying leads to sequestration of cholesterol and nidus formation. Therefore gall bladder functions should be evaluated routinely in such patients and early intervention is recommended.

physiology of the biliary tree motility of the gallbl bladder-part 1

An incomplete picture has emerged of the complex means by which gallbladder motility is controlled under normal and pathophysiological conditions. In the first part of this review an overall account is presented. The mechanisms of cholecystokinin release, its stimulation by dietary factors and peptides elaborated by both pancreas and small intestine are discussed. The inhibition of cholecystokinin release by bile acids and proteases is also described. In the second part attention is focussed on other peptides affecting motility. These include [a] octreotide, effective for treatment of acromegaly, [b] peptide YY, contributing to a "colonic brake", [c] motilin, associated with interdigestive contractions, analogues of which possibly correct gallbaldder hypomotility, and d] substance P and calcitonin gene- related peptide, which facilitate ganglionic transmission after release from exrinsic sensory neurones and alter gallbladder responses to vagal stimulation. The sympathetic nervous system and diabetes mellitus also influence vagal responses. The former, acting presynaptically, may provide a "brake" to prevent vagal overactivity. The latter could cause hypomotility via autonomic neuropathy, although hyperglycaemia, itself, may play a role. The role of nitric oxide, released from neurones also producing vasoactive intestinal peptide is recognized. Both lengthen muscle, the former producing responses without requiring plasma membrane receptors. Gallbaldder motility also changes during pregnancy and stone formation. Progesterone and cholesterol can limit G protein actions, thus impairing contractions. Inflammation is associated with abnormal motility. The production of reactive Oxygen metabolites, acting directly or releasing prokinetic prostaglandins, may be responsible. It has been proposed that the gastrointestinal tract may be normally in a state of controlled inflamation, primed to react to harmful challenges