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Biomedical subjects

R L Owen

Publications and source records attributed to R L Owen.

At least 19 recordsLinked to original sources
PubMed1998

The infusion rate dependent influence of acute metabolic acidosis on pulmonary vascular resistance in broilers.

Experiments were conducted to evaluate the pulmonary vascular responses of lightly anesthetized clinically healthy male broilers during acute metabolic acidosis induced by bolus i.v. injections or constant i.v. infusions of HCl. In Experiment 1, broilers received consecutive 1.5 mL i.v. bolus injections of 2.5% mannitol (volume control) and 0.4 N, 0.8 N, and 1.2 N HCl in 2.5% mannitol. Following each injection, equivalent concentrations of mannitol or HCl were infused i.v. at a rate of 0.05 mL/min.kg BW. In Experiment 2, repeated bolus injections of 2.5% mannitol and 1.2 N HCl were administered during ongoing constant infusion of 2.5% mannitol. The following variables were evaluated: pulmonary arterial pressure, pulmonary vascular resistance, mean arterial pressure, total peripheral resistance, cardiac output, stroke volume, heart rate, respiratory rate, hematocrit (HCT), and arterial blood gas (PaO2, PaCO2, pH, HCO3-). Mannitol alone did not alter any of the variables. The HCl loading protocols acidified the arterial blood to sustained (constant infusion) or transient (bolus injection) values averaging between pH 7.2 and 7.3. In both experiments, bolus injections of 1.2 N HCl caused transient increases in pulmonary vascular resistance and pulmonary arterial pressure, coincident with decreases in mean arterial pressure and cardiac output. When HCl was infused at a constant rate in Experiment 1, the arterial blood hydrogen ion concentration, [H+], was positively correlated with pulmonary arterial pressure and cardiac output, negatively correlated with mean arterial pressure and total peripheral resistance, and was not correlated with pulmonary vascular resistance. During constant i.v. infusion of mannitol or HCl in both experiments, pulmonary arterial pressure was positively correlated with pulmonary vascular resistance and cardiac output. Overall, bolus injections of 1.2 N HCl consistently triggered transient pulmonary vasoconstriction (increased pulmonary vascular resistance), leading to a transient increase in pulmonary arterial pressure in spite of opposing changes in cardiac output and mean arterial pressure. In contrast, equivalent or greater increases in [H+] during constant i.v. infusion of HCl caused a substantially lower increment in pulmonary arterial pressure, which, in, turn was primarily attributable to increases in cardiac output rather than pulmonary vascular resistance. Increments in either pulmonary vascular resistance or cardiac output induced by metabolic acidosis would be expected to contribute to the onset of pulmonary hypertension syndrome (PHS, ascites) in broilers.

Acidosis↗
PubMed1998

Premature trypsinogen activation during cerulein pancreatitis in rats occurs inside pancreatic acinar cells.

Although it is widely accepted that trypsinogen activation is an initiating event in the development of acute pancreatitis, its location inside the pancreas is not known. In our studies, acute edematous pancreatitis was induced in rats by one or two intraperitoneal injections of 50 microg cerulein/kg body weight. The pancreas was removed for examination 1 or 2 h after the first and the second cerulein injection, respectively. The cleavage product of trypsinogen activation, trypsinogen activation peptide, was specifically labeled on pancreatic tissue sections by a corresponding antibody, the signal enhanced by a biotin-avidin conjugate, and the site then visualized by coupled peroxidase activity on diaminobenzidine. The sections were examined by light microscopy. Trypsinogen activation peptide, reflecting activation of the pancreatic digestive enzyme trypsinogen, was detected inside pancreatic acinar cells in this animal model of acute pancreatitis. As early as 1 h after the first injection of cerulein, protease activation was seen within the apical pole of acinar cells. Protease activation was increased 2 h after the latter of two injections of cerulein and more evenly distributed within the cells. For the first time morphologic evidence confirms that the activation originates within the acinar cell, rather than from the interstitium or the duct lumen. The location of this activation at the apical site of the acinar cell indicates its origin from subcellular compartments involving the late steps in the secretory pathway.

Animals↗
PubMed1998

Mid-life crisis for M cells.

The epithelium that lines the gut is impermeable to macromolecules and microorganisms, except in Peyer's patches (PP), where the lymphoid follicle-associated epithelium (FAE) contains M cells that transport antigens and microorganisms. A cultured system that reproduces the main characteristics of FAE and M cells was established by cultivation of PP lymphocytes with the differentiated human intestinal cell line Caco-2. Lymphocytes settled into the epithelial monolayer, inducing reorganization of the brush border and a temperature-dependent transport of particles and Vibrio cholerae. This model system could prove useful for intestinal physiology, vaccine research, and drug delivery studies.

Caco-2 Cells↗
PubMed1998

M cells as portals of entry for HIV.

Accumulating evidence points toward active uptake by mucosal antigen sampling cells as the mechanism for rectal HIV acquisition. Organized lymphoid tissue in the intestine consists of lymphoid follicles with an epithelium containing M cells specialized for uptake and transport of microorganisms, bringing them into contact with lymphoid cells. M cells have been found in the human colon and rectum, and adherence and uptake of HIV by M cells in mouse and rabbit Peyer's patches has been demonstrated in vitro. In an in vivo mouse model of viral acquisition, reovirus is actively taken up by M cells into rectal lymphoid tissue containing CD4 lymphocytes and macrophages, which are targets and replication sites for HIV. Immunization strategies for prevention of HIV transmission should include a mucosal component to prevent initial entry, since elimination from cellular sanctuaries remains an elusive goal.

Animals↗
PubMed1998

Small intestine pathogens in AIDS: conventional and opportunistic.

The small intestine, coming in direct contact with ingested potential pathogens, depends on active mucosal immunity to withstand invasion and damage. In patients with AIDS and severe impairment of immunoregulatory lymphocytes, proliferation of protozoal, viral, bacterial, and fungal pathogens produces diarrhea and malabsorption. When noninvasive tests of stool and blood fail to identify responsible organisms, endoscopy can reveal mucosal lesions which are suggestive if not diagnostic. Cryptosporidium, cf2E. intestinalis, cf1CMV, MAC, and other infections can be identified by intestinal biopsy quicker and often at lower overall cost than they can be by culture.

AIDS-Related Opportunistic Infections↗
PubMed1997

Chronic unilateral occlusion of an extrapulmonary primary bronchus induces pulmonary hypertension syndrome (ascites) in male and female broilers.

Previously, it was demonstrated that acute (4 min) and chronic (12 d) occlusion of an extrapulmonary primary bronchus triggers pulmonary hypertension but not pulmonary hypertension syndrome (PHS, ascites) in broilers. The present study was conducted to determine whether a more prolonged period of bronchus occlusion causes PHS similar to that induced by clamping one pulmonary artery. Male and female broiler chicks, 14 to 18 d old, were anesthetized, the thoracic inlet was opened, and a silver clip was positioned to fully obstruct the left extrapulmonary primary bronchus (BRONCHUS CLAMP group) or the left pulmonary artery (PA-CLAMP group). Sham-operated chicks were anesthetized and the thoracic inlet was opened; however, neither the pulmonary artery nor the bronchus was clamped (SHAM group). An electrocardiogram (ECG) was obtained whenever clinical ascites became apparent in individual broilers, or prior to the final necropsy for broilers surviving to the end (Day 36) of the experiment. The right:total ventricular weight ratio (RV:TV) was evaluated as an index of pulmonary arterial pressure. Early post-surgical mortality (up to 21 d of age) was higher in the PA-CLAMP group (27% for males and females combined) than in the BRONCHUS CLAMP (10%) and SHAM (2%) groups. Cumulative ascites mortality (Days 22 to 36) also was higher in the PA-CLAMP group (86% for males, 77% for females) than in the BRONCHUS CLAMP (69% for males, 41% for females) and SHAM (23% for males, 0% for females) groups. Ascitic birds in all treatment groups had higher RV:TV ratios and more negative ECG Lead II S-wave amplitudes than nonascitic birds, reflecting the right ventricular hypertrophy and generalized ventricular dilation typically associated with PHS. These results demonstrate that unilateral bronchus occlusion is an effective experimental model for triggering ascites at a lower incidence than that obtained by occluding one pulmonary artery. Following the onset of pulmonary hypertension, the pathophysiological progression leading to ascites appears to be similar for broilers with either unilateral bronchus or pulmonary artery occlusion.

Animals↗
PubMed1997

Mucosal abnormalities in microsporidiosis.

OBJECTIVE: To determine the prevalence of microsporidiosis in HIV-infected patients with and without diarrhoea and to characterize alterations in mucosal architecture and brush border enzyme activities in patients with microsporidiosis. PATIENTS: A total of 259 HIV-infected patients undergoing oesophago-gastroduodenoscopy because of diarrhoea (n = 123) or other symptoms (n = 136) were studied. METHODS: Patients were evaluated for the presence of microsporidia by electron microscopy of duodenal biopsies. Brush border enzyme activities were measured by histochemistry and mucosal architecture was determined by three-dimensional morphometry in biopsies from patients with microsporidiosis and compared with biopsies from a subgroup of HIV-infected patients with or without other enteropathogens. RESULTS: Enterocytozoon bieneusi was detected in 17 patients and Encephalitozoon intestinalis was detected in two patients. Microsporidiosis was significantly more frequent in patients with chronic diarrhoea (19.1%; P < 0.0001) or in patients with acute diarrhoea (7.2%; P = 0.04) than in patients without diarrhoea (1.5%). Microsporidiosis was associated with lactase deficiency (P = 0.03) and a reduced activity of alkaline phosphatase (P = 0.028) and alpha-glucosidase (P = 0.025) at the basal part of the villus compared with brush border enzymes in patients without enteropathogens. Patients with microsporidia had reduced villus height (P = 0.043) and a villus surface reduced by 40% (P = 0.004) compared with patients with enteropathogens other than microsporidia. CONCLUSIONS: Our study confirms the association between microsporidia and diarrhoea. The pathophysiologic mechanism by which microsporidia cause diarrhoea appears in part to be malabsorption, caused by a reduction of absorptive mucosal surface and impairment of enterocyte function.

AIDS-Related Opportunistic Infections↗
PubMed1996

Impact of aging on gastrointestinal mucosal immunity.

There is considerable evidence that the mucosal or secretory immune response in the gastrointestinal tract is compromised by aging. The generation of a mucosal immune response is an extremely complex process that involves antigenic stimulation of a specific subpopulation of immunologically competent cells in the Peyer's patches, differentiation and migration of these cells to the small intestinal lamina propria, initiation and regulation of local antibody production in the intestinal wall, and mucosal epithelial cell receptor-mediated transport of antibodies to the intestinal lumen. Available data suggest that gastrointestinal mucosal immunosenescence reflects deficits in: (1) the differentiation and/or migration (homing) of immunoglobulin A immunoblasts to the intestinal lamina propria, and (2) the initiation and/or regulation of local antibody production. The significant age-related increases in the incidence and severity of gastrointestinal infectious diseases, coupled with the potential for immunopharmacologic manipulation of the mucosal immune compartment, substantiate the merit of studies designed to resolve the etiology of mucosal immunodeficiency in the elderly.

Aging↗
PubMed1995

Immunochemical localization of type I VIP receptor and NK-1-type substance P receptor in rat lung.

Peptidergic nerves in the respiratory tract release vasoactive intestinal peptide (VIP) and substance P (SP), which mediate physiological and immune functions. Antipeptide antibodies to type I VIP receptor (VIPR) and NK-1-type SP receptor (SPR) were used to identify these receptors in normal rat lungs. VIPRs and SPRs were detected on airway epithelium from the trachea to the respiratory bronchioles but not in alveoli, submucosal glands, or pulmonary smooth muscle, except for that of some pulmonary veins. VIPRs also were expressed on macrophages around capillaries, in tracheal and bronchial connective tissue, in alveolar walls, and in the subintima of pulmonary veins and some arterioles. The absence of receptors from airway smooth muscle and submucosal glands implies that mediation of some known effects of SP and VIP may be epithelial or macrophage dependent. Other types of VIPRs and SPRs on airway glands and smooth muscle may transduce direct effects. The similar localization of VIPRs and SPRs in rat lung suggests that VIP and SP may coordinately regulate some pulmonary functions.

Animals↗
PubMed1995

Changes in pulmonary arterial and femoral arterial blood pressure upon acute exposure to hypobaric hypoxia in broiler chickens.

An experiment was conducted to investigate the pulmonary arterial and femoral arterial pressure responses to acute hypobaric hypoxia. Twenty-four, 7-wk-old Hubbard x Hubbard male chickens were lightly anesthetized and catheters were introduced into the right femoral artery and the pulmonary artery. The birds were then placed in a hypobaric chamber, and blood pressure responses were monitored during acute (15 min) exposures to simulated altitudes of 2,000 and 4,000 m. The pulmonary artery pressure increased .7 and 4% during the first and second exposures to a simulated altitude of 2,000 m, whereas the femoral artery pressure decreased 6 and 8% during exposures to this altitude. The pulmonary artery pressure increased 7% on the first exposure and 23% (P < .05) on the second exposure to a simulated altitude of 4,000 m. The femoral arterial pressure decreased (P < .05) on both exposures to this altitude (29 and 24%, respectively). The initial femoral and pulmonary artery pressures and changes in these pressures upon exposure to hypobaric hypoxia were not consistently correlated with the characteristics of the electrocardiogram, packed cell volume, body weight, or the right:total ventricular weight ratio. These results indicate that acute hypobaric hypoxia elicits a hypotensive response in the systemic arterial circulation and a hypertensive response in the pulmonary arterial circulation of broiler chickens.(ABSTRACT TRUNCATED AT 250 WORDS)

Altitude↗
PubMed1995

Growth of broiler chickens in response to feed restriction regimens to reduce ascites.

A trial was conducted to investigate the impact of early feed restriction on ascites induced by cold temperatures and the subsequent effect on the whole body and breast muscle growth of broilers. Two feed restriction regimens were tested, consisting of limiting daily feed intake of the birds to 75% of the ME required for normal growth from either 4 to 11 d or from 7 to 14 d. At 21 d, half of the birds were moved to a cold house (17.8 C) to induce ascites. Five birds from each pen were killed for the breast muscle growth, Pectoralis major and Pectoralis minor, and heart and abdominal fat pad weights at 4, 7, 11, 14, 21, 35, and 49 d of the experiment. Birds in the cold house were heavier and had better feed conversion than birds in the control house at 49 d of age. This could be attributed to the high ambient temperatures (27 to 33 C) in the control house. The ad libitum birds had a significantly greater percentage of P. major than the feed-restricted birds. Exposure to cold temperatures caused significantly higher percentage of ascites from 21 to 49 d. Cold temperatures also increased the percentage of total heart and the right ventricle weight relative to total heart weight ratio at 35 and 49 d of age, suggesting that the surviving birds were more likely to develop ascites. Although catch-up growth was observed, the final body weight of feed-restricted birds was not the same as ad libitum birds. Early feed restriction reduced the incidence of ascites, but at the cost of breast muscle growth.

Age Factors↗
PubMed1994

Immunohistochemical localization of peptidergic nerve fibers and neuropeptide receptors in Peyer's patches of the cat ileum.

This study examined the distribution of peptidergic nerve fibers in Peyer's patches to determine whether appropriate receptors were present. Vasoactive intestinal peptide (VIP), substance P (SP), calcitonin gene-related peptide (CGRP) and receptors for VIP and SP were localized in lymphoid follicles of the cat ileum using a combined indirect horseradish peroxidase and streptavidin-biotin method. The margins of follicles were innervated by nerve fibers containing VIP, SP and CGRP. Nerve fibers were predominantly around lymphatics and high endothelial venules at the edges of follicles. Specific receptors for VIP and SP were present at the margins of follicles and in the lamina propria around crypts. VIP receptors were numerous on T cells within and around high endothelial venules and lymphatic vessels and at the margins of follicles. SP receptors were identified on a small number of T and B cells, granulocytes and macrophages, restricted to the margins of follicles. The defined distribution in ileal lymphoid tissue of nerve fibers containing VIP and SP and the corresponding localization of their appropriate receptors support immunoregulatory roles for neuropeptides in mucosal immunity.

Animals↗