Search PubMed⌕ Search
Home/Archive/PubMed

PubMed · 10489931

Inflammation does not decrease intraluminal pH in chronic inflammatory bowel disease.

K Ewe·S Schwartz·S Petersen·A G Press
View original source ↗Export metadata ↓

Abstract

Intestinal inflammation may influence intraluminal pH. Profiles of the gastrointestinal pH were evaluated in 15 patients with active Crohn's disease of the ileocecal area. In addition, five patients with moderate (1) or severe (4) ulcerative colitis were studied. Fifteen healthy subjects served as controls. Intraluminal pH of the different parts of the gastrointestinal tract was measured by a free-floating pH-sensitive telemetering capsule. A metal sphere was attached to the capsule for exact localization by a metal detector. Physiological patterns of pH were maintained throughout the gastrointestinal tract including the inflamed segments. Median pH in the terminal ileum of the patients with Crohn's disease was 7.5 vs. 7.7 and in the rectum in ulcerative colitis 7.8 vs. 7.2 in the controls. In conclusion, intraluminal pH is not decreased by inflammatory changes in Crohn's disease and ulcerative colitis, allowing eudragit-coated pH-controlled-release formulations of mesalazine to dissolve in diseased areas also.

Explore related subjects

Acid-Base EquilibriumAdultColitis, UlcerativeCrohn DiseaseFemaleHumansHydrogen-Ion ConcentrationIleumIntestinal MucosaMaleMiddle AgedRectumReference ValuesTelemetryJournal Article

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

K Ewe, S Schwartz, S Petersen, A G Press. 1999. Inflammation does not decrease intraluminal pH in chronic inflammatory bowel disease.. https://doi.org/10.1023/a%3A1026664105112

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2001

A role for intracellular pH in membrane IgM-mediated cell death of human B lymphomas.

We show that anti-IgM-induced cell death in a human B lymphoma cell line, B104, is associated with early intracellular acidification and cell shrinkage. In contrast, another human B cell lymphoma line, Daudi, less susceptible to B cell antigen receptor-mediated cell death, responded to anti-IgM with an early increase in intracellular pH (pH(i)). The anti-IgM-induced changes of pH(i) were associated with different levels of activation of the Na(+)/H(+) exchanger isoform 1 (NHE1) as judged by its phosphorylation status. Prevention of anti-IgM-induced cell death in B104 cells by the calcineurin phosphatase inhibitor, cyclosporin A, abrogated both intracellular acidification and cell shrinkage and was associated with an increase in the phosphorylation level of NHE1 within the first 60 min of stimulation. This indicates a key role for calcineurin in regulating pH(i) and cell viability. The potential role of pH(i) in cell viability was confirmed in Daudi cells treated with an Na(+)/H(+) exchanger inhibitor 5-(N,N-hexamethylene)amiloride. These observations indicate that the outcome of the anti-IgM treatment depends on NHE1-controlled pH(i). We suggest that inactivation of the NHE1 in anti-IgM-stimulated cells results in intracellular acidification and subsequently triggers or amplifies cell death.

Acid-Base Equilibrium↗
PubMed2001

Insulin-like growth factor I alters renal function and stimulates renin secretion in late gestation fetal sheep.

While it is known that treatment with insulin-like growth factor I (IGF-I) stimulates growth of the fetal kidney, nothing is known about the short term or long term effects of IGF-I on fetal renal function. To investigate the acute effects of IGF-I on fetal renal function and on the activity of the fetal renin-angiotensin system, studies were carried out in 12 chronically catheterized fetal sheep aged 120 +/- 1 days, before and during a 4 h I.V. infusion of IGF-I at 80 ug h-1. Seven control fetuses were infused over the same period with vehicle (0.1% bovine serum albumin in 0.15 M saline). IGF-I infusion increased plasma IGF-I concentrations by about 80%. There was a small fall in arterial PO2 (P < 0.01), arterial PCO2 increased (P < 0.05), plasma lactate levels increased (P < 0.01) and arterial pH fell (P < 0.05). Fractional bicarbonate reabsorption increased and bicarbonate excretion decreased (P < 0.05). Infusions of IGF-I had no sustained effect on fetal arterial pressure. Glomerular filtration rate (GFR) did not change significantly during IGF-I infusion, but renal blood flow (RBF) fell (P < 0.05). Therefore filtration fraction relative to control values increased (P < 0.05), suggesting that efferent arteriolar vasoconstriction had occurred. IGF-I infusion led to an antidiuresis (P < 0.01), a rise in urinary osmolality (P < 0.05) and a fall in free water clearance (P < 0.01). Since fetal PO2 fell, it is probable that these effects were mediated by arginine vasopressin. The excretion rates of sodium, chloride and phosphate were all reduced by 4 h of infusion (P < 0.05), because their fractional reabsorption rates were all increased (sodium, P < 0.01; chloride, P < 0.01; and phosphate, P < 0.05). Plasma renin concentration increased by 275 +/- 52% during infusion of IGF-I (P < 0.005). Plasma renin activity also increased (P < 0.005), while circulating angiotensinogen concentrations fell (P < 0.05). In the adult, IGF-I increases both RBF and GFR, enhances tubular reabsorption and stimulates the renin-angiotensin system. In the fetus, however, it decreased RBF and had no effect on GFR, but was associated with enhanced tubular function and intense stimulation of renin secretion. Some of these effects of IGF-I on fetal renal function may be involved in maturation of the kidney in preparation for life after birth.

Acid-Base Equilibrium↗
PubMed2001

Exercising skeletal muscle blood flow in humans responds to reduction in arterial oxyhaemoglobin, but not to altered free oxygen.

We hypothesised that reducing arterial oxyhaemoglobin (O2Hba) with carbon monoxide (CO) in both normoxia and hyperoxia, or acute hypoxia would cause similar compensatory increases in human skeletal muscle blood flow and vascular conductance during submaximal exercise, despite vast differences in arterial free oxygen partial pressure (Pa,O2). Seven healthy males completed four 5 min one-legged knee-extensor exercise bouts in the semi-supine position (30 +/- 3 W, mean +/- S.E.M.), separated by approximately 1 h of rest, under the following conditions: (a) normoxia (O2Hba = 195 ml l-1; Pa,O2 = 105 mmHg); (b) hypoxia (163 ml l-1; 47 mmHg); (c) CO + normoxia (18% COHba; 159 ml l-1; 119 mmHg); and (d) CO + hyperoxia (19% COHba; 158 ml l-1; 538 mmHg). CO + normoxia, CO + hyperoxia and systemic hypoxia resulted in a 29-44% higher leg blood flow and leg vascular conductance compared to normoxia (P < 0.05), without altering blood pH, blood acid-base balance or net leg lactate release. Leg blood flow and leg vascular conductance increased in association with reduced O2Hba (r2 = 0.92-0.95; P < 0.05), yet were unrelated to altered Pa,O2. This association was further substantiated in two subsequent studies with graded increases in COHba (n = 4) and NO synthase blockade (n = 2) in the presence of normal Pa,O2. The elevated leg blood flow with CO + normoxia and CO + hyperoxia allowed a approximately 17% greater O2 delivery (P < 0.05) to exercising muscles, compensating for the lower leg O2 extraction (61%) compared to normoxia and hypoxia (69%; P < 0.05), and thereby maintaining leg oxygen uptake constant. The compensatory increases in skeletal muscle blood flow and vascular conductance during exercise with both a CO load and systemic hypoxia are independent of pronounced alterations in Pa,O2 (47-538 mmHg), but are closely associated with reductions in O2Hba. These results suggest a pivotal role of O2 bound to haemoglobin in increasing skeletal muscle vasodilatation during exercise in humans.

Acid-Base Equilibrium↗