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Biomedical subjects

P H Rowe

Publications and source records attributed to P H Rowe.

At least 37 records · Page 2Linked to original sources
PubMed1987

Parenteral aspirin and sodium salicylate are equally injurious to the rat gastric mucosa.

The effects of parenteral aspirin (ASA) or sodium salicylate (SA) on the gastric mucosa were investigated in anesthetized pylorus-ligated rats 3 h after a bolus intravenous injection of ASA or SA, 150 mg/kg, or NaCl (control). Aspirin or SA produced similar extensive gross mucosal hemorrhagic lesions and similar microscopic damage in the presence of luminal acid (luminal pH 1.3 +/- 0.05). Neither ASA nor SA produced gastric mucosal injury with intragastric instillation of saline (luminal pH 3.7 +/- 0.5). Pretreatment for 1 h with luminal or subcutaneous 16,16-dimethyl prostaglandin E2 completely prevented the formation of red streaks in ASA-treated rats but not in SA-treated rats, although prostaglandin E2 pretreatment significantly reduced the gross lesion area in SA-treated rats (p less than 0.05). We conclude the following: (a) Intravenous SA is as damaging as intravenous ASA as long as luminal acid is present. (b) 16,16-Dimethyl prostaglandin E2 completely protected the gastric mucosa from injury by intravenous ASA, and to a lesser extent by intravenous SA. (c) In view of the damaging effects of SA on the gastric mucosa and the rapid conversion of ASA to SA, the mechanism of the gastric mucosal injury by intravenous ASA is much more complex than simple inhibition of endogenous prostaglandin synthesis.

Animals↗
PubMed1987

Cricopharyngeal Crohn's disease.

We report a case of Crohn's disease of the cricopharyngeal oesophagus which presented with complete dysphagia and was successfully treated by balloon dilatation. We can find no previous reports of such a case.

Cricoid Cartilage↗
PubMed1987

Gastroduodenal mucosal defence mechanisms and the action of non-steroidal anti-inflammatory agents.

This review summarises gastroduodenal protective mechanisms, the actions of non-steroidal anti-inflammatory (NSAI) agents on mucus and HCO3 secretions, and the basis of gastric mucosal injury induced by acetylsalicylic and salicylic acids (ASA and SA). Resistance to autodigestion by acid and pepsin present in gastric juice is multifactorial involving pre-epithelial (mucus-bicarbonate barrier) and post-epithelial (blood flow, acid-base balance) factors in addition to properties of the surface cell layer per se. The latter includes mucosal re-epithelialisation, a property which appears particularly important with respect to recovery from acute injury. A range of NSAI agents (ASA, fenclofenac, ibuprofen and indomethacin) inhibit gastric HCO3 transport in isolated mucosal preparations. Inhibition of duodenal HCO3 transport has been demonstrated in response to indomethacin in vitro and in vivo. These effects on secretion can be antagonised by exogenous prostaglandins of the E series. The layer of secreted mucus gel overlying the epithelial surface is not affected by NSAI drugs in the short term. However a number of these agents have been shown to inhibit glycoprotein biosynthesis by the epithelial cells. Thus loss of this protective coat could be anticipated during chronic drug exposure since erosion of adherent mucus by luminal shear and proteolysis would not be compensated by continued secretion. Detailed analysis of the gastric mucosal injury induced by salicylates both in vitro and in vivo reveals that much of the damage previously attributed to ASA is in fact due to the metabolic product SA. In this respect it is concluded that mucosal injury caused by ASA is due to a combination of two factors.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Late rupture of ligated common iliac arteries.

Late rupture may follow simple ligation of the common iliac arteries after aortobifemoral grafting. Oversewing the origins of the arteries may prevent this rare but dangerous complication. A CT scan is recommended to investigate unexplained abdominal pain following aortic surgery.

Aged↗
PubMed1986

Effect of simulated systemic administration of aspirin, salicylate, and indomethacin on amphibian gastric mucosa.

The effects of 20 mM aspirin (ASA), 20 mM sodium salicylate (SA), or 10(-4) M indomethacin placed in the nutrient solution (N) to stimulate systemic administration were investigated at pHN 7.3 in Ussing-chambered amphibian gastric mucosae. In histamine-stimulated tissues, the initial rise and subsequent rapid fall in potential difference, rise in resistance, and inhibition of hydrogen ion (H+) secretion induced by SAN did not occur with ASAN unless hydrolysis of ASAN produced a SAN of greater than 3 mM. In metiamide-treated tissues, 20 mM SAN caused an immediate fall in potential difference and an increase in resistance; 2 mM SAN and 20 mM ASA produced similar qualitative electrical changes, but only those induced by ASA were reversible. IndomethacinN caused no significant changes in potential difference, resistance, or H+ secretion in histamine- or metiamide-treated tissues. Despite producing highly significant reductions in generation of prostaglandin E2, and prostaglanndin F2 alpha and 6-keto prostaglandin F1 alpha, ASAN and indomethacin caused no surface ulceration. Sodium salicylate placed in the nutrient solution caused only a small reduction in prostaglandin F2 alpha, without change in the other prostaglandins, and produced extensive edema in the lamina propria, histologically. We conclude the following: (a) The inhibition of H+ secretion and electrical changes caused by SAN in histamine-treated gastric fundus are not observed with ASAN unless there is hydrolysis to [SAN] greater than 3 mM. (b) Our data strongly implicate the SAN in ASAN-containing solutions as being responsible for the electrical effects and inhibition of H+ secretion. (c) There is no correlation in vitro between inhibition of prostaglandin synthesis and the electrical or morphologic changes produced by nutrient exposure to ASA, SA, or indomethacin.

16,16-Dimethylprostaglandin E2↗
PubMed1986

Chloride transport of frog gastric fundus: effects of omeprazole.

Omeprazole (10(-4) M) inhibited H+ secretion and increased potential difference (PD), resistance, and short-circuit current (Isc) in chambered bullfrog gastric mucosa, but the electrical changes developed only in tissues previously exposed to histamine. Net chloride transport (JnetCl) did not change after omeprazole under short-circuited conditions, and Isc increased to become equal to JnetCl. Under open-circuit conditions, JnetCl was reduced by 38%, the decrement attributable to the concomitant increase in PD, as evidenced by a linear relationship between JnetCl and PD in omeprazole-treated mucosae clamped to different PD (0-45 mV). The effect of omeprazole on PD and Isc could be blocked by metiamide and was absent in spontaneously resting tissues. HEPES nutrient solutions did not alter the electrical response or Cl- transport after omeprazole. In Na+-free solutions, omeprazole induced only a transient rise in PD and Isc. We conclude that omeprazole uncouples H+ and Cl- secretion. This Cl- secretion is electrogenic and dependent upon stimulation by histamine. Both Na+ and HCO3- seem to be involved in movement of Cl- across the basolateral membrane.

Animals↗
PubMed1985

In vitro protection of amphibian gastric mucosa by nutrient HCO3- against aspirin injury.

The effects of luminal aspirin [acetylsalicylic acid (ASA)] at luminal pH 4.5 and pH 3.0 on Ussing chambered amphibian gastric fundic and antral mucosae were investigated using different concentrations of HCO3- ([HCO3-]) in the nutrient solution in histamine-stimulated or metiamide-treated tissues. The severe surface cell and oxyntic gland injury seen in histamine-stimulated tissues after a 3-h exposure to 20 mM ASA at luminal pH 4.5 in HCO3- -free nutrient solution (HEPES) was prevented by including 18 mM or 48 mM HCO3- in the nutrient solution. At luminal pH 3.0, 48 mM HCO3- in the nutrient solution delayed the histologic damage to the surface epithelium and oxyntic glands caused by a 30-min exposure to 20 mM luminal ASA, but it afforded no protection to a 60-min exposure. This protection of the gastric epithelium by a high nutrient [HCO3-] did not occur in metiamide-treated tissues at luminal pH 3.0. Although the injury to antral epithelial cells exposed to 20 mM luminal ASA at luminal pH 3.0 or 4.5 was less severe than that in fundic mucosae, 48 mM HCO3- in the nutrient solution also afforded clear protection in this tissue. A high nutrient [HCO3-] prevented the sharp fall in the potential difference observed in fundus exposed to ASA at luminal pH 4.5 and delayed the fall in potential difference observed in fundic and antral mucosae exposed to ASA at luminal pH 3.0. The high nutrient [HCO3-] did not prevent the increase in resistance observed in tissues during ASA exposure at luminal pH 4.5 and 3.0. The electrical data reflect not only the damaged surface and oxyntic cells caused by ASA, but also the complex effects of ASA on active and passive ion transport. We conclude the following: (a) The mucosal injury to the fundus and antrum caused by luminal ASA is prevented by 48 mM HCO3- in the nutrient solution when luminal pH is 3.0 and by 18 mM HCO3- when luminal pH is 4.5. Absence of nutrient HCO3- accentuates the injury caused by luminal ASA. (b) The luminal pH, concentration, and time of exposure influence the depth and severity of ASA injury to the fundic and antral mucosa. (c) The electrophysiologic and morphologic changes after ASA exposure are not interrelated, due to the complex effects of ASA on the ion transport and morphology of the gastric epithelium.

Animals↗
PubMed1985

Characteristics of sudden potential drop in bullfrog gastric mucosa.

An unusual sudden potential drop (SPD) has been described by Kidder in bullfrog gastric mucosa exposed to anoxia and a serosal pH less than or equal to 7.1. We found that anoxia was not a prerequisite, since under fully oxygenated conditions the SPD occurred reliably in metiamide-treated tissues when the pH of the nutrient solution (pHN) was below 7.1. The SPD was observed also in metiamide-treated tissues exposed to 20 mM luminal or nutrient acetylsalicylic acid (ASA) with pHN = 7.3, an effect that was abolished by increased nutrient HCO3- concentration. The SPD occurred when NO3- but not isethionate or acetate replaced Cl- in the bathing media. A marked increase in potential difference in response to changing luminal Cl- concentration was observed after the SPD, uptake of Cl- from the luminal solution into the tissue increased, but transmural fluxes of Cl- decreased bidirectionally. Permeability to H+ was unaltered in the post-SPD state. An SPD never occurred in antrum under conditions causing SPD in fundus, suggesting that oxyntic cells are prerequisite. We conclude that, under conditions which cause tissue or cellular acidosis and cessation of H+ secretion, fundic mucosae respond with an anion-selective increase in apical permeability manifest as the SPD.

Animals↗
PubMed1985

Fixation of Hohmann's osteotomy for hallux valgus.

We modified Hohmann's (1923) osteotomy for hallux valgus by internal fixation of the metatarsal head with no need for a plaster cast. Five (2-10) years post-operatively, all 20 patients (32 feet) had complete relief and all but one was satisfied with the cosmetic result. However, we now routinely add osteotomies of the second and third metatarsal neck to prevent, albeit asymptomatic, callosities.

Adolescent↗
PubMed1985

Oedème bleu involving the lower limb.

Oedème bleu may masquerade as an acute vascular disorder of the limb. We present a case of this syndrome occurring in a young female with the physical signs involving the lower limb.

Adolescent↗
PubMed1984

An investigation of the effects of phenobarbitone on the pharmacokinetics of norethindrone in the rat using liver perfusion and everted gut sacs.

Previous in vivo studies have suggested that phenobarbitone increases the first pass clearance of norethindrone in the rat by induction of enzymes both in the gut wall and liver. In the present study phenobarbitone caused an increase in both the production of highly polar ether-extractable metabolites and the conjugation of the steroid as it crossed the wall of the everted gut sac preparation. In addition, there was a marked increase in the uptake of norethindrone into the liver followed by increased phase I metabolism in the isolated perfused liver. As expected for a highly cleared drug, enzyme induction had no measurable effect on the terminal half-life of norethindrone in the perfused liver preparation.

Animals↗