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G Paulsen

Publications and source records attributed to G Paulsen.

12 recordsLinked to original sources
PubMed1979

Effect of parental aspirin on the gastric mucosal barrier in the rat.

The purpose of the present study was to determine in the rat whether parenteral aspirin, like topical aspirin, injures the gastric mucosa by diffusely disrupting the gastric mucosal barrier to hydrogen ion back-diffusion. Back-diffusion studies, including the ion fluxes and lumenal potential difference, were performed in control situations and either 0.5 or 4 h after the intraperitoneal administration of sodium acetylsalicylate. Gastric mucosal lesions were scored. After 0.5h, lesions developed but the barrier was intact. However, after 4 h, lesion formation was more severe and changes characteristic of diffuse barrier disruption, fall in potential difference and increased loss of hydrogen ion occurred. Since lesions occurred before evidence of diffuse barrier disruption could be detected, we conclude that in the present model diffuse barrier disruption is a consequence rather than a cause of lesions.

Animals↗
PubMed1979

Topical aspirin plus HCl gastric lesions in the rat. Cytoprotective effect of prostaglandin, cimetidine, and probanthine.

The effect of representative agents of three classes of antisecretory compounds; prostaglandins, histamine H2-receptor antagonist, and anticholinergic agents, on acute gastric mucosal lesions produced by topical aspirin (200 mg/kg) plus HCl (150 mM) in the pylorus-ligated rat was studied. Acid was given exogenously so as to negate any antisecretory effect of the drugs studied. Both nonantisecretory and antisecretory doses of each agent as determined by preliminary secretory studies were employed. The postaglandin analogue 16,16-dimethyl prostaglandin E2, the H2-receptor antagonist cimetidine, and the anticholinergic agent probanthine, in both doses studied, all significantly reduced lesion formation. The H1-receptor antagonist mepyramine neither protected by itself nor enhanced the protective effect of cimetidine. Pepsin release into the gastric content increased with increasing mucosal damage. However, addition of pepsin to the gastric instillate had no effect on severity lesions in any group, which indicates that the increased pepsin was the result of, and not the cause of, the mucosal damage. The findings indicate that all three classes of antisecretory agents studied are also cytoprotective, i.e., they can protect against gastric mucosal injury by topical aspirin plus HCl by some mechanism other than inhibition of acid and pepsin secretion.

Animals↗
PubMed1976

(32P) phosphate incorporation into ATP during ATP hydrolysis and its dependence on the interaction of actin and myosin.

The incorporation of 32Pi into ATP has been found to be catalyzed by myosin only when and if it interacts with actin. This exchange reaction is inhibited in natural but not in desensitized actomyosin after removing of trace Ca2+ with ethyleneglycol bis(2-aminoethyl)-N,N'-tetraacetic acid (EGTA). In desensitized as well as in synthetic actomyosin the exchange reaction can be fully inhibited by the addition of troponin I (0.5 mg troponin I/mg actomyosin results in a 50% inhibition) or after replacing the Mg activator by CaCl2. The exchange rate is about 1:500 of the ATPase rate in presence of 2 mM phosphate. These results suggest the existence of an 'energy-rich' actin -- myosin -- nucleoside-diphosphate intermediate during the cross-bridge cycle.

Actins↗
PubMed1976

Mechanism of prevention of aspirin-induced gastric lesions by bile duct legation in the rat.

UNLABELLED: Gastric reflux of bile has been reported to be essential for the production of acute gastric mucosal lesions by intragastric aspirin in the rat. The purpose of the present study was to determine whether bile duct legation of pylorus ligation in the rat inhibits asprin-induced gastric lesions, and, if so, what the protective mechanisms are. Operations were performed under ether anesthesia. Asprin, 200 mg per kg, was instilled into the stomach 1/2 hr postsurgery (bile duct ligation or pylorus ligation). Four hours later the rats were killed, the stomachs were examined, and mucosal lesions were scored. Bile duct ligation, but not pylorus ligation, significantly protected against aspirin-induced gastric-lesions. Bile duct ligation, in pylorus-ligated rats, inhibited gastric acid output by 78%. Instilling HCl + aspirin in bile duct-ligated rats restored lesion formation. Shunting bile to the colon (to prevent bile reflux) did not prevent aspirin lesions. Salicylate determination, to ascertain whether bile duct ligation altered asprin absorption, revealed no significant differences between bile duct ligation and aspirin, shunt + aspirin, and sham shunt + aspirin in plasma and gastric tissue salicylate concentrations. CONCLUSIONS: (1) Bile duct legation protects against aspirin-induced gastric mucosal lesions by inhibiting gastric HCl secretion. As a corollary, a certain amount of acid in the stomach is necessary for aspirin-induced gastric lesions to form. (2) Bile reflux is not necessary for aspirn-induced gastric lesions in the rat.

Animals↗
PubMed1975

Experimental chronic gastric ulcer due to ischemia in rats.

Ligation of the left gastric and right gastroepiploic arteries and veins resulted in chronic gastric ulcer formation in the rat. Linear mucosal corpus hemorrhages appeared within 8 hr of ligation. By 2 days large corpus hemorrhagic erosions were present. A single, large ulcer involving nearly the entire corpus was present at 3-5 days. In the ulcerated area the mucosa and muscularis mucosae were destroyed, thick granulation tissue filled the submucosa and the muscularis propria was severely damaged. Progressive healing occurred thereafter and 75% of the ulcers healed completely grossly in 2-8 weeks. Histologic studies showed that healing and mucosal regeneration occurred by the outgrowth of a layer of cells from the adjacent intact epithelium extending over the surface of the ulcer. Invaginations from this covering layer of cells formed a glandular mucosa composed of mucous cells. Later parietal and chief cells appeared, and eventually (6 months) a normal corpus-type mucosa covered the entire corpus. With time smooth-muscle fibers appeared in the outer half of the dense submucosal granulation tissue and eventually a normal muscularis mucosae, submucosa, and muscularis propria were present (6-12 months). These studies show that: (1) ischemia can give rise to chronic gastric ulcer, and (2) all elements of the gastric wall, including the mucosa, the muscularis mucosae, and the muscularis propria can fully regenerate.

Animals↗
PubMed1975

Parenteral aspirin produces and enhances gastric mucosal lesions and bleeding in rats.

The effect of parenteral sodium acetylsalicylate (Na ASA) on the development of gastric mucosal lesions and bleeding was studied in control rats and in rats subjected to cold-restraint stress. Although both doses of Na ASA studied, 15 and 60 mg/kg intraperitoneally, alone resulted in lesion formation, only with the larger dose did this reach the level of statistical significance. However both doses of Na ASA alone significantly increased blood loss as measured by a decrease in hematocrit value. The administration of Na ASA 15 MG/kg intraperitoneally to animals subjected to cold-restraint significantly increased blood loss, but not lesion formation, while the larger dose of Na ASA significantly increased both parameters. Thus parenteral aspirin not only can cause gastric mucosal damage and bleeding, but it can enhance lesion formation and blood loss produced by cold-restraint. Two mechanisms may be involved: a smaller dose of Na ASA significantly affecting hemostasis but a larger dose being required for gastric mucosal damage.

Animals↗
PubMed1975

The role of bile reflux in the development of cold-restraint gastric lesions.

The study was designed to test whether or not bile reflux is necessary for the development of gastric mucosal lesions during cold-restraint stress in the rat. 40 male Sprague-Dawley rats were studied. They were randomized into 4 groups. Group 1 underwent sham operations with no cold-restraint stress. Group 2 underwent sham operations. Group 3 underwent pyloric ligation. Group 4 underwent bile duct ligation. Groups 2, 3, and 4 were subjected to cold-restraint stress for 3 hours at 4-6 degrees C in a Bollman cage. After the experimental procedure, the stomachs were removed under ether anesthesia, the severity of lesions was recorded, and blood from the hearts was obtained for hematocrit readings. The mean lesion scores of all groups exposed to cold-restraint stress were similar and much higher than that of the unrestrained sham-operated group (P smaller than 0.001). Also, mean hematocrit readings in all groups exposed to cold-restraint stress were lower than in the control group (P smaller than 0.05). There was a correlation between severity of mucosal lesions and hematocrit reading (rs=0.57, P smaller than 0.001). The results obtained allow the following conclusions: (1) Bile reflux is not necessary for formation of cold-restraint stress lesions in the rat. (2) Hematocrit readings appear to be a useful measure of blood loss secondary to experimental mucosal lesions.

Animals↗
PubMedDate not supplied

Secretion of nickel in rabbit saliva.

Secretion of nickel into unstimulated and stimulated saliva of rabbits was studied after a single intraperitoneal injection of nickel chloride labelled with 63Ni. Maximum 63Ni in unstimulated saliva was obtained in specimens collected one hr after maximum serum-63Ni was reached and two hrs after the nickel administration. Compared to serum-63Ni, the secretion of isotope into saliva was low whether or not stimulation was carried out. After 24 hrs, only traces of radioactivity were left in saliva. Forty to 60 percent of salivary-63Ni was ultrafiltrable. Most nickel associated with salivary proteins was weakly bound. Two acidic protein fractions obtained by gel filtration of saliva seemed to bind nickel firmly at neutral pH. No such binding of nickel to salivary proteins was observed after the in vitro addition of normal saliva to 63NiCl2.

Animals↗