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Biomedical subjects

W E Perkins

Publications and source records attributed to W E Perkins.

28 records · Page 2Linked to original sources
PubMed1985

Lack of effect of metoclopramide on cisplatin-induced nephrotoxicity in rats.

Metoclopramide has gained acceptance as an effective drug for the control of nausea and vomiting in cancer patients receiving cisplatin chemotherapy. In addition to its emetogenic side effects, cisplatin is known to be nephrotoxic. This animal study was undertaken to determine if the severity of cisplatin-induced nephrotoxicity is altered by the coadministration of metoclopramide. Female F-344 rats received subcutaneous saline or metoclopramide 30 min before and 120 min after intravenous administration of saline or cisplatin. Animals were sacrificed on the 5th day following treatment. Decreases in body weight, elevations in serum urea nitrogen and histopathological changes were of similar magnitude in all cisplatin treated groups regardless of concomitant metoclopramide administration. Saline dosed control animals did not exhibit these changes. It is concluded that the coadministration of metoclopramide did not significantly alter the nephrotoxic effects of cisplatin in this experiment.

Animals↗
PubMed1984

Somatostatin modulation of peptide-induced acetylcholine release in guinea pig ileum.

The peptides caerulein, neurotensin, somatostatin, and substance P modulate the activity of intestinal neurons and alter gut motility. We examined the effects of these peptides on acetylcholine release from the myenteric plexus and intestinal contractility in vitro. Caerulein (1 X 10(-9) M), neurotensin (1.5 X 10(-6) M), and substance P (1 X 10(-7) M) significantly enhanced the release of [3H]acetylcholine from the myenteric plexus of the guinea pig ileum. This effect was inhibited by tetrodotoxin (1.6 X 10(-6) M). Somatostatin (10(-6) M) inhibited caerulein- and neurotensin-evoked release of acetylcholine but did not inhibit release induced by substance P. Caerulein, neurotensin, and substance P caused contraction of the guinea pig ileal longitudinal muscle. Somatostatin inhibited the contractions induced by caerulein and neurotensin. In contrast, substance P-induced contraction was not inhibited significantly by somatostatin. Thus, in the guinea pig ileum, caerulein-, neurotensin-, and substance P-induced contractility is due, at least in part, to acetylcholine release from the myenteric plexus. The ability of somatostatin to inhibit peptide-induced contractility is selective, and its mechanism may be attributed to inhibition of acetylcholine release.

Acetylcholine↗
PubMed1984

Myocardial effects of mitoxantrone and doxorubicin in the mouse and guinea pig.

Mitoxantrone (DHAQ) was compared to doxorubicin for myocardial effects in the mouse and the guinea pig. Histologically, DHAQ induced a high incidence of focal myocardial damage in mice, similar to that observed with doxorubicin. Functionally, like doxorubicin, DHAQ significantly reduced the rate of contraction and histamine responsiveness of guinea pig right atria in vitro. Additionally, long-term ip administration of either DHAQ or doxorubicin reduced the atrial response to histamine in vitro. These data suggest that DHAQ may have a spectrum of myocardial activity similar to that of doxorubicin.

Animals↗
PubMed1982

Effects of caerulein on rat small and large intestinal fluid transport in vivo.

We have examined the effect of caerulein on intestinal fluid transport in vivo. Rat jejunal, ileal, and colonic segments were perfused with a physiologic buffer for a 60-min control period, followed by a 60-min period after caerulein, prostaglandin E2 (PGE2), or saline (0.9%, w/v) were given by intramuscular (i.m) injection. At a dose of 5 micrograms/kg caerulein had no effect on ileal fluid transport. Lower doses of caerulein (300 ng and 1 microgram/kg) also had no effect. PGE2 significantly (P less than 0.05) inhibited net ileal absorption by 94 +/- 24% from pre-dose levels. Caerulein (300 ng/kg) had no effect (P greater than 0.05) on jejunal or colonic fluid transport. Intestinal fluid accumulation assessed by the 'enteropooling' assay did not increase after 30 ng or 1 microgram/kg of caerulein, whereas in animals given PGE2 of (5 mg/kg) the fluid accumulation more than doubled (P less than 0.001): control 1.59 +/- 0.15 ml; cerulein (1 microgram/kg) 1.36 +/- 0.20 ml; and PGE2 4.7 +/- 0.50 ml. Serum levels of caerulein (after a 1 microgram/kg dose), measured by radioimmunoassay, were elevated up to 30 min after i.m. injection. The data indicate that caerulein has no direct effect on rat small or large intestinal fluid transport.

Animals↗
PubMed1982

Effect of ICRF-187 on doxorubicin-induced myocardial effects in the mouse and guinea pig.

ICRF-187 was tested for cardioprotective activity in doxorubicin-treated mice and guinea pigs. Pretreatment with i.p. ICRF-187 caused a significant decrease in the indicence of i.v. doxorubicin-induced myocardial histological damage in the mouse. I.p. ICRF-187 did not, however, reduce the effect of i.p. doxorubicin on a functional myocardial effect of this antitumour drug, a reduced histamine responsiveness of right atria in vitro. These data suggest that ICRF-187 may not be specific for all the cardiac effects of doxorubicin.

Animals↗
PubMed1975

Effect of 3,4-toluenediamine on output from in situ rat Brunner's glands pouches.

Duodenal and gastric glandular mucosal damage have been observed 24 hr following single subcutaneous doses of 3,4-TDA in fed, unrestrained rats. 3,4-TDA significantly reduced secretion from in situ Brunner's glands pouches in pentobarbital anesthetized rats. The reduction in volume output with a definitely duodenal ulcerogenic dose of this compound was more than twice that observed with a minimally ulcerogenic dose, suggesting a correlation between the duodenal ulcerogenic and duodenal anti-secretory activities of this compound. The animal model described in this communication should facilitate experimentation to establish the inhibitory effect of compounds on the output of protective fluids from the proximal duodenum.

Animals↗
PubMed1973

Effects of carbenoxolone sodium on stress-induced gastric damage in rats.

Carbenoxolone sodium was studied to determine its effect against restraint-induced gastric mucosal damage in the rat. Significant anti-ulcer activity was observed following intraperitoneal administration in nonfasted but not in either 24 or 48 h fasted rats. Orally, carbenoxolone had no statistically significant effect in non-fasted rats although the data suggest that it may have afforded some protection. These results indicate that the use of non-fasted rats is most probably a requirement for demonstrating the protective activity of this type of anti-ulcer compound in stressed rat assays.

Animals↗