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Biomedical subjects

D R Franz

Publications and source records attributed to D R Franz.

28 records · Page 2Linked to original sources
PubMed1986

Organophosphate-induced histamine release from mast cells.

To examine the hypothesis that soman intoxication leads to degranulation of mast cells with the release of histamine, we studied the effects of soman on rat peritoneal mast cells (RPMC) in vitro and in vivo. In vitro studies were performed with RPMC harvested from Edgewood rats, and challenged with soman (10(-8)-3 X 10(-3) M) in Tyrode's buffer. The RPMC exhibited a dose-dependent release of histamine, with maximal release of 50% at 3 to 6 X 10(-4) M. The release process is an active, secretory, noncytotoxic event, which is calcium and temperature dependent, requires metabolic energy and is influenced by intracellular levels of cyclic AMP. We next studied the in vivo effects of disodium cromoglycate (DSCG, 10(-4) M) on soman and Compound 48/80-induced histamine release. In vivo studies were performed by the i.p. injection of 5 ml of Tyrode's buffer containing soman (O-1 LD50), or Compound 48/80 as a positive control, with or without DSCG. The fluid recovered after approximately 10 min in the peritoneal cavity was examined for percentage of histamine release. In vivo, Compound 48/80 induced 49 +/- 1% histamine release, with no inhibition by DSCG (Compound 48/80 plus DSCG induced 49 +/- 0.4% histamine release). On the other hand, soman (1 LD50) induced 17 +/- 5% extracellular histamine release, with complete inhibition by DSCG (soman plus DSCG induced 3 +/- 1% histamine release). The data indicate that soman induced a dose-dependent release of histamine from RPMC, and provide evidence that histamine is a potentially important mediator of the pathophysiological response to organophosphate intoxication.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

The effects of cyanide and its interactions with norepinephrine on isolated aorta strips from the rabbit, dog, and ferret.

Effects of sodium cyanide on isolated strips of rabbit, dog, and ferret aorta were determined. In the rabbit aorta strip, cumulatively added cyanide caused small contractions beginning at approximately 10(-11) M cyanide and reaching a maximum response at 10(-5) M. A concentration of cyanide between 10(-5) M and 10(-3) M produced relaxation. When cyanide was cumulatively added to norepinephrine (NE)-contracted rabbit aorta strips, no contractions were observed. Cyanide concentrations above 10(-5) M produced relaxation in the NE-contracted vessels. Sensitivity of the aorta strips to NE differed among the species examined. The ED50 for contractions in the dog and ferret aorta was 4 X 10(-4) M and in the rabbit was 5 X 10(-6) M. Pretreatment with cyanide in concentrations up to 10(-2) M did not reduce contractions of dog aorta to NE, although 10(-2) M cyanide abolished contractions of rabbit aorta to NE and reversed NE-contractions of ferret aorta to relaxation. The antagonism of cyanide for NE-induced contractions was completely reversible with cyanide concentrations up to 10(-3) M. Cyanide pretreatment of strips of aorta increased the rate of contraction to NE. A concentration of 10(-2) M cyanide caused small contractions of aorta strips from each species. Thus, cyanide exerts dose and species dependent responses on vascular smooth muscle.

Animals↗
PubMed1984

Cyanide loss from tissue baths in the presence and absence of tissue.

Loss of cyanide from Krebs-Henseleit solution (KHS) was studied in aerated tissue baths at 38 degrees C in the presence and in the absence of tissue. The rate of cyanide loss was greater from 300-microM than from 30-microM solutions and still greater from 300-microM solutions in the presence of vascular tissue. Initial cyanide loss was much greater from the tissue-containing bath, and the half-time was shorter in the presence of tissue (54 min) than in its absence (98 min) in baths containing the same initial cyanide concentration (300 microM).

Animals↗
PubMed1981

Effect of prostaglandin E2 on gastric mucosal bleeding caused by aspirin.

The effect of prostaglandin E2 on gastric mucosal bleeding caused by aspirin was studied. Blood in serial gastric washings was measured chemically for 30 min. Normal blood loss was equivalent to 0.05 ml/day. Aspirin, 600 mg four times daily, increased gastric bleeding on day 1; bleeding was further increased on day 2. On day 2, ingestion of 0.5 mg of prostaglandin E2 15 min before 600 mg of aspirin reduced the gastric microbleeding caused by aspirin. Prostaglandin E2, 0.5 mg four times daily, did not change the normal blood loss. No consistent changes in gastric emptying or in secretion of chloride were detected.

Aspirin↗
PubMed1980

Collection of urine from caged laboratory cats.

Twenty-four hour urine specimens were collected from caged domestic cats using modified rubber dish pans. This simple method provided an uncontaminated specimen, total daily urine output and required no training of the animals.

Animals↗
PubMedDate not supplied

Hemodynamic and calorimetric changes induced by microcystin-LR in the rat.

Microcystin-LR, a cyclic peptide from the cyanobacterium Microcystis aeruginosa, given at acutely toxic doses causes severe hepatic interstitial hemorrhage. Hemodynamic, calorimetric and acid-base balance changes after i.v. microcystin were measured. The effect of isoproterenol, dopamine, methylprednisolone and whole-blood volume expansion on the immediate hemodynamic effects after toxin administration were also evaluated. A dose of 100 micrograms kg-1 was invariably lethal for rats in all studies. Pathophysiological changes included: a sustained, rapid decline in cardiac output and stroke volume; an acute hypotension responsive to volume expansion with whole blood; a decreased heart rate, responsive to both isoproterenol and dopamine; an early decline in oxygen consumption, carbon dioxide production and metabolic rate accompanied by progressive hypothermia; and acid-base balance changes indicating partially compensated metabolic acidosis. The lethal effects of microcystin-LR were previously attributed to hypovolemic shock as a result of hepatic interstitial hemorrhage. These results indicate that, in addition, there may be a cardiogenic component that limits the physiological cardiac reserve, compromising a normal response to circulatory inadequacy.

Acid-Base Equilibrium↗