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Biomedical subjects

E J Barbieri

Publications and source records attributed to E J Barbieri.

29 records · Page 2Linked to original sources
PubMed1981

The effects of adrenergic agonists and antagonists on vesicourethral smooth muscle of rabbits.

The effects of alpha and beta adrenergic agonists and antagonists on isolated smooth muscle preparations from the rabbit bladder body, bladder base and proximal urethra have been studied. The predominance of alpha receptors in the proximal urethra and the bladder base was observed via contraction of these areas by norepinephrine and blockade by phentolamine. Alpha receptor-mediated contractile activity could be unmasked in the bladder body when beta receptors were blocked with propranolol. Isoproterenol, 1 X 10(-10) to 3 X 10(-7) M, had a strong, dose-related relaxant effect on the bladder body, but little effect on the bladder base or proximal urethra. Selective beta-2 agonists such as terbutaline, salbutamol and ritodrine elicited tissue responses similar to those of isoproterenol. The pD2 values for isoproterenol, terbutaline, salbutamol and ritodrine were 8.59, 7.87, 7.34, and 6.52, respectively. Dobutamine, a selective beta-1 agonist, failed to cause significant relaxation of these tissues. The nonselective beta receptor blocker, propranolol, and the selective beta-2 receptor blocker, butoxamine, competitively antagonized the relaxant effects of the four active beta agonists; however, atenolol, a selective beta-1 receptor blocker, was inactive. On the basis of the selective action of these agonists and antagonists, we concluded that beta-2 receptors mediate relaxation of the vesicourethral smooth muscles of the rabbit and the participation of beta-1 receptors in the areas is insignificant.

Animals↗
PubMed1979

In vitro study of antispasmodic effects of dicyclomine hydrochloride on vesicourethral smooth muscle of guinea pig and rabbit.

Dicyclomine inhibition of acetylcholine-induced and barium chloride-induced isotonic contractions of the smooth muscle from three segments of the lower urinary tract (bladder body, bladder base, and proximal urethra) of the guinea pig and the rabbit was studied in vitro. In the guinea pig dicyclomine caused competitive inhibition of acetylcholine-induced contraction of the bladder body (1 x 10(-7) M to 1 x 10(-5) M) and the bladder base (1 x 10(-6) M, 1 X 10(-5) M) and was less potent than atropine and propantheline. In the rabbit significant blockade of acetylcholine-induced contractions occurred at dicyclomine concentrations of 5 x 10(-6) M to 3 x 10(-5) M in the bladder body and at 1 x 10(-5) M and 3 x 10(-5) M in the bladder base. In both species dicyclomine inhibitory effects were most marked in the bladder body, moderate in the bladder base, and minimal in the proximal urethra. Dicyclomine failed to cause inhibition of the barium chloride-induced contractions in the guinea pig vesicourethral smooth muscle. In rabbits, however, significant antagonism P less than 0.01) of barium chloride-induced muscle contraction was observed with dicyclomine at concentration 1 x 10(-5) M in both bladder body and the bladder base. The clinical implication of such properties of dicyclomine are discussed.

Acetylcholine↗
PubMed1979

Depression of drug metabolism in the mouse by a combination of Mycobacterium butyricum and anaesthetics.

1 Subcutaneous injection of Mycobacterium butyricum suspended in mineral oil into the mouse hind paw caused an oedematous local inflammation. Hind paw swelling was maximum 5 days after injection and was still apparent at day 30. 2 Drug metabolism in vivo (as monitored by ketamine- or pentobarbitone-induced sleeping times) was not affected by the inflammatory disease. However, administration of ketamine or pentobarbitone at day 1 led to significantly elevated sleeping times when the mice showing local inflammation were retested at day 5 with the anaesthetics. 3 Indomethacin inhibited hind paw oedema in the mouse but did not affect ketamine-Mycobacterium butyricum-induced depression of drug metabolism. 4 Prolongation of ketamine-induced anaesthesia by combination with Mycobacterium butyricum at day 5 correlated with the degree of hind paw inflammation at this time. 5 The data suggest that anaesthetics (i.e., ketamine and pentobarbitone) may sensitize hepatic membranes to the effect of Mycobacterium butyricum or some toxic compound elaborated during the active phase of inflammation.

Anesthetics↗
PubMed1978

Effects of prostaglandins on vesicourethral smooth muscle of rabbit. Therapeutic implications.

The effects of PGF 2-alpha and PGE2 on the vesicourethral smooth muscle of the rabbit were studied in vitro. PGF2-alpha had potent contractile effects on the bladder body and comparatively less in the bladder base and the proximal urethra. PGE2 contractile effects were two times greater than PGF 2-alpha on the bladder body but minimal or absent on the base and the urethra. The effects of PGF2-alpha and PGE2 seem to be mediated through a prostaglandin receptor as indicated by competitive antagonism of both prostaglandins by N-0164, a synthetic phenyl phosphonate. It also appears that the effects of PGF2-alpha PGE2 may not be mediated through muscarinic, adrenergic, nicotinic, or histaminic receptors or direct smooth-muscle action. The therapeutic implications of PGE2 in the patients with problems of bladder emptying are discussed.

Acetylcholine↗
PubMed1977

Measurement of prostaglandin E2 in an inflammatory exudate: effects of nonsteroidal anti-inflammatory agents.

A method was developed for extracting and measuring nanogram quantities of prostaglandin E2 (PGE2) from carrageenan-induced abscess in the rat. PGE2 concentration, quantitated by radioimmunoassay, was 42.5 and 92.9 ng/g of abscess in two studies. Anti-inflammatory activity, based on reduction in abscess weight, was observed with indomethacin, phenylbutazone, SC-19220 and A-22981; however, only indomethacin (10 mg/kg i.p.) significantly reduced PGE2 levels in the abscess tissue. Dose-related anti-inflammatory activity of indomethacin (1-10 mg/kg i.p.) was directly correlated with reductions of PGE2 content in the abscess. These data support the theory that the anti-inflammatory activity of indomethacin in the carrageenan abscess model involves inhibition of prostaglandin formation. Dose-related suppression of abscess formation by SC-19220 (7.5-30 mg/kg i.p.) was not related to changes in PGE2 levels at the inflammatory site, which suggests that the anti-inflammatory mechanism of SC-19220 is not mediated via inhibition of prostaglandin synthesis.

Abscess↗
PubMedDate not supplied

The interaction of dopamine, cocaine, and cocaethylene with ethanol on central nervous system depression in mice.

The interactions between dopamine, cocaine, cocaethylene, and ethanol were studied in Swiss-Webster mice. The loss of the righting reflex (LORR) was used as a measure of CNS depression. Animals were injected intraperitoneally (IP) with ethanol (4.0 g/kg). which caused a LORR. Immediately upon regaining of the righting reflex, mice were injected intracerebroventricularly (ICV) with saline, dopamine (0.1, 0.5, or 1.0 mumol/kg), cocaine (1, 15, or 25 mumol/kg), or cocaethylene (1, 15, or 25 mumol/kg). In the presence of systemic ethanol, all three compounds produced CNS depression in a dose-dependent manner. The dopamine D2-receptor antagonist sulpiride and the D1-receptor antagonist fluphenazine were given acutely ICV with dopamine in the presence of systemic ethanol to examine whether these antagonists could block the return to the LORR produced by dopamine. Sulpiride, however, actually enhanced the interaction between ethanol and dopamine in a dose-dependent manner as measured by the LORR; fluphenazine neither blocked nor enhanced the effect of dopamine in the presence of systemic ethanol. In addition, these antagonists had no effect on cocaine- and cocaethylene-induced CNS depression in the presence of systemic ethanol. The results of this study showed that the neurotransmitter dopamine and both cocaine and cocaethylene can promote further CNS depression in the presence of systemic ethanol, and that dopamine was significantly more potent than cocaine and cocaethylene as measured by the return to the LORR.

Animals↗