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Reprod Fertil Dev. 1996;8(3):335-46.
Effects of lung expansion on lung liquid production in vitro by lungs from fetal guinea-pigs. I. Basic studies and the effects of amiloride and propranolol.

Nelson PG, Perks AM.

Department of Zoology, University of British Columbia, Vancouver, Canada.

Lungs from near-term fetal guinea-pigs were supported in vitro for 3 h; lung liquid production was measured by a dye-dilution method using Blue Dextran 2000 (fetuses 62 +/- 2 days of gestation, 97.6 +/- 19.0 (SD) g body weight; n = 134). Untreated control preparations produced fluid at 1.30 +/- 0.22 ml/kg body weight per h, and showed no significant changes during incubation (n = 30). After 1 h of incubation, experimental lungs were expanded with Krebs-Henseleit saline in volumes estimated to be below or approximating those of the first breath (n = 30; first breath, 0.6-1.2 ml). Expansions were graded at 18 +/- 4%, 31 +/- 4%, 43 +/- 3%, 50 +/- 3% and 72 +/- 2% of lung volume (volumes used for expansion at the maximal level, 0.64 +/- 0.25 ml). All expansions of 31% or above produced reductions in fluid production significant by analysis of variance (P < 0.01-0.001); production halted at 50% expansion, and there was strong reabsorption at 72% expansion (-0.87 +/- 0.45 ml/kg body weight per h by the final hour). There was an exponential relationship between percentage expansion and percentage fall in production (r = 1.00). There was no evidence for excessive pressure, and no evidence for lung damage as judged by electron microscopy or entry of intracellular materials into the fluid (lactic dehydrogenase, protein, K+). In studies based on 36 preparations, 10(-6) M amiloride present in the lung lumen (apically) abolished the reabsorptions seen at 70 +/- 3% expansion, but not the arrest of production; it had no effect on control preparations. Studies based on 24 preparations showed that responses to 72 +/- 2% expansion were not affected by 10(-7) M propranolol placed in the outer saline. In studies of 14 fetuses of widely different body weights (68.3-124.9 g), responses to 74 +/- 2% expansion showed an exponential increase with increasing body weight (r = 0.96). Although caution is needed, the results suggest that expansion of the lungs at birth may induce fluid reabsorption by an action independent of tissues outside the lungs, probably involving both activation of a Na(+)-based reabsorptive system and arrest of production, but not requiring beta-receptor activation. The probability that the responses are maximal at birth is discussed, and it is suggested that the effect of expansion may be a specialization of the perinatal lung.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8795095&dopt=Abstract




J Biochem (Tokyo). 1996 May;119(5):852-6.
Beta-Adrenergic receptors in rat fat cells and their relationship with lipolysis.

Okuda H, Morimoto C, Tsujita T.

2nd Department of Medical Biochemistry, School of Medicine, Ehime University.

Norepinephrine stimulated lipolysis in rat fat cells while (-)-alprenolol completely inhibited this lipolysis. (-)-Alprenolol competed for (-)-[3H] dihydroalprenolol (DHA) binding sites on rat fat cells. The specific (-)-[3H]DHA binding sites identified by competition with (-)-alprenolol were found to be transferred to the solubilized supernatant during preparation of endogenous lipid droplets from the fat cells. Although the lipid droplets did not exhibit specific (-)-[3H]DHA binding, norepinephrine induced lipolysis in a cell-free system consisting of the lipid droplets and hormone-sensitive lipase (HSL). Norepinephrine-induced lipolysis in the cell-free system was inhibited by propranolol and (-)-alprenolol, but not by phenoxybenzamine. The lipolytic action of norepinephrine and the anti-lipolytic actions of propranolol and (-)-alprenolol disappeared after sonication of the lipid droplets in the cell-free system. These results suggest that the adrenergic receptor concerned with lipolysis in fat cells may not be a specific (-)-[3H]DHA binding site, but may be closely related to the lipid droplets.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8797083&dopt=Abstract




Br J Pharmacol. 1996 Jun;118(4):865-70.
Effects of beta-adrenoceptor antagonists on Ca(2+)-overload induced by lysophosphatidylcholine in rat isolated cardiomyocytes.

Chen M, Hashizume H, Abiko Y.

Department of Pharmacology, Asahikawa Medical College, Japan.

1. The effects of beta-adrenoceptor antagonists including (-)- and (+)-propranolol, (-)- and (+)-penbutolol, timolol, pindolol, atenolol, acebutolol and practolol on the Ca(2+)-overload induced by lysophosphatidylcholine (LPC) were examined in isolated cardiomyocytes of the rat. 2. Fura-2 was used for measurement of the intracellular calcium concentration ([Ca2+]i). LPC (15 microM) produced a rapid increase in [Ca2+]i from 72 +/- 5 to 3042 +/- 431 nM which coincided with a decrease in the percentage of rod-shaped cells from 69 +/- 2 to 5 +/- 2%. 3. Preincubation with (-)-propranolol (20 microM), (+)-propranolol (50 microM), or (-)- or (+)-penbutolol (20 microM), the lipophilicity of which is higher than other beta-adrenoceptor antagonists, significantly inhibited both the increase in [Ca2+]i and the cell-shape change induced by 15 microM LPC. The inhibitory effects of the four drugs on the LPC-induced increase in [Ca2+]i and cell-shape change were concentration-dependent. The IC50S of (-)-propranolol, (+)-propranolol, (-)- and (+)-penbutolol for the increase in [Ca2+]i were 1.28, 10.50, 0.67 and 0.76 microM, respectively. 4. Pretreatment with pindolol, timolol, acebutolol, practolol, atenolol or lignocaine did not inhibit the increase in [Ca2+]i and the morphological change induced by LPC. 5. LPC markedly increased the release of creatine phosphokinase from 9 +/- 1 to 45 +/- 2% which could be significantly reduced by (-)- or (+)-propranolol but not by acebutolol or timolol. 6. The protective effects of (-)- and (+)-propranolol, (-)- and (+)-penbutolol against the Ca(2+)-overload induced by LPC were not associated with the beta-adrenoceptor antagonistic action, but probably with an unknown action which is related to the preservation of membrane integrity. Further studies are necessary to clarify the exact mechanisms of the protective action of these beta-adrenoceptor antagonists against the Ca(2+)-overload induced by LPC.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8799555&dopt=Abstract












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