Inhibition of human premature labor by indomethacin.
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Biomedical subjects
Publications and source records attributed to I Rubinstein.
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1. Twenty-two sterols were identified in the starfish Asterias rubens (Phylum, Echinodermata; Class, Asteroidea). 2. The major 4-demethyl sterols had a Delta(7) bond and the C(27) compound 5alpha-cholest-7-en-3beta-ol predominated over other mono- and di-unsaturated sterols belonging to the C(26), C(27), C(28) and C(29) series. 3. Small amounts of cholest-5-en-3beta-ol and 5alpha-cholestan-3beta-ol were also present. 4. The minor sterols identified all contained either one or two methyl groups at C-4 and are considered to be potential biosynthetic precursors of 5alpha-cholest-7-en-3beta-ol. 5. Three sterols possessing a 9beta,19-cyclopropane ring were also isolated and were probably derived by the starfish from a dietary source.
The purpose of this study was to determine the effects of bradykinin (BK), substance P (SP) and histamine on plasma exudation in the skin of conscious dogs with and without pacing-induced heart failure. We also determined the role tissue angiotensin I-converting enzyme (ACE) and neutral endopeptidase (NEP) play in modulating these responses. We found that intradermal injection of BK, SP and histamine induced a significant, concentration-dependent Evans blue exudation in normal dogs (p < 0.05). Bradykinin-induced responses were significantly potentiated by captopril (p < 0.05). In contrast, phosphoramidon potentiated BK-induced responses only at low concentrations of BK. Both captopril and phosphoramidon had no significant effects on SP- and histamine-induced Evans blue exudation. BK- and SP-induced responses were significantly attenuated, whereas histamine-induced Evans blue exudation was significantly potentiated in dogs with heart failure. We conclude that heart failure is associated with attenuation of BK- and SP-, but not histamine-induced plasma exudation in the peripheral microcirculation and that these responses are not modulated by tissue ACE and NEP.
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Our goal was to examine the effects of endothelin-1 and endothelin-3 on hamster cheek pouch arterioles in vivo in the absence and presence of endothelin receptor antagonists. Endothelin-1 (0.1, 1.0 and 10 pM) and endothelin-3 (0.1 and 1.0 nM) produced dose-related constriction of cheek pouch arterioles which was inhibited by the endothelin ETAB receptor antagonist PD 142893 (Ac-D-Dip-Leu-Asp-Ile-Ile-Trp) and endothelin ETA receptor antagonist PD 147953 [FR 139317: (hexahydro-1H-azepinyl)carbonyl-Leu-(N-Me)-D-Trp- D-2-Pya]. The thromboxane analogue, U-46619 (0.1 and 1.0 nM) also produced dose-related constriction of cheek pouch arterioles, but in contrast to endothelin-1 and endothelin-3 this vasoconstriction was not abolished by endothelin receptor antagonists. These findings suggest that endothelin-1 and endothelin-3 produce marked constriction of cheek pouch arterioles which appears to be mediated by activation of endothelin ETA receptors.
The hamster cheek pouch has been used extensively to study the modulation of microvascular responsiveness of native and transplanted tissues, because it is immunologically privileged. The purpose of this study was to determine the structural changes that occur over time in bovine lung tissue (donor) that was grafted into the hamster cheek pouch (recipient). Lungs from adult cows were cut into 1-mm-thick slices and grafted into the cheek pouch of adult Syrian golden hamsters (n = 60). After induction of anesthesia, bovine lung tissue was placed under the avascular tissue covering the cheek pouch, and the overlying skin was sutured. Intravital microscopy (IM) and transmission electron microscopy (TEM) of the cheek pouch and grafted tissue were performed 1, 7, 14, and 28 days after grafting. By using IM, we found blood flow throughout the grafted bovine lung tissue between days 7 and 14 post-transplantation. Both IM and TEM showed that the grafted tissue contained patent microvessels anastomosing with cheek pouch microvessels, alveolar structures, and interstitial tissue. Mast cell infiltration around microvessels of the grafted tissue was evident in all animals between days 14 and 28 post-grafting. No other inflammatory cells were identified throughout the observation period. By day 28 post-grafting, the entire lung tissue became fibrotic. We conclude that bovine lung tissue can be successfully transplanted into the hamster cheek pouch, that blood flow is established throughout the graft, and that prominent mast cell infiltration is associated with fibrosis of the graft 28 days after transplantation. We suggest that this model can be useful in studying pulmonary microvascular responses in situ.
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