Release of slow-reacting substance from guinea-pig and human lung by calcium ionophore A23187 [proceedings].
Explore the source record for details and available documents.
SEARCH · Search PubMed
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Sodium can inhibit the specific binding of leukotriene D4 (LTD4) to its receptors. The effects of sodium on the biological activity of slow-reacting substance (SRS) which contains LTD4 are studied here. SRS was produced in leukocytes from seven normal donors. Its activity was bioassayed by guinea pig ileum contraction in an organ bath containing Tyrode's solution with 0.11 M NaCl. With higher concentrations of NaCl, the SRS-induced ileum contraction increased 45% at 0.14 M of NaCl (P less than 0.02), and 55% at 0.18 M NaCl (P less than 0.02). When NaCl concentration was increased to 0.21 M, the contractibility only increased 18% from the baseline (0.11 M NaCl), evidencing no statistical difference. The direct effect of changing NaCl solution from 0.11 to 0.21 M was to induce a significant ileum contraction with dose-related pattern.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Effect of IV infusions of smooth and rough Pasteurella hemolytica lipopolysaccharides (LPS; 24 ng/kg/min for 500 min) on circulating levels of arachidonic acid, prostaglandins (PG), thromboxane B2 (TxB2), histamine, and serotonin in calves was evaluated. Both smooth and rough LPS had no effects on plasma PGE but caused maximal increases in arachidonic acid, TxB2, and PGF2 alpha at 1 hr and 6-keto-PGF1 alpha at 3 hr of infusion, respectively. The increases in arachidonic acid and its metabolites were greater and more prolonged for smooth LPS than for rough LPS. Although both rough and smooth LPS increased plasma serotonin transiently at 25 min of infusion, only rough LPS decreased serotonin in the later period of endotoxemia. In contrast, smooth, but not rough, LPS decreased plasma histamine during endotoxemia. These results indicate that during endotoxemia there is increased PG and TxA2 synthesis secondary to marked arachidonic acid release into circulation. The data also demonstrate that smooth and rough LPS differ in their abilities to release histamine, serotonin, and eicosanoids. These effects might be due to differences in the in vivo mechanisms of action of smooth and rough LPS and may partly explain the differential potency of smooth and rough LPS in producing pathophysiological changes.
Explore the source record for details and available documents.
The presence of alpha 1-receptors has been demonstrated in numerous venous fragments for various animal models. On the other hand, the presence of alpha 2-receptors in the saphenous of the dog is a matter of debate. Beta 2-receptors are activated by isoproterenol, noradrenaline and adrenaline in precontracted veins (part of the facial vein of the rabbit may be an exception). Preferential blocking by atenolol of beta 1-receptors in the jugular veins of the rat suggests that these receptors may mediate vasodilation. The saphenous veins of the dog provide the only example where specific dopaminergic receptors have been noted following partial antagonism with haloperidol. The vasoconstrictive action of acetylcholine has been seen in venous segments of numerous species and indicates the presence of muscarinic receptors. The existence of angiotensin receptors can be postulated despite the weak and inconstant in vitro and in vivo (the dorsal cerebral sinus in the dog excepted) reactions observed and the use of a non-specific antagonist. The same is true for bradykinin and vasopressin. The marked vasoconstrictive action of serotonin on all veins studied is evidence for the presence of receptors. The nature of the antagonists is subject to some divergence of opinion. Nevertheless, D tryptamine muscular receptors (or 5 HT2) can be identified due to the lack of morphine-mediated response and the efficacy of methysergide. The presence of a third type of serotoninergic receptor has only been reported once, following observations of vasodilation in the sheep. H1 receptors are involved in histamine-mediated vasoconstriction. The presence of H2 receptors which mediate vasodilation in precontracted veins remains hypothetical. Prostaglandins exhibit different efficacies in producing contraction in isolated veins; PGF2 alpha is more efficacious than PGE1 and PGE2. Prostacyclin induces contraction of human saphenous veins in a dose-dependent manner. PGE2 and particularly PGE1 can induce relaxation in precontracted veins, as is also true for prostacyclin. Receptors for these prostaglandins must exist at the post-junctional level. P2-receptors mediate transmission of the vasoconstrictive action of various purine derivatives.
These discussions are selected from the weekly staff conferences in the Department of Medicine, University of California, San Francisco. Taken from transcriptions, they are prepared by Drs Homer A. Boushey, Professor of Medicine, and David G. Warnock, Associate Professor of Medicine, under the direction of Dr Lloyd H. Smith, Jr, Professor of Medicine and Associate Dean in the School of Medicine. Requests for reprints should be sent to the Department of Medicine, University of California, San Francisco, School of Medicine, San Francisco, CA 94143.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Serotonin (5-HT), histamine (HA), angiotensin II (ATII), prostaglandin F2 alpha (PGF2 alpha) and thromboxane A2 (TxA2) are known as vasoactive substances, each producing a characteristic contraction of cerebral arteries. These contractions are considered to be mediated by their specific receptors. Recent studies suggest that the activations of these receptors primarily stimulate the phospholipase C and/or phospholipase A2 localized within the same membrane. Stimulation of these enzymes consequently induces production of the second or third messengers such as inositol triphosphate (IP3), diacylglyceride (DAG), arachidonic acid (AA), and ultimately various prostaglandins. The present study is to examine how oxyhemoglobin (Oxy-Hb), another vasoactive substance, can modify these receptor-mediated contractions, and to compare the effects on high K+-, caffeine-and 1-oleoyl-2-acetyl-rac-glycerol (OAG)-induced contractions which are not mediated by the receptors on the cytoplasmic membrane. Helical strips of the bovine middle cerebral arteries (M2) were mainly used in this experiment, and the changes in muscular tensions during isometric contractions were recorded on the polygraph. 5-HT, HA, ATII, PGF2 alpha and cTxA2 (carbocyclic thromboxane A2) were used for each receptor activation. Indomethacin (IDM), a cyclooxygenase inhibitor and 2-nitro-4-carboxyphenyl-n, n-diphenyl-carbamate (NCDC), a phospholipase C inhibitor were used to analyze a possible acting site of Oxy-Hb in modifying these reseptor-mediated enzyme reactions. The results obtained are summarized as follows. (1) All contractions induced by either 5-HT, PGF2 alpha, cTxA2, HA or ATII (concentrations less than 10(-6) M) were markedly augmented as much as 4-8 times the normal, when they were examined in the presence of 10(-5)M Oxy-Hb.(ABSTRACT TRUNCATED AT 250 WORDS)
Explore the source record for details and available documents.
Drugs used to control inflammation in the rheumatic diseases are extremely diverse. Despite this, the pattern of clinical response and similarities in side-effects allow them to be subdivided into groups. These patterns also provide clues about the mode of action of the drugs. Conversely, studies of the mechanisms of action of drugs used to treat rheumatoid arthritis are beginning to throw light on the pathological process.
Vasomotor rhinitis is commonly defined as an unspecific hyperractivity of the nasal mucosa. The symptoms might be due to increased parasympathetic activity to the nose with the release of vaso-secretory active substances. Experimental data from the cat suggest that the postganglionic parasympathetic mediator of nasal secretion is cholinergic, whereas the vascular responses appears to be due to a different mechanism. Apart from a rich sympathetic and parasympathetic innervation of the nasal mucosa there are other nerve fibres containing substance-P (SP) and vasoactive intestinal polypeptide (VIP). The secreto-vasomotor responses can be influenced by activation of these fibres and the atropine resistant vasodilatation seen following Vidian nerve stimulation thus may partly be due to activation and release of SP and VIP. Furthermore, other vasoactive substances released such as e.g. SRS or Kallikrein may participate in these reactions.
Explore the source record for details and available documents.
Explore the source record for details and available documents.