Mode of action of disodium cromoglycate.
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Antigen-Antibody Reactions↗
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Inhibition by suprofen and other non-narcotic analgesic drugs of the effects of prostaglandin precursor on isolated tissues and platelets.
Contractions caused by Slow Reacting Substance C(SRS-C) and by Arachidonic Acid hydroperoxide (AAP) in the guinea-pig ileum and by AAP in the rat fundus were studied in the presence of suprofen and of 3 reference compounds. The dose-related inhibitions were not due to antagonism of prostaglandins. Other agonists of gastrointestinal smooth muscle were not or only weakly antagonized. For the study of selective inhibition of AAP-induced contractions by non-narcotic analgesics, the rat fundus is the preferred preparation. In this model suprofen had an ED50 of 1.27 x 10(-7) M (0.033 mug/ml), being 1.5, 94 and 2, 020 times more potent than indomethacin, phenybutazone and acetylsalicylic acid, respectively. Suprofen also strongly inhibited malondialdehyde formation by guinea-pig platelets incubated with arachidonic acid. The reported effects point to inhibition by suprofen of prostaglandin biosynthesis. The antagonism of AAP-induced contractions in the rat fundus is a valuable test system for inhibitors of prostaglandin biosynthesis.
Analgesics↗
Effects of inflammatory mediators on electrolyte transport across the porcine distal colon epithelium.
The epithelium from the porcine distal colon was mounted in Ussing chambers and bathed in plasma-like Ringer's solution. Histamine produced increases in current which were not affected by pretreatment with the neural conduction blocker tetrodotoxin. Both the H1-histamine antagonist pyrilamine and the cyclooxygenase inhibitor indomethacin produced dextral shifts in the histamine concentration-response curve. Replacement of Cl with gluconate or HCO3 with tris(hydroxymethyl)aminomethane(tris)-N-2- hydroxyethylpiperazine-N'-2-ethanesulfonic acid in the bathing solution inhibited the mucosal response to histamine by 74 and 23%, respectively. In addition, histamine increased the serosal-to-mucosal Na and Cl fluxes and inhibited the mucosal-to-serosal Na flux, resulting in a reduction of net Na and Cl absorption. Prostaglandin E2 also produced increases in short-circuit current which remained unaffected by tetrodotoxin. Replacement of either Cl or HCO3 inhibited these increases by 85%. Prostaglandin E2 inhibited the mucosal-to-serosal and net Cl fluxes. Leukotriene C4 produced oscillating increases in the short-circuit current which were completely blocked by tetrodotoxin. These increases in current were attributed to an increase in the serosal-to-mucosal Cl flux which resulted in a decrease in net Cl absorption. From these data it was concluded that: 1) histamine interacts with H1-receptors to increase Na and Cl secretion and inhibit Cl absorption; 2) prostaglandin E2 inhibits a HCO3-dependent Cl absorptive pathway, possibly involving Cl/HCO3 exchange and 3) leukotriene C4 acts on enteric nerves to stimulate Cl secretion.
Animals↗
[Drug therapy of rheumatoid arthritis].
Continuous, computer-aided registration of large numbers of patients with rheumatoid arthritis (RA) had lead to a revised concept of the prognosis. More patients than previously throught develop severe progressive, erosive, deforming, and crippling disease. Most of the permanent damage develops within the first 10 years of the course of the disease. The patients die 10-15 years before the background population, even though the cause of death is rarely a direct consequence of the disease. Because of these observations, the treatment strategy is now becoming more aggressive than previously. Treatment with slow acting anti-rheumatic drugs (SAARDs) is started within the first year. Synovitis activity is monitored continuously, and in case of primary or secondary resistance to one SAARD the drug is replaced by another one for as long as the disease is active. This procedure makes it necessary that all patients with suspected RA be evaluated early and repeatedly by rheumatologists during the whole course of the disease. The drug treatment should be conducted with close cooperation between the general practitioners and the rheumatologists.
Anti-Inflammatory Agents↗
Ultrastructural localization of substance P-like immunoreactivity in the intermediolateral column of spontaneously hypertensive rats and Wistar-Kyoto rats.
The distribution of substance P in the intermediolateral column of the upper thoracic spinal cord of spontaneously hypertensive (SHR) rats and Wistar-Kyoto (WKY) rats was studied by combined retrograde tracing of choleragen subunit-B horseradish peroxidase (CB-HRP) and immuno-electronmicroscopy. In the T(1)-T(3) segments of the spinal cord, SP-like immunoreactive products were localized in the cell bodies and dendrites of the sympathetic preganglionic neurons as well as in a few pre-axon terminals or axon terminals. In the neuropil of the intermediolateral column (ILN), different synaptic configurations were observed including synaptic contacts between SP-like positive dendrites and negative axon terminals, and between SP-like positive axon terminals and SP-like positive dendrites. Furthermore, a single SP-like positive dendrite was sometimes postsynaptic to several axon terminals, a feature typical of glomerular synapses. The present findings suggest that most of the SP-like immunoreactive elements in the ILN were of intraspinal origin derived mainly from the sympathetic preganglionic neurons in SHR and WKY rats. Since there was no ultrastructural difference in the distribution of SP between the neural elements in the ILN of SHR and WKY rats, the present findings also suggest that SP may not be directly involved in the hyperactivity of the sympathetic nervous system in hypertension.
Animals↗
[Humoral and immunological aspects of acute respiratory failure].
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Anaphylaxis↗
[Lymphocytes as markers of etiologic and pathogenetic factors of infectious diseases].
In the examination of patients with the dermato-respiratory syndrome, peptic ulcer, pyoderma and surgical wounds for their immune status for the expression of receptors of immunocytokins (interferon, interleukin-2), autocoids (histamine, serotonin), neuromediators (acetylcholine, dopamine, epinephrine, norepinephrine) and for the presence of Staphylococcus aureus and Helicobacter pylori antigens have revealed that lymphocytes are the markers of the presence of infection in the body, pathogenetic systemic and intersystemic disturbances, adequately chosen therapy and its effectiveness.
Autacoids↗