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PubMed1977

Study of the repercussions on blood of acute experimental inflammation in rats. II. Blood changes in the course of carrageenin induced inflammation.

Repercussions on blood of inflammation induced by carrageenin injection in the four paws of rats were studied. Two stages were observed. 4 h after carrageenin injection, a high fall in leucocyte count and a small decrease in blood total proteins and blood fibrinogen were registered. ADP mediated platelet aggregation and sedimentation rate were not modified. 24 h after carrageenin injection, sedimentation rate and blood fibrinogen were increased; some platelet hyperaggregation with ADP was also observed.

Adenosine Diphosphate↗
PubMed1998

Double-masked, placebo-controlled evaluation of loteprednol etabonate 0.5% for postoperative inflammation. Loteprednol Etabonate Post-operative Inflammation Study Group 1.

PURPOSE: To compare the efficacy and safety of loteprednol etabonate 0.5% with those of a placebo (vehicle) in controlling anterior chamber cell and flare reaction in patients having cataract surgery with intraocular lens (IOL) implantation. METHODS: This randomized, double-masked, placebo-controlled, parallel-group multicenter study comprised patients who exhibited a minimum anterior chamber inflammation (ACI) score (sum of cell and flare reaction) of 3 (0 to 9 scale) on the day after cataract removal with posterior chamber IOL implantation. All 227 patients received loteprednol etabonate 0.5% or the placebo 4 times a day in the operated eye for up to 14 days after surgery. Five patients without valid on-treatment follow-up visits were not evaluated for efficacy. RESULTS: By the final visit, the ACI had resolved in 64% (70/109) of patients in the loteprednol etabonate group and 29% (33/113) of those in the placebo group (P < .001). The resolution rate and mean change from baseline of the individual components of ACI (cell and flare), as well as other signs and symptoms, was better in the loteprednol etabonate group. Both treatments were well tolerated. Among the 53 patients who did not complete the study, 34 (29%) were placebo patients discontinued for inadequate anti-inflammatory effect. The treatment failure rate and the time course of failures were lower in the loteprednol etabonate group; the differences were clinically meaningful and statistically significant (P < .001). Three patients in the loteprednol etabonate group had an intraocular pressure elevation of 10 mm Hg or more over the preoperative screening value. CONCLUSION: Loteprednol etabonate 0.5% led to a clinically meaningful reduction in the signs and symptoms of postoperative ACI and had an acceptable safety profile when compared with a placebo.

Adult↗
PubMed1975

Inflammation of the skin. I. Phospholipid metabolism in some experimental inflammations of mouse skin.

Phospholipid metabolism in inflamed tissue of the mouse skin which had been induced by the application of 1-chloro-2, 4-dinitrobenzene (DNCB), croton oil, or irradiation of ultraviolet rays was examined, and it was found that phospholipid levels had increased in theinflamed tissues. In the case of ultraviolet rays, the increase was temporary, and the level returned to that of control after 3 or 4 days. In the case of DNCB or croton oil, the level increased after a decrease for a short period. The pattern of the increase between physical and chemical irritation was different. Increase of incorporation of 32-P into phospholipid in inflamed tissue was examined, and it was observed that the level reached a maximum after one day. It is thus assumed that phospholipid plays an important role in the mechanism of inflammation.

Animals↗
PubMed1975

Anaphylactoid-inflammation-promoting factor. An insulin-induced factor derived from non-sensitized lymphocytes increases anaphylactoid inflammation in rats.

The experiments reported here indicate that, when exposed to insulin, viable lymphocytes rapidly released into the incubation medium a factor capable of increasing the dextran-induced anaphylactoid reaction, but having no effect on the inflammatory response evoked by 5-HT. This pro-inflammatory factor was shown to be elaborated by cell suspensions derived from lymph nodes of rats, rabbits, pigs or calves as well as from human tonsils. Thymus cells showed no such activity. The pro-inflammatory factor was termed as anaphylactoid-inflammation-promoting factor (AIPF). Its production depended upon the dose of insulin, and the time of exposure. AIPF was found to have an elution pattern in Sephadex G-100 gels similar to that of BSA (67,000 daltons). The activity was abolished by heat or incubation with DNase or a-chymotrypsin, but was not influenced by RNase. AIPF by itself did not induce increased vascular permeability, and proved to be distinct from the permeability factors present in the lysate of lymph node cells.

Adrenalectomy↗
PubMed1990

[Clearance rate of gingiva and content of collagen of inflammated and clinically non-inflammated papilla interdentalis].

UNLABELLED: The gingiva vessel function has been defined by gingivitis (A), clinical sound gingiva without (B) and with loss in attachment (C) as well as the collagen fraction by biopsy material. The division of the probands at the age between 20 and 24 years into groups has been carried out after checking the SBI, PII (Silness/Loe) and the loss of attachment of the teeth 43-33. The vessel function has been found out through the impulse rate of the gingiva Xenon-133-clearance by calculating the clearance rates (CR) (groups: A1 n = 15; B1 n = 18; C1 n = 16). The vestibular interdental papillae have been elaborated in a second study for finding out the collagen fractions with the Stegemann method modified by Woessner (groups: A2 n = 18; B2 n = 10; C2 n = 12). The statistical reliability has been checked by the t-test (F-test) and the u-test by Mann and Whitney. RESULTS: In the clearance study the CR in group A1 are higher and in group C1 lower than in group B1. In the second study the increased collagen solubility in group A2 by inflammation is confirmed, in group C2 a significant higher share in unsoluble collagen and total collagen has been defined than in group B2.

Adult↗
PubMed1981

Antigen handling in antigen-induced joint inflammation: kinetics of a second intra-articularly injected dose of antigen in an already established antigen-induced joint inflammation.

The fate of a second intra-articularly (i.a.) injected dose of bovine serum albumin (BSA) in an already established BSA-induced knee-joint inflammation was compared with that of a paired first arthritis-inducing injection of the same dose of BSA into the contralateral knee of immunized rabbits. External counting of i.a. radiolabelled BSA indicated more rapid initial elimination but approximately two-fold increase in long-term retention of BSA after a second i.a. injection as compared with a first one. Direct counting of dissected joint structures confirmed these data and localized the retained BSA predominantly in hyaline articular cartilage, menisci and ligaments, both after a first and after a second injection. Since the protocol used in these studies per se excluded systemic factors as possible determinants of the difference in antigen retention observed, local alterations in the already inflamed joint caused this difference. Control studies indicated that both humoral immune factors and non-specific inflammatory changes within the chronically inflamed joint determine the phenomenon. Local alterations in an immune-induced chronically-inflamed joint increase its antigen-binding capacity, a mechanism of possible relevance to the chronic course and the occurrence of exacerbations characteristic of some forms of human arthritis.

Animals↗
PubMed2006

Pravastatin reverses the down-regulating effect of inflammation on beta-adrenergic receptors: a disease-drug interaction between inflammation, pravastatin, and propranolol.

Inflammatory conditions reduce the potency to prolong the PR interval of certain cardiovascular drugs including propranolol, sotalol, and verapamil in rats and humans despite elevated plasma drug concentrations. We tested whether pravastatin restores altered action and disposition of propranolol as well as inflammatory mediators concentrations in the Pre-Adjuvant Arthritis (Pre-AA) Sprague-Dawley rat model. Rats [Healthy/Placebo, Arthritis/Placebo, Healthy/Statin, and Arthritis/Statin groups (n=14-16/group)] received Mycobacterium butyricum on day 0 followed by 6 mg/kg pravastatin or placebo twice daily during days 4-8. PR-interval response to 25 mg/kg oral propranolol was measured on days 0, 4 and 8. On day 8, blood samples were collected for interferon-gamma, interleukin-10, C-reactive protein, and nitrite measurements. Propranolol enantiomer pharmacokinetics were delineated using another 4 groups (healthy n=5, Pre-AA n=9) on day 8. Pre-AA significantly reduced propranolol response despite a 10-fold increase in concentrations. Pravastatin restored the response but not the drug concentrations. Area under the % effect-time curve (% min) was 714+/-214 in Healthy/Placebo, 256+/-249 in Arthritis/Placebo, 1534+/-367 in Healthy/Statin, and 1713+/-393 in Arthritis/Statin. While pravastatin reduced elevated serum interferon-gamma concentration in the Pre-AA model, it did not influence other biomarkers. Pravastatin restores response to propranolol in inflamed rat but has no effect on the elevated propranolol concentrations. This was associated with lower serum interferon-gamma concentrations.

Adrenergic beta-Antagonists↗