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At least 1,171 records · Page 65Linked to original sources
PubMed1983

Control of Arthus tonsillitis by the administration of an antiplasminic agent.

Previous reports have shown that fibrinolytic activity was increased in the circulatory blood of rabbits with Arthus tonsillitis. In this study, t-AMCHA was administered intravenously to rabbits, in order to clarify its role as an antiplasminic agent in the control of Arthus tonsillitis. First, to establish the proper method of administration of t-AMCHA and the quantity to be administered, a preliminary estimation was made of the requisite concentration of t-AMCHA in the circulating blood and tonsillar tissue. Then macroscopic observations and histopathological studies were performed on the tonsils of rabbits with Arthus tonsillitis after t-AMCHA administration at various doses. Finally, after injection of the antiplasminic agent, estimations were made of the plasma fibrinolytic activity in the blood of the rabbits under study. It was decided that administration of t-AMCHA at 3-hourly intervals could maintain a constant concentration of the substance in the tonsillar tissue. The marked hyperaemia and bleeding which were observed macroscopically and histopathologically at 1-2 days after the onset of tonsillitis, disappeared from the parenchyma of the tonsils and pharyngeal tissue surrounding the tonsils in the group receiving regular injections of t-AMCHA at 3-hourly intervals. After estimating certain parameters of the fibrinolytic system in the blood, it was found that fibrinolytic activity decreased and whole plasmin was not consumed as a result of the administration of t-AMCHA during the early stage of tonsillitis. The process of Arthus tonsillitis can thus be controlled by the administration of the antiplasminic agent.

Animals↗
PubMed1981

Antifibrinolytic therapy in patients with aneurysmal subarachnoid hemorrhage. A report of the cooperative aneurysm study.

Antifibrinolytic therapy was used in 1,114 patients who had aneurysmal subarachnoid hemorrhage (SAH) and who were treated by the 13 institutions of the Cooperative Aneurysm Study. Patients were started on treatment within one week after SAH was diagnosed, and therapy was discontinued 14 days after the ictus. Rebleeding occurred in 10% of the treated patients. Overall mortality among the treated patients during the two weeks following hemorrhage was 10.7%. Though some minor and a few major side effects occurred, serious complications of therapy were infrequent.

Adolescent↗
PubMed1988

Outcome of aneurysmal subarachnoid hemorrhage in patients 66 years of age and older.

The outcome at three months after aneurysmal SAH in a group of older patients and a group of younger patients is compared. The patients were admitted within 72 hours of their SAH. Of 61 patients 66 years of age and older, comprising 13% of the whole patient group, 52% died, 12% remained dependent and 36% became independent. In the younger group, 55% had an independent outcome (p less than 0.01). In contrast to what we expected in the older patient group, not extracranial, but intracranial events (re-bleeds, infarcts, hydrocephalus) were by far the most frequent cause of deterioration.

Age Factors↗
PubMed1988

Cytoprotective action of cetraxate against HCl.ethanol-induced gastric lesion in rats.

The protective effect of cetraxate, an antiulcer and antigastritis agent, on HCl.ethanol-induced gastric lesions was investigated in rats. Oral administration of 1 ml of HCl.ethanol (60% ethanol in 150 mM HCl) induced within 1 hr linear hemorrhagic necrosis in the gastric mucosa. Either oral or intraperitoneal treatment with cetraxate (30-300 mg/kg) significantly inhibited such macroscopic gastric lesions in a dose-related manner, and the inhibition at the oral highest dose (300 mg/kg) was practically complete. Histological analysis also confirmed that cetraxate effectively prevented deep mucosal necrosis, but showed that it was without protective effect on the surface epithelial disruption and submucosal edema in response to HCl.ethanol. The antilesion activity of cetraxate was of statistically significance for at least 3 hr after a single injection, and it was hardly affected by the removal of the gastric contents just prior to application of the necrotizing agent. However, subcutaneous treatment of rats with indomethacin (5 mg/kg) resulted in a partial but significant attenuation in the protection afforded by cetraxate, suggesting that dual mechanisms related and unrelated to endogenous prostaglandins may be involved in its protective activity. The results demonstrate that cetraxate is a potent cytoprotective agent effectively preventing the formation of gastric mucosal necrosis induced by HCl.ethanol.

Animals↗
PubMed1982

[Experimental studies on the diffusion of antifibrinolytic agents in fibrin thrombi. A contribution to intrathecal antifibrinolytic therapy in subarachnoid hemorrhages].

The diffusion behaviour and the diffusion coefficients of antifibrinolytics in fibrin thrombi were determined by in vitro incubating attempts with tritium marked compounds of PAMBA, AMCA, and ECA as well as by chromogenic substrate determination for contrykal. The great diffusion ability of PAMBA supports the usefulness of intrathecal therapy of subarachnoidal bleeding for blocking endogenous fibrinolysis, whereas the exogenous fibrinolysis of the fibrin thrombus closing aneurysm is inhibited by the intrathecal application.

4-Aminobenzoic Acid↗
PubMed1983

Therapeutic effects of cetraxate against acute gastritis and acute aggravation of chronic gastritis. Endoscopic investigation by the double-blind method.

To determine the efficacy of cetraxate against acute gastritis and acute aggravation of chronic gastritis, a comparison was made with aldioxa as the standard drug by the double-blind method based mainly on observations by gastroscopy. There were four types of gastroscopic findings used: hemorrhage, erosion, redness and edema. Observations were performed whenever possible before and 1, 2 and 4 weeks after administration, and the cure and improvement rates were investigated. The cure rates for each finding except edema after 1 and 2 weeks were better (in the order of redness, erosion and hemorrhages) in the cetraxate group than in the aldioxa group, and there was a significant difference for redness in the 1st week (p less than 0.05). The no change and aggravating rates were also lower for redness in the 1st week (p less than 0.05) and edema in the 1st week (p less than 0.10) in the cetraxate group than in the aldioxa group. There were almost no differences in the effects of both drugs on subjective symptoms. The safety based on type and incidence of side effects was considered to be high for both drugs. From these results, it appeared that cetraxate is effective against acute gastritis and acute aggravation of chronic gastritis.

Acute Disease↗
PubMed1983

Chemical control of hyperfibrinolytic states by synthetic inhibitors of fibrinolytic enzymes.

The effects of two types of synthetic inhibitor of fibrinolytic enzymes (omega-aminocarboxylic acids, benzamidine derivatives) on intravascular fibrinolysis and fibrinogenolysis were studied in rats. Generalised primary fibrinogenolysis was produced by infusion of human plasminogen-streptokinase complex, secondary fibrinolysis was induced by infusion of the thrombin-like enzyme batroxobin. The inhibitors exerted different effects on the hyperfibrinolytic states. The omega-aminocarboxylic acids (PAMBA, AMCA) inhibited fibrinolysis more effective than fibrinogenolysis. In contrast, the benzamidines (APPA, NANP) were more potent inhibitors of fibrinogenolysis. Aprotinin examined for comparison behaved like the benzamidine derivatives.

4-Aminobenzoic Acid↗
PubMedDate not supplied

Influence of some monoamine oxidase inhibitors on the sleep-wakefulness cycle of the cat.

The influence of some monoamine oxidase inhibitors (phenelzine, transamin [tranylcypromine], nialamide) on the structure of the sleep-wakefulness cycle of the cat was studied. It was shown that these monoamine oxidase inhibitors elicit and increase in slow-wave sleep in the sleep-wakefulness cycle due to complete suppression of paradoxical sleep and significant decrease in wakefulness. After the cessation of the action of the monoamine oxidase inhibitors, a selective rebound of wakefulness is observed against the background of complete or partial absence of paradoxical sleep. The gives grounds for the hypothesis that during partial deprivation of wakefulness under the influence of monoamine oxidase inhibitors an intensification occurs on the accumulation of specific need for this physiological state, the satisfaction of which is accomplished as the result of its rebound in the post-deprivational cycle, i.e., after the termination of the EEG of the synchronizing effect of the monoamine oxidase inhibitors.

Animals↗
PubMed2004

Hemostatic agents.

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Aminocaproic Acid↗
PubMed1999

Hemostatic agents and their safety.

The pharmacologic management of hemostasis in patients undergoing cardiopulmonary bypass may be accompanied by adverse responses. Evaluating the safety profile of hemostatic agents (eg, lysine analogs, aprotinin, protamine, or even donor blood) should be done objectively. Subsequent to early anecdotal reports, the safety profile of aprotinin, a broad-spectrum serine protease inhibitor, has been thoroughly evaluated in multiple double-blind, placebo-controlled, multicenter studies. Although associated with decreased fibrinolysis, aprotinin has not been associated with an increased risk of post-cardiopulmonary bypass myocardial infarction, graft closure, stroke, or increased risk of renal dysfunction from US studies. As with any polypeptide, there is a risk of anaphylaxis, which is influenced not only by prior exposure but also by time since prior exposure. In a similar fashion, after early anecdotal reports, evaluations involving large numbers of patients have helped define adverse reactions to protamine. Adverse reactions to blood products also must be considered in any safety comparisons involving hemostatic agents.

Aminocaproic Acid↗
PubMed2003

Antifibrinolytics.

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Aminocaproic Acid↗