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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↗
PubMedDate not supplied

Inosiplex: metabolism and excretion of the dimethylaminoisopropanol and p-acetamidobenzoic acid components in rhesus monkeys.

The principal excretion products derived from radiolabeled N,N-dimethylaminoisopropanol (Dip) and p-acetamidobenzoic acid (PAcBA) components of inosiplex (Isoprinosine) were identified and quantified in urine following single iv and oral administration of the drug in rhesus monkeys. The major metabolite derived from [3H] PAcBA was identified as PAcBA-O-acylglucuronide by 1) positive naphthorescorcinol reaction for glucuronic acid and 2) hydrolysis of the metabolite to PAcBA and glucuronic acid, using either dilute base (but not acid) or beta-glucuronidase. This metabolite accounted for 50% of the administered dose in orally dosed animals and 31% in iv dosed animals. A minor metabolite, which constituted approximately 5% of the excreted 3H from either iv or orally dosed animals, was identified as the hippuric acid conjugate of PAcBA by co-chromatography with a commercial standard. A single metabolite derived from [14C]Dip was identified as Dip-N-oxide by co-chromatography with synthetic material in several chromatographic systems; this metabolite accounted for 17 to 18% of the administered 14C in either the iv or orally dosed animals.

4-Aminobenzoic Acid↗
PubMed1984

A possible explanation of mechanisms inducing inhibition of vascularization of tumours by antifibrinolytic drugs--the influence of migratory behaviour of endothelial cells.

The observation that administration of antifibrinolytic drugs results in tumour growth stasis, having possibly its origin in reduced vascularization of the tumour, led us to investigate the migratory behaviour of bovine endothelial cells under in vitro conditions in the presence of drugs known to influence the activity of fibrinolytic enzymes. The Boyden-technique and microcinematography were used for this analysis. It could be shown that aprotinin, an inhibitor of serine proteinases and para-methylaminobenzoic acid, a specific inhibitor of plasminogen activation and plasmin action greatly reduced the migratory rate of the cells. Streptokinase, a plasminogen activator, stimulated the cell migration in optimal concentrations. The authors hypothesize that tumour vascularization is initiated by immigration of endothelial cells into the tumour by fibrinolytic action following a fibrin gradient induced by the tumour themselves. Fibrinolytic inhibitors suppress this process.

4-Aminobenzoic Acid↗
PubMed1984

Inhibitors of poly(ADP-ribose) synthesis enhance X-ray killing of log-phase Chinese hamster cells.

Postirradiation incubation of V79 Chinese hamster cells with inhibitors of poly(ADP-ribose) synthesis was found to potentiate the killing of cells by X rays. Potentiation increased with incubation time and with concentration of the inhibitor. Preirradiation incubation had only a small effect. The enhanced response correlated well with the known extent of the inhibition of poly(ADP-ribose) synthesis. A radiation-sensitive line, V79- AL162 /S-10, was affected to a lesser extent than the normal cells. Cells repaired the radiation damage with which the inhibitors interacted within 1 hr, a process that has similar kinetics to what is observed when a postirradiation treatment with hypertonic buffer is used [H. Utsumi and M. M. Elkind , Radiat . Res. 77, 346-360 (1979)]. However, the sectors of damage affected by inhibitors of poly(ADP-ribose) synthesis and hypertonic buffer do not entirely overlap. The inhibitor nicotinamide enhanced the killing mainly of late S-phase cells and did not affect cells at the G1/S border. It is concluded that the repair process(es) involving poly(ADP-ribose) synthesis is important for cell survival in repair-competent cells and that the radiation-sensitive cells that were examined are partially deficient in a repair pathway in which poly(ADP-ribose) participates.

4-Aminobenzoic Acid↗
PubMed1984

A single-specimen fecal chymotrypsin test in the diagnosis of pancreatic insufficiency: correlation with secretin-cholecystokinin and NBT-PABA tests.

An investigation of fecal chymotrypsin activity on spot fecal specimens was carried out in three groups of subjects, divided as follows: 45 healthy controls (group C); 36 patients with gastroenterological diseases of extrapancreatic origin (group VP); and 42 patients with chronic pancreatitis (group CP). Nineteen patients of group CP underwent pancreozymin-secretin and NBT-PABA tests. The following results, expressed as mg of chymotrypsin/g of feces, were obtained: C = 0.610 +/- 0.203; CP = 0.291 +/- 0.154, p less than 0.001; VP = 0.560 +/- 0.234. FCT showed a sensitivity rate of 78.5% and a specificity rate of 71.6%. The fecal output of chymotrypsin correlated well with the pancreatic secretion of chymotrypsin (r = 0.59, p less than 0.01) and with the percentage of recovery of urinary PABA (r = 0.44, p less than 0.05). We conclude that chymotrypsin assay by the described method on spot stool specimens is a simple, reliable technique which may be considered a good screening test for pancreatic insufficiency. The test will not detect minimal pancreatic disease or minimal pancreatic dysfunction.

4-Aminobenzoic Acid↗
PubMed1984

[Activation of the blood kallikrein-kinin system in disseminated intravascular coagulation in rats. The significance of the pulmonary component and an attempt at correction with aspirin].

It has been shown that the development in animals of disseminated intravascular coagulation (DIC) caused by long-term intravenous infusion of thrombin was accompanied by appreciable activation of the kallikrein-kinin system, being characteristic of acute pathological processes. In the initial stages of the process development, prekallikrein and kallikrein inhibitor were observed to be secreted from the lungs to arterial blood. Further development of DIC led to the depletion of the reserves of the kinin system. Pretreatment with a single low dose of acetylsalicylic acid considerably reduced the total animals' lethality and postponed blood kinin system activation determined by the development of DIC.

4-Aminobenzoic Acid↗
PubMedDate not supplied

Serine esterase inhibitor reduces contractions with isolated trachea and lung strips from guinea pigs induced by phospholipase A2.

The regulation of the phospholipid metabolism (arachidonic acid (AA) cascade) plays a key role in the pathogenetic mechanisms of the various forms of bronchial asthma. This pathogenetic mechanism offers also important therapeutic implications. Since AA liberation is modulated by phospholipase A2 (PLP-A2) the authors studied the effects of PLP-A2 on guinea pig airways under in vitro conditions and their responses to action of protease inhibitor. Experiments were performed in organ bath with lung strips and tracheal spirals from male guinea pigs. PLP-A2 caused in both models dose-dependent contractions. Para-aminomethyl-benzoic acid reduced PLP-A2-induced contractions in lung strips and trachea in a similar way. This reduction is apparently due to inhibition of AA liberation. These experimental findings underline the relevance of AA cascade to pathogenesis of bronchoconstriction and bronchial hyperreactivity. They support the clinical effectiveness of para-aminomethylbenzoic acid demonstrated earlier. The search for new potential antiasthmatic drugs with the site of action on AA liberation from phospholipids requires in vitro test systems. Guinea pig airway preparations proved to be a suitable in vitro model. The inhibition of PLP-A2 by protease inhibitors seems to be a principal (corticosteroid-like) way for modulation of bronchoconstriction.

4-Aminobenzoic Acid↗
PubMed1984

[Effectiveness of the calcium antagonist nifedipine and the protease inhibitor with plasmin inactivating effect para-aminomethylbenzoic acid on stress-induced bronchial asthma].

In 15 asthmatics (7 females, 8 males, average age 23.3 years) the efficacy of the calcium antagonist nifedipine (Corinfar) and of PAMBA on the exercise-induced asthma was investigated. The patients underwent for 6 minutes a submaximal exercise (80 +/- 5% of the age-related maximum pulse rate) on the bicycle ergometer or by free running. Nifedipine exhibited a highly significant inhibition of the exercise-induced bronchial obstruction (p less than 0.001). Under the PAMBA-medication no significant differences could be stated in comparison to the exercise test without medicament (p greater than 0.5). A standardization of the exercise tests is to be aspired to.

4-Aminobenzoic Acid↗
PubMedDate not supplied

[Study of the histaminergic mechanisms of the action of malaben].

In rabbits (intact and with experimental myocardial infarction) histamine metabolism (histamine content and diaminoxidase activity) following introduction of malaben was studied. In intact animals the ability of malaben to reduce the blood histamine level and to activate diaminoxidase was discovered. Administration of malaben in experimental myocardial infarction promotes a quicker normalization of the disturbed metabolism of histamine.

4-Aminobenzoic Acid↗