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F B Ubatuba

Publications and source records attributed to F B Ubatuba.

16 recordsLinked to original sources
PubMed1989

An animal model for the study of arterial thrombosis.

1. Thrombus formation induced by electrical stimulation of the carotid artery was investigated in anesthetized rabbits and rats. Occlusive Grade III thrombi were produced consistently in 34 normal New Zealand rabbits and 58 untreated albino Wistar rats. Thrombus formation was monitored continuously in some of the animals with a magnetic flowmeter or a thermistor probe applied on the carotid. 2. The usefulness of the model for the screening of drugs was tested by treating the animals with warfarin, heparin, prostacyclin (PGI2), dihydroprostacyclin (DiHPGI2), prostaglandin E1 (PGE1), and prostaglandin D2 (PGD2). 3. All of the drugs except warfarin were infused continuously into the venous circulation during the entire experimental period at a rate of 0.2 ml/min. 4. Warfarin (10 mg/kg), administered by gavage 24 h before the experiment, prevented thrombus formation, as did heparin iv (greater than 34 U/kg). 5. Of the four platelet antiaggregatory prostaglandins tested, PGI2 was the most potent inhibitor of thrombus formation and DiHPGI2 the least active, as evaluated by visual inspection of stimulated arterial segments which were excised 30 min (rabbits) or 15 min (rats) after the stimulation was stopped. PGI2 was less active in rats than in rabbits (Threshold Protective Dose ratio ca. 4:1). PGE1 and PGD2 showed intermediate activity in both animal models.

Animals↗
PubMed1988

[Intestinal absorption of glucose in anesthetized rats. I. Standardization of a method for screening of oral hypoglycemic agents].

This paper presents a method for the screening of natural hypoglycaemic drugs that interfere with the intestinal absorption of glucose. Luminal perfusion of the small intestine (whole length) was carried out on 24 h fasted adult Wistar rats, anaesthetized with sodium pentobarbital. Two rubber Nelaton cannulae were introduced into the organ, the first at the proximal end of the duodenum, just after the pylorus and a second larger one near the ileo-cecal valve. After a preliminary washing with warm physiological saline to remove any alimentary residues and secretions, warm saline containing glucose (plain or with added putative absorption inhibitors), was then introduced into the gut. Ten minutes later the contents was expelled with air and the preparation fully washed with plain warm saline. All perfusates were separately collected up to volume in graduated flasks kept in chipped ice. The glucose concentration was measured in triplicate samples by the specific glucose-oxidase method. The intestinal absorption of the sugar was calculated by difference from the glucose concentration found in the initial solution and in the final perfusate. The method is reliable and highly reproducible.

Animals↗
PubMed1985

Do platelets migrate into inflammatory exudates?

Rat platelets and the corresponding rabbit IgG antibodies mixed in polyester sponges implanted under the skin of normal animals caused an enhanced 24-h inflammatory response and a significant increase of prostaglandins in the exudate. These experimental results contrast with those obtained for normal rats implanted with sponges containing only IgG anti-platelet antibodies. The present experiments show that circulating platelets were not concentrated at the inflamed site and can hardly be considered of importance in acute inflammation.

Animals↗
PubMed1979

The effect of prostacyclin (PGT2) on platelet behaviour. Thrombus formation in vivo and bleeding time.

Prostacyclin (PGI2) infused intravenously into anaesthetized rabbits inhibited electrically-induced thrombus formation in the carotid artery, increased bleeding time and inhibited ex vivo platelet aggregation induced by ADP or arachidonic acid. The increase in bleeding time and the inhibition of ex vivo platelet aggregation lasted for as long as the infusion of PGI2 was maintained but rapidly disappeared after infusion was stopped. Prostacyclin is a more potent inhibitor of platelet function, in vivo than prostaglandin E1 (PGE1) or prostaglandin D2 (PGD2). The effects of prostacyclin on all parameters studied except blood pressure were potentiated by the concomitant administration of theophylline, a phosphodiesterase inhibitor.

Animals↗
PubMed1979

Preparation and biochemical properties of PGH3.

PGH3 was biosynthesised from all-cis-5,8,11,14,17-eicosapentaenoic acid (20:5 omega 3) by an acetone-pentane powder of ram seminal vesicles and its structure was confirmed by GLC-MS after its reduction to PGF 3 alpha. PGH3 was transformed by horse platelet microsomes to TXB3, and by aortic microsomes to delta 17-6-keto-PGF 1 alpha. The structures of these compounds were confirmed by GLC-MS.

Animals↗
PubMed1978

Transformation of arachidonic acid and prostaglandin endoperoxides by the guinea pig heart. Formation of RCS and prostacyclin.

The metabolism of arachidonic acid (AA) was studied in perfused isolated hearts from guinea pigs. The coronary effluent was continuously bioassayed for prostaglandin-like substances (PLS) using the cascade technique of Vane. Injections of AA in doses between 1--50 microgram into the perfusion fluid prior to the heart produced vasodilatation of the coronary vascular bed followed by a contraction of the rat stomach strip (RSS), chick rectum (CR) and rat colon (RC) as well as relaxation of the bovine coronary artery (BCA). At the higher doses of AA there was also contraction of the rabbit aorta (RbA). The same pattern of effects on the bioassay tissues was seen when prostaglandin endoperoxide (PGH2) was perfused through the heart. The response of the bank of superfused tissues provided evidence for the formation of prostacyclin (PGX or PGI2), PGE2 and PGF2alpha. Chromatographic studies showed that 6-oxo-PGF1alpha together with other prostaglandins was present in the perfusate after acidification, which suggested that the bovine coronary relaxing substance consists mainly of PGI2. Moreover, the rabbit aorta contracting substance (RCS) released in the perfusate was due to prostaglandin endoperoxides and not to thromboxane (TXA2). The formation of PLS from AA was completely blocked after treatment of the heart with the cyclo-oxygenase inhibitors, indomethacin or meclofenamic acid. Pretreatment of the heart with 15-hydroperoxyarachidonic acid (15-HPAA), a selective inhibitor of prostacyclin synthetase, inhibited the effect of AA on the coronary vasculature and diverted the metabolic transformation of AA towards PGE2 and PGF2alpha.

Animals↗
PubMed1977

Enzymatic preparation of prostaglandin endoperoxides.

A simple and reliable method is described for the preparation of the endoperoxide intermediates (PGG2 and PGH2) in the biosynthesis of prostaglandins. The endoperoxides are thermolabile and easily decomposed by water (t 1/2 congruent to 5 min at 37 degrees C). Because of this, special precautions must be taken to work at low temperature and to minimize contact with moisture. Milligram quantities of PGG2 and PGH2 were obtained by running several reactions successively and pooling the extracts before chromatographic fractionation. The method is now being developed further to scale up the procedure.

Animals↗
PubMed1976

Platelets, acute inflammation and inflammatory mediators.

The anti-inflammatory activity of aspirin-like drugs could derive, at least in part, by inhibiting synthesis and release of prostaglandins or rabbit aorta-contracting substance from platelets. Indeed, aggregation of platelets and the consequent release of inflammatory mediators has been frequently evoked as a factor in the development of the inflammatory reaction. The participation of platelets in acute inflammation was tested in three types of trauma in rats rendered thrombocytopenic with anti-platelet serum. Oedema in response to carrageenin, anti-platelet serum or passive cutaneous anaphylaxis was no different from the controls in thrombocytopenic rats.

Acute Disease↗
PubMed1976

Platelets, Arthus-type reactions and inflammatory mediators.

The release of inflammatory mediators and the appearance of necrohaemorrhagic lesions induced by subcutaneous implantation of sponges containing antiplatelet serum globulins were studied in control and thrombocyto-penic rats. In thrombocytopenic animals, antiplatelet globulins caused a greater release of prostaglanding-like material and 5-hydroxytryptamine as well as larger inflammatory lesions. Thus, platelet integrity is not necessary for the induction of lesions by antiplatelet globulins and the mediators in the sponge exudates must have originated from leucocytes or damaged tissues. Mast cells seem not to be involved in the production of 5-hydroxytryptamine in this inflammatory reaction. It is suggested that in idiopathic thrombocytopenic purpura (ITP) an Arthus-type hypersensitivity reaction, rather than the thrombocytopenia itself, is the cause of the vascular lesions and their manifestations.

Animals↗
PubMed1975

Platelets, Arthus-type reactions and inflammatory mediators.

The release of inflammatory mediators and the appearance of necrohaemorrhagic lesions induced by subcutaneous implantation of sponges containing antiplatelet serum globulins were studied in control and thrombocytopenic rats. In thrombocytopenic animals, antiplatelet globulins caused a greater release of prostaglanding-like material and 5-hydroxytryptamine as well as larger inflammatory lesions. Thus, platelet integrity is not necessary for the induction of lesions by antiplatelet globulinrom leucocytes or damaged tissues. Mast cells seem not to be involved in the production of 5-hydroxytryptamine in this inflammatory reaction. It is suggested that in idiopathic thrombocytopenic purpura (ITP) an Arthus-type hypersensitivity reaction, rather than the thrombocytopenia itself, is the cause of the vascular lesions and their manifestations.

Animals↗
PubMed1975

Are platelets important in inflammation?

The participation of platelets in acute inflammation was tested by three different traumas in rats rendered thrombocytopenic with anti-platelet serum. Thrombocytopenic rats showed normal oedema response to carrageenin, anti-platelet serum and passive cutaneous anaphylaxis.

Animals↗
PubMed1973

The use of the hamster stomach in vitro as an assay preparation for prostaglandins.

1. Hamster stomach strips in vitro are useful test preparations for the assay of prostaglandins E and F in the nanogram concentration range. Three-minute cycles can be used for long periods without spontaneous contractions or significant base-line instability.2. The mean percentage error and the precision index of six 4-point assays of prostaglandin E(2) were 7.8 and 0.057, respectively.3. The relative sensitivity to different prostaglandins was E(2)/E(1) approximately 1, E(2)/F(1alpha) approximately 65 and E(2)/A(1) approximately 400.4. These preparations were relatively insensitive to 5-hydroxytryptamine (prostaglandin E(2)/5-HT approximately 20,000) and histamine (prostaglandin E(2)/histamine approximately 200).5. These results suggest that the hamster stomach preparation can be used to differentiate between 5-hydroxytryptamine and prostaglandins.

Animals↗