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Biomedical subjects

C Gomes

Publications and source records attributed to C Gomes.

At least 37 records · Page 2Linked to original sources
PubMed1989

Screening in mice of some medicinal plants used for analgesic purposes in the state of São Paulo. Part II.

Seventeen medicinal plants used popularly in Brazil for their reputed analgesic properties were tested in mice by the writhing and tail flick methods. All extractions were made in 50% aqueous ethanol at low temperatures. The oral dose administered was always 1 g extract/kg. Significant effects in both tests were produced by Lippia alba, Piper abutiloides, Piper cincinnatoris, Piper lindbergii and Tillandsia usneoides.

Analgesics↗
PubMed1989

[Influence of age on the morbidity and mortality in coronary artery surgery].

To study the effects of age on the results of coronary artery bypass grafting (CABG), 250 patients operated on from 1986 to 1989 were divided into two groups: 1) less than 65 years of age and 2) older than 65. Pre, intra and postoperative data collected in all patients included: sex, type and class of angina, associated diseases, previous myocardial infarction, previous CABG, left ventricular aneurysm, bypass time, aortic cross-clamp time, number of grafts per patient, need for prolonged inotropic support, postoperative complications, and mortality. A large number of elderly patients had unstable angina (20.3% vs 6.2%), post-infarction angina (10.1% vs 7.8%), angina at rest (10.1% vs 3.6%), peripheral vascular disease (8.4% vs 2.6%), required prolonged inotropic support (18.6% vs 3.1%), had major neurological complications (8.4% vs 0.1%) and perioperative myocardial infarction (5.0% vs 0.5%). Overall mortality was 3.6% but mortality rates were significantly higher in elderly patients (11.8% vs 1.0%). These data suggest that elderly patients have an increased risk of cardiac and neurologic morbidity and mortality. It appear that the increased morbidity and mortality is related to an increased susceptibility of the elderly to serious postoperative complications.

Adult↗
PubMed1988

Acute diuretic effects in conscious rats produced by some medicinal plants used in the state of São Paulo, Brasil.

Extracts of 32 medicinal plants used popularly for their presumed diuretic and/or antihypertensive properties were tested for diuretic effects in conscious unrestrained rats. Extracts were made using aqueous ethanol (50:50, v/v) at 4-10 degrees C. When given orally at a dose of 40 ml/kg, a majority of the ethanol-free extracts produced a more pronounced diuresis than would be expected from the potassium concentration of the extracts. The most significant diuretic effect was observed with Hedychium coronarium sheath and leaf-blade extracts.

Animals↗
PubMed1988

Screening in mice of some medicinal plants used for analgesic purposes in the state of São Paulo.

Twelve medicinal plants used popularly for their reputed analgesic properties were tested in mice by the writhing and tail-flick methods. All extractions were made using 50% aqueous ethanol at low temperatures. The oral dose administered was always 1 g solids/kg. While several extracts showed a positive effect in one of the tests, significant effects in both tests were produced by Serjania communis only. Morphine and acetylsalicylic acid were used as reference drugs.

Abdomen↗
PubMed1988

The effect of supplementary oral nutrition in poorly nourished patients with chronic obstructive pulmonary disease.

We carried out a prospective, randomized, controlled trial to investigate the effect of a 3-month period of supplementary oral nutrition in 14 poorly nourished outpatients with COPD. Seven patients were randomized into Group 1 who received their normal diet during Months 1 to 3, a supplemented diet during Months 4 to 6, and their original normal diet during Months 7 to 9. The other 7 patients received their normal diet for the entire 9-month study period (Group 2). Seven well-nourished patients (Group 3) matched for age and severity of air-flow obstruction served as control subjects; they received their normal diet for the 9-month study period. Measurements of nutritional status, respiratory muscle and handgrip strength, sternomastoid muscle function (including frequency/force curves, maximal relaxation rate, and a fatigability test), lung function, arterial blood gas tensions, general well-being and breathlessness scores, and 6-min walking distances were carried out monthly in all patients. At the start of the study, the poorly nourished patients had lower mean daily calorie and protein intakes than did the well-nourished patients. The poorly nourished patients had lower respiratory muscle and handgrip strength, and abnormal contractility and increased fatigability of the sternomastoid muscle compared with those in the well-nourished patients. After 3 months of supplementary oral nutrition, there was a significant improvement in the nutritional status of Group 1 patients, as evidenced by an increase in body weight, triceps skinfold thickness, and midarm muscle circumference. Respiratory muscle and handgrip strength increased in parallel with nutritional status, although there were no significant changes in lung function or arterial blood gas tensions.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1986

Acute antihypertensive effect in conscious rats produced by some medicinal plants used in the state of São Paulo.

Thirty two medicinal plants used popularly for their proposed diuretic and/or antihypertensive properties have been tested for antihypertensive effects in conscious unrestrained rats. All extractions were made in aqueous ethanol (50:50 by vol.) at low temperature. Before administration of the extracts the alcohol was evaporated. The extracts (40 ml/kg) were always administered per os. Antihypertensive effects in SHR rats were observed after the administration of Allium sativum Linn. (bulb), Olea europaea Linn. (leaf) and Hedychium coronarium Koen. (leaf-blade).

Animals↗
PubMed1984

Central nervous effects of the convulsant protein canatoxin.

Some pharmacological-toxicological effects of canatoxin, a toxic protein purified from the seeds of Canavalia ensiformis have been studied in mice and rats. The most obvious effect, a lethal tonic convulsion, was generally produced 10-15 min. after intravenous injection of 2-3 mg/kg of the highly purified protein (mol. wt. 88,000). After intraperitoneal, intramuscular or subcutaneous administration the convulsion produced by the same toxin dosis occurred within 24 hours. A spinal transection at the midthoracic level did not abolish the convulsions of the hindlimbs while destruction of the medulla below this level completely blocked the convulsions of the hindlimbs. The convulsions of the head and forelimbs were unaffected by these surgical pretreatments. The toxic protein did neither affect the isolated skeletal muscle nor did it potentiate nerve impulse induced contractions. The convulsive effect of canatoxin was potentiated by reserpine and attenuated by phenobarbital, diazepam, methenesine and also by haloperidol and spiroperidol. The total concentration of brain and spinal cord neurotransmitters seemed to remain unchanged after subconvulsive and convulsive doses of canatoxin. In the conscious rat the toxic protein did not change the blood pressure except for a shortlasting hypertensive response observed immediately before the onset of the convulsions. The heart frequency was lowered at subconvulsive and convulsive doses but no effect was seen on the frequency of the rat isolated right atria exposed to high doses of canatoxin. The body temperature was lowered by a convulsive doses of the toxic protein.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Aminooxyacetic acid induced accumulation of GABA in the rat brain. Interaction with GABA receptors and distribution in compartments.

The effect of aminooxyacetic acid (AOAA, 90 mg/kg i.v.) on bicuculline, picrotoxin and 3-mercaptopropionic acid (3-MPA) induced convulsions and on GABA concentrations in cerebellum, whole brain and a synaptosomal fraction of whole brain was investigated. At various intervals after AOAA the rats were either injected with one of the convulsive drugs or sacrificed for analysis of the GABA concentration. AOAA caused a rapid initial (0-30 min) and a later slower increase of GABA in cerebellum and whole brain. In the synaptosomal fraction the GABA accumulation was delayed and less pronounced when compared to the whole brain. The bicuculline induced convulsions were markedly potentiated during the first hour but completely blocked from 2-6 h after AOAA. Picrotoxin showed a somewhat different pattern to bicuculline in the interactions with AOAA. The initial strong potentiation was not observed but the later phase of protection was present. In the interactions with 3-MPA, the effect of AOAA was always protective. The time to onset of convulsions was gradually increased during the first 30 min after AOAA. This protective effect remained practically unchanged up to 6 h after AOAA. However, once started, the convulsions were generally of the same duration and intensity. The results can be interpreted as GABA accumulating after AOAA stimulates GABA receptors to a degree more or less proportional to the whole brain GABA concentration and further that GABA synthetized in neurons is liberated, stimulates inhibitory bicuculline sensitive (predominant) and excitatory bicuculline insensitive receptors and is captured to a large extent by non-neuronal cells.

3-Mercaptopropionic Acid↗
PubMed1982

GABA turnover in mouse brain: agreement between the rate of GABA accumulation after aminooxyacetic acid and the rate of disappearance after 3-mercaptopropionic acid.

GABA levels of the whole mouse brain were studied after in vivo inhibition of GABA synthesis by 3-mercaptopropionic acid (3-MPA, 100 mg/kg i.p.) and of GABA degradation by aminooxyacetic acid (AOAA, 3.8-60 mg/kg i.v.). The influence of 3-MPA on GABA levels was investigated in brains where postmortal GABA accumulation was allowed to occur and in brains where this phenomenon was avoided by very rapid dissection and homogenization of the brain in acid (within 50 sec after decapitation). The post-mortal GABA increase was blocked by 86% after injection of 3-MPA and 3 min before decapitation. In the group where the postmortal accumulation was avoided by very rapid homogenization of the brain in acid, GABA levels decreased by 15% within 2 min after 3-MPA (mean turnover time = 14 min). From 2 to 4 min the GABA concentration remained stable at this decreased level. GABA accumulation after AOAA was maximal after a dose of 7.5 to 15 mg/kg. i.v. Doses higher than 60 mg/kg always produced convulsions. The phase of most rapid accumulation of GABA after AOAA indicates a mean turnover time of about 10 min. The first rapid phase of accumulation was followed by a slower phase. It is probable that the turnover time of whole mouse brain GABA is approximately 10-14 min. It is also concluded that AOAA in a dose of around 15 mg/kg i.v. hardly can inhibit GAD in vivo in the mouse brain and that this dose, by this route of administration, could be used for studies of GABA synthesis in vivo in the mouse.

3-Mercaptopropionic Acid↗
PubMed1980

Effect of aminooxyacetic acid (AOAA) on GABA levels in some parts of the rat brain.

The accumulation of GABA in the cerebellum and medulla oblongata-pons of rats has been studied after inhibition of GABA-T (EC 2.6.1.19) by different doses of AOAA. It was found that intraperitoneal (i.p.) injections of AOAA were, at least during the first hour after injection, much less effective than intravenous (i.v.) injections probably due to poor absorption i.p. After i.v. injection, AOAA caused a maximal accumulation of GABA in the cerebellum at a dose of 50 mg/kg. This maximal effect was virtually unchanged up to a dose of 150 mg/kg (the highest dose tested i.v.). If GAD (EC 4.1.1.15) was inhibited by 3-mercaptopropionic acid 30 min after AOAA (90 mg/kg i.v.) the GABA level was stable for at least another 30 min. The rate of GABA accumulation in the cerebellum during the first 15 min after AOAA (50-150 mg/kg i.v.) was 0.086 mumol/g/min and thereafter 0.034 mumol/g/min. It is concluded that AOAA in vivo in a wide dose range inhibits GABA-T almost 100% without affecting GAD to any great extent, and that the onset of action is rapid after i.v. but not after i.p. injection.

3-Mercaptopropionic Acid↗
PubMed1980

On the importance of GABA-ergic neurons for the AOAA induced accumulation of GABA in the rat brain.

The accumulation of GABA induced by an intravenous injection of aminooxyacetic acid (AOAA) was followed for 1 h in five parts of the rat brain, i.e. cerebellum, medulla oblongata-pons, striatum, ventral mesencephalon and hypothalamus. The accumulation was similar in all brain parts studied when expressed as percentual increase from the basal value; an initial rapid accumulation indicating a mean turnovertime of 12--16 min during the first 5 min was gradually decreased to turnovertime of about 1--3 h during the last 30 min of observation. In order experiments brains were transected unilaterally between the substantia nigra and the striatum. Six days after the hemisection the GABA concentration of the substantia nigra of the transected side had decreased to less than 30% of the control side. The AOAA induced accumulation of GABA in the substantia nigra of the transected side was less pronounced than that of the control side. The initial rapid accumulation seen in all brain parts studied was completely lacking in the substantia nigra of the transected side. In the striatum, the transection did neither alter the GABA concentration nor the AOAA induced accumulation of GABA. As the initial rapid accumulation of GABA disappears after degeneration of GABA-ergic neurons, it is suggested that this initial phase of GABA accumulation produced by an intravenous injection of AOAA probably is the result of GABA accumulation in neurons.

Acetates↗
PubMed1980

Purification of GABA on small columns of Dowex 50W; Combination with a method for separation of biogenic amines.

Elution of GABA has been included in the method for separation of biogenic amines on small Dowex 50W columns described by Atack & Magnusson (1978). After extraction with perchloric acid and neutralization to pH 3.0, the sample is passed through the column. 5-HIAA might thereafter be eluted as described by Lindqvist (1971). After washes with water and 8 ml of a 0.025 M sodium citrate buffer pH 4.5, GABA is eluted in 3 ml of a 0.05 M sodium citrate buffer pH 5.3-5.4. The elution of tryptophane and the above mentioned amines can thereafter be performed. The recovery of GABA from the column is 100%. Silica thin-layer chromatography of the GABA eluate gives only one ninhydrine positive spot with a Rf value identical to GABA standard. When the GABA eluate from a whole brain and spinal cord is run on an automatic amino acid analyser, only one peak is detectable, eluted in the same position as GABA standard. Fluorescence analysis of the GABA eluate gives similar values if a( ninhydrine, b) acetylacetone plus formaldehyde or c) fluorescamine is used to form the flurophore. The GABA values are identical whether the samples reacted with ninhydrine are diluted with water or copper tartrate. The GABA concentrations found in some parts of the rat brain are of the same order of magnitude as reported by other authors.

5-Hydroxytryptophan↗
PubMed1980

Pre- and postsynaptic alpha-adrenoceptor antagonists: differentiated cardiovascular effects in the rat.

Intravenous (i.v.) injections of yohimbine, phentolamine, prazosine and phenoxybenzamine lowered blood pressure and increased heart rate in conscious rats. Intracerebroventricular (i.c.v.) injections of yohimbine and phentolamine increased blood pressure and heart rate; this was antogonized by pretreatment with clonidine. Phenoxybenzamine and prozosine had no effect or gave hypotension and tachycardia on i.c.v. injection. Pentobarbitone anaesthesia partly antagonized the cardiovascular effects of all alpha-adrenoceptor antagonist. Synthesis and utilization of central noradrenaline was increased by i.v. or i.c.v. yohimbine; anaesthesia partly antagonized this effect. In peripheral tissues others have found that yohimbine, tolazoline, piperoxan and phentolamine are potent blockers of the presynaptic alpha-adrenoceptors while phenoxybenzamine and prazosine act preferentially on postsynaptic alpha-adrenoceptors. The differentiated cardiovascular response to i.c.v. injection of these blockers may reflect their different affinity to central pre- and postsynaptic alpha-adrenoceptors.

Adrenergic alpha-Antagonists↗