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Biomedical subjects

R Guerra

Publications and source records attributed to R Guerra.

At least 73 records · Page 4Linked to original sources
PubMed1990

Increased resistance against oxidative stress is observed during a short period of renal reperfusion after a temporal ischaemia.

Reperfusion of rat kidney submitted to temporal ischaemia induces a decrease in glutathione content. Lipid peroxidation is not detected in kidney homogenates but microsomes obtained after periods of reperfusion longer than 60 minutes show increased malondialdehyde values correlated with high oxygen consumption and superoxide free radical generation. Microsomes obtained from kidneys submitted to 15 or 60 minutes of reperfusion are resistant to NADPH-induced lipid peroxidation but after 120 minutes of reperfusion an increased lipid peroxidative response is observed. Although the mechanism of the protection found in microsomes against the induction of oxidative stress in the first 60 minutes of reperfusion is unknown, it is postulated that this subcellular fraction plays an important role in the oxidative stress observed after longer periods of reperfusion.

Animals↗
PubMed1989

Effect of silybin dihemisuccinate on the ethanol metabolizing systems of the rat liver.

Silybin dihemisuccinate produces a decrease in the ethanol metabolic rate of rats. This effect is ascribed to an inhibition of the microsomal ethanol oxidizing system (MEOS). Alcohol dehydrogenase activity, catalase activity and NADPH cytochrome c reductase activity are not affected by the flavonoid. It is proposed that the inhibition of MEOS by silybin dihemisuccinate is related to its antioxidant properties, acting as a scavenger of the free radicals involved in ethanol metabolism by this enzymatic system. This observation may have therapeutical implications because microsomal lipid peroxidation induced by hydroxyl free radicals has been related to the etiology of hepatic alcoholic disease.

Animals↗
PubMed1989

Ingestion of high doses of fish oil increases the susceptibility of cellular membranes to the induction of oxidative stress.

Feeding rats with 4 g/kg body weight of sardine oil during 7 or 14 days increases the content of eicosapentaenoic acid and docosahexaenoic acid in the erythrocyte and hepatic microsomal membranes by 2 to 6%. These membranes show increased susceptibility to the induction of oxidative stress, expressed as lipid peroxidation, when they are exposed to Fe2+-ascorbate and to NADPH-FE3+-ADP, respectively. The results indicate that in order to prevent the increased susceptibility to lipid peroxidation, supplementation with larger amounts of antioxidants may be needed than those required to stabilize the oil.

Animals↗
PubMed1989

Silybin dihemisuccinate protects against glutathione depletion and lipid peroxidation induced by acetaminophen on rat liver.

Acetaminophen hepatotoxicity is characterized by glutathione depletion, cellular necrosis, and, in some instances, by the induction of lipid peroxidation. Silybin dihemisuccinate, a soluble form of the flavonoid silymarin, protects rats against liver glutathione depletion and lipid peroxidation induced by acute acetaminophen intoxication. Other biochemical parameters such as serum transaminases did not show the drastic increase observed under acetaminophen intoxication when animals were treated with the flavonoid. Preliminary results suggest that silybin dihemisuccinate may be another antidote against acetaminophen hepatotoxicity.

Acetaminophen↗
PubMed1989

Selectivity of silymarin on the increase of the glutathione content in different tissues of the rat.

Silymarin, a flavonoid extracted from the seeds of the milk thistle, Silybum marianum, increases the redox state and the total glutathione content of the liver, intestine, and stomach of the rat. The same treatment does not affect the levels of the tripeptides in the kidney, lung, and spleen. This selective effect of the flavonoid on the digestive organs is ascribed to its pharmacokinetics on the digestive track, where the biliary concentration of silymarin is increased and maintained via the entero-hepatic circulation.

Animals↗
PubMed1989

Release of NO and EDRF from cultured bovine aortic endothelial cells.

The endothelium-derived relaxing factor (EDRF) has recently been reported to be nitric oxide. This study was performed to determine whether the vasorelaxant activity of EDRF could be accounted for by nitric oxide released from cultured endothelial cells. Nitric oxide released from cultured bovine aortic endothelial cells was monitored using a chemiluminescence technique with and without reflux processing of the effluent with a strong reducing environment (1% sodium iodide in glacial acetic acid). In the presence of indomethacin, basally released EDRF was sufficient to relax a bioassay detector vessel (preconstricted with prostaglandin F2 alpha) by 41 +/- 8%. Bradykinin (0.01 microM) and A23187 (10 microM) produced relaxation of the bioassay detector vessel equal to 74 +/- 7 and 69 +/- 13%, respectively. In both the absence and the presence of reflux preprocessing of the cell effluent in a reducing environment, the amount of nitric oxide detected by chemiluminescence was 7-10-fold less than that required to account for the detector vessel relaxation (determined from responses of the detector vessel to standard infusions of authentic nitric oxide). These experiments contradict the view that nitric oxide is the sole or principal EDRF. It is likely that either other nonprostanoid vasodilator substances are released in addition to nitric oxide or that EDRF is a nitric oxide containing or forming compound that is substantially more potent than authentic nitric oxide.

Animals↗
PubMed1989

Characteristics of canine coronary resistance arteries: importance of endothelium.

Canine coronary resistance vessels were studied in vitro to examine the role of the endothelium in modulating responses to acetylcholine, vasopressin, and thrombin and to compare these responses to those found in large epicardial vessels. Acetylcholine had no effect on passively distended microvessels; however, after preconstriction with the thromboxane analogue, U 46619 caused dose-dependent vasodilation [50% effective concentration (EC50), 0.05 microM; maximum response, 97.9 +/- 2.1% relaxation]. Large epicardial arterial rings studied in organ chambers similarly relaxed to acetylcholine (EC50, 0.07 microM; maximum response, 79 +/- 5% relaxation). Hemoglobin was utilized to inactivate endothelium-derived relaxing factor (EDRF), resulting in reversal of acetylcholine vasodilation in both the microvessels (92 +/- 3.2% reversal) and the large epicardial vessels (117 +/- 9%). Hemoglobin had no effect on passively distended or preconstricted microvessels. Vasopressin constricted resistance vessels by 22.3 +/- 5.9 microns at 500 microU/ml. Hemoglobin potentiated this response by 100%, suggesting that vasopressin elicited EDRF release. In large coronary arteries, however, vasopressin elicited endothelium-dependent dilation with maximal relaxation of 36 +/- 9% at 3,000 microU/ml. Thrombin produced endothelium-dependent relaxation of large epicardial arterial rings but only constricted coronary microvessels. The response to thrombin was not altered by hemoglobin. This study demonstrates that the endothelium of coronary microvessels, like that of larger vessels, importantly modulates vascular reactivity to selected agents. Furthermore, major differences exist between large and small coronary arteries in their response to vasopressin and thrombin.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1989

Mechanisms of abnormal endothelium-dependent vascular relaxation in atherosclerosis: implications for altered autocrine and paracrine functions of EDRF.

The present studies were performed to determine if abnormal endothelium-dependent vascular relaxation in atherosclerosis is due to decreased production or release of endothelium-derived relaxing factor (EDRF) by atherosclerotic rabbit vessels or if atherosclerotic vessels are less sensitive to the relaxing effects of EDRF. EDRF release was quantified using two approaches, by the response of bioassay detector vessels and also by the activation of guanylate cyclase within cultured endothelial cells. Using these assays, atherosclerotic vessels were found to release significantly less EDRF than normal vessels in response to both receptor- and nonreceptor-mediated stimuli. Relaxations of normal and atherosclerotic vessels to luminally applied EDRF (derived from normal rabbit aortas stimulated by the calcium ionophore, A23187) and nitric oxide, a putative EDRF, were also studied. Atherosclerotic vessels were more sensitive to EDRF than normal vessels, and equally sensitive to nitric oxide. Additional studies performed in organ chambers failed to demonstrate augmented constriction of atherosclerotic vessels in response to acetylcholine in the presence or absence of methylene blue or LY83583, compounds which inhibit the effect of EDRF. We conclude that decreased EDRF release is the principal underlying mechanism responsible for abnormal endothelium-dependent vascular relaxation in atherosclerosis.

Acetylcholine↗
PubMed1989

[Infections by anaerobes in children: frequency of isolation and antimicrobial resistance].

We studied the frequency of isolation and antimicrobial susceptibility of strict anaerobic bacteria isolated in a paediatric hospital. A total of 1,753 samples from purulent material and hemocultures were processed. One hundred and thirty strains were isolated from 95 children: 44 from 48 cases of peritonitis (91.7%), 2 from 8 brain abscesses (25%), 23 from 124 soft tissue abscesses (18.5%), 4 from 64 empyemas or lung abscesses (6.3%) and 22 from 1,509 hemocultures (1.5%). Mixed infection (anaerobic and aerobic bacteria) was detected in 38.5% of the cases; however, in peritonitis 81.3% of the cases showed mixed infection. The more frequently isolated bacteria were: Bacteroides (44.6%), Clostridium (19.2%), Fusobacterium (7.7%) and gram positive cocci (7.7%). Propionibacterium acnes was isolated in 15 specimens; however, most of them were considered as contamination. Bacteroides was isolated more frequently from patients with peritonitis (51.6%). The susceptibility to five antibiotics was tested in 124 strains using the method of serial dilutions in agar plates. The genus Bacteroides showed a high resistance to penicillin (73.1%), moderate to clindamycin (11.5%) and low to cefoxitin, chloramphenicol and metronidazole (6.8%, 2% and 5.8%). The rest of the anaerobic strains tested (other gram negatives and grampositives) were highly sensitive to all the antimicrobials tested, except for clindamycin (26.7% and 36.9% resistance, respectively). Cefoxitin, chloramphenicol and metronidazole had the lower CMI50 and CMI90 for the genus Bacteroides; and for the rest of the bacteria, penicillin had the highest activity (CMI90 less than 0.025). Since the frequency of isolation of anaerobic bacteria in children with severe infections, presumably originated from the digestive tract, paranasal sinus and middle ear is high, anaerobic cultures must be practiced in these patients. Empiric antimicrobial treatment should also be started. This treatment should be with penicillin when the probability of isolation of Bacteroides is low (infections in the face, neck, thorax and soft tissues) and with metronidazole in intraabdominal infections. Because of the severity and probable etiology of brain abscesses, treatment with penicillin and chloramphenicol or metronidazole is recommended in these cases.

Anti-Bacterial Agents↗
PubMed1986

Differential prooxidative effect of adult and fetal hemoglobin.

Human fetal hemoglobin assayed in a peroxidizing system shows an increased prooxidative effect when compared to human adult hemoglobin. This effect is related only to the oxyhemoglobin form since both fetal and adult methemoglobins did not show any prooxidative effect. The prooxidative effect of the oxyhemoglobin form is ascribed to its increased sensitivity to form superoxide free radicals when transformed to the methemoglobin form. It is proposed that the structure of the heme pocket of fetal oxyhemoglobin enhances free radical release when compared to adult oxyhemoglobin. This difference may be important in some hematological disorders presented by the newborn.

Female↗
PubMed1986

Differential effect of silybin on the Fe2+-ADP and t-butyl hydroperoxide-induced microsomal lipid peroxidation.

We have observed a differential effect of silybin dihemisuccinate on rat liver microsomal oxygen consumption and on lipid peroxidation induced by NADPH-Fe2+-ADP and t-butyl hydroperoxide. These results are ascribed to the antioxidant properties of the flavonoid. The differences observed in the effect of the catalysts may be a consequence of the different capacity of silybin to act as a scavenger of free radicals formed by NADPH-Fe2+-ADP or t-butyl hydroperoxide.

Adenosine Diphosphate↗
PubMed1985

Protective effect of the flavonoid silybin dihemisuccinate on the toxicity of phenylhydrazine on rat liver.

Phenylhydrazine is a hemolytic agent whose mechanism of action is related with the formation of free radicals and the induction of lipid peroxidation. The flavonoid silybin dihemisuccinate is an antihepatotoxic principle used in the treatment of many liver diseases; its mechanism of action has been ascribed to its antioxidant properties. This work demonstrates, using a hemoglobin-free perfusion system, the protective effect of the in vivo treatment of the rat with silybin dihemisuccinate on the hepatic glutathione depletion and lipid peroxidation induced by the infusion of phenylhydrazine into the perfusion buffer.

Animals↗