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Biomedical subjects

G G Corbucci

Publications and source records attributed to G G Corbucci.

32 records · Page 2Linked to original sources
PubMed1990

The role of reduced glutathione during the course of acute haemolysis in glucose-6-phosphate dehydrogenase deficient patients: clinical and pharmacodynamic aspects.

Tissue hypoperfusion leads to cellular oxidative and peroxidative damage due to biochemical disorders in the oxygen and substrate metabolism. The metabolic turnover of glutathione (GSH) represents one the main cytoprotective systems against the peroxide attack and the depletion or defect in resynthesis of this compound is accompanied by pathological consequences. In the present study the clinical effects of glutathione depletion were investigated in conditions of acute tissue hypoxia due to marked haemolysis in glucose-6-phosphate dehydrogenase deficient patients (favism syndrome). In these subjects a significant marker of the tissue oxidative damage was represented by the uric acid blood levels, presumably linked to xanthine-hypoxanthine altered metabolism. To antagonize the effects of oxyradical pathology, reduced glutathione was administered to a group of patients and the results confirmed the cytoprotective role played by the GSH supplementation. The GSH action was evident on the tissue metabolism and this supports the opinion that reduced glutathione could represent a new and interesting therapeutic approach in marked and acute hypoxic conditions.

Adolescent↗
PubMed1990

Metabolic effects induced by L-carnitine and propionyl-L-carnitine in human hypoxic muscle tissue during exercise.

An experimental model was developed to investigate some metabolic effects of strenuous exercise in hypoxic muscle tissue of human volunteers. The incidence of carnitine supplementation was studied, assuming as marker the thiobarbituric acid reaction products analysed in plasma samples collected during the course of the protocol programme. Propionyl-L-carnitine appears to antagonize in a significant degree the damaging effects of muscle fatigue combined with hypoxic status. Under these conditions the detoxifying role played by propionyl-L-carnitine, previously reported in various tissues and in other pathological conditions, appears to be relevant, although further studies are needed to elucidate the pharmacodynamics of this molecule.

Carnitine↗
PubMed1987

Some aspects of the mitochondrial oxidative metabolism in human atrial tissue during cardiopulmonary by-pass.

Following previous research on the hypoxic cell in human circulatory shock, the present work has investigated some mitochondrial oxidative aspects in atrial biopsies taken during cardiopulmonary by-pass. Cardioplegic solution and hypothermia were administered to 10 patients and the atrial samples were collected before and after aortic clamping. The results show a cellular protective effect of cardioplegia and hypothermia on the electron-transport chain, even if the enzymes with high KmO2 appear to be more sensitive to ischaemia. The results suggest a metabolic injury rather than an oxidative damage due to the induced ischaemia, alterations to fatty-acid beta-oxidation being especially notable. Because of the unchanged oxidative capacities, the oxyradical generation and the peroxidative damage appear to be irrelevant in the ischaemic period and during the course of reperfusion. Further studies are needed to elucidate the metabolic damage and the therapeutic implications due to the induced ischaemia in the myocardial cell during the aortic clamping.

Adult↗
PubMed1986

Changes in the levels of coenzyme Q homologues, alpha-tocopherol and malondialdehyde in human tissue during the course of circulatory shock.

Following our previous findings on mitochondrial oxidative damage during the course of circulatory shock in human muscular tissue, in the present work we examined the pathogenic connections between the electron-transport-chain enzymic activity and the ubiquinone metabolism. The effects of the oxidative damage on the alpha-tocopherol content and malondialdehyde (MDA) levels were also studied. The results reveal an involvement of cytochrome oxidase and coenzyme Q10 in the oxidative damage due to shock; alpha-tocopherol seems to show a particularly increased antioxidant activity contemporary with the marked increase in MDA levels. These findings suggest that the significant fall in the mitochondrial oxidative capacity could generate an oxygen free-radical production with subsequent peroxidative damage of the mitochondrial inner-membrane bilayer.

Blood Pressure↗
PubMed1985

Shock-induced damage to mitochondrial function and some cellular antioxidant mechanisms in humans.

The effects of circulatory shock on skeletal muscle mitochondrial oxidative activity in various substrates and cytochrome oxidase activity have been investigated using samples of muscle obtained by the needle biopsy technique from human subjects. The effect of shock on superoxide dismutase activity and glutathione content of skeletal muscle was also examined. The results show that there is a large decrease in cytochrome oxidase activity during shock and also in the capacity of the mitochondria to oxidize either succinate, or pyruvate, or palmitoyl carnitine. There is a fall in the tissue content of superoxide dismutase and in the total glutathione present. Furthermore, an increased oxidized glutathione content causes a decrease in the molar ratio of reduced to oxidized glutathione present in the muscle. These findings suggest that mitochondrial electron transport chain (ETC) oxidative damage can play a relevant role in the pathogenesis of circulatory shock and support the hypothesis of oxygen-free radical involvement in the cellular injury.

Biopsy, Needle↗
PubMed1985

Effects of L-carnitine administration on mitochondrial electron transport activity present in human muscle during circulatory shock.

Carnitine was administered to a group of patients in shock, and the activities of cytochrome oxidase and succinate cytochrome c reductase in muscle needle biopsies from these patients were compared to those activities present in a non-carnitine treated control group of patients. Carnitine seemingly exerted a significant protective action on cytochrome oxidase activity during the initial phases of shock, but not to such an extent on succinate cytochrome c reductase activities.

Carnitine↗
PubMedDate not supplied

Adaptive changes in response to acute hypoxia, ischemia and reperfusion in human cardiac cell.

BACKGROUND: Previous studies have shown that biomolecular and biochemical adaptive changes antagonize oxidative damage due to hypoxia and ischemia in myocardial cells. The aim of our study was to verify in human ischemic and reperfused cardiac tissue the relationship between mitochondrial enzyme activities and the activation of HSP70 and c-fos synthesis in the context of a cytoprotective mechanism. Nitric oxide (NO) modulating effects on mitochondrial respiratory chain enzyme activities in ischemic and reperfused tissue were investigated (preliminary report). METHODS: During elective coronary artery bypass grafting, in 30 consecutive patients ventricle samples were taken one before aortic clamping the second after 55 +/- 8 min ischemic period and the third 34 +/- 5 after final reperfusion. Coronary sinus blood samples were taken in parallel to assess free radical release measured by malondialdehyde (MDA) levels. In a small number of patients (N = 5) nitric oxide tissue levels were analyzed. RESULTS: When compared with normoxic tissue, a significant decrease in cytochrome oxidase (COX) and succinate Cyt-c reductase (SCR) activities in ischemic and reperfused samples were observed. The activation of HSP70-72 and c-fos transcription factor was evident in courses of ischemia and reperfusion. Blood MDA levels underline the concept that oxyradical generation characterizes peroxidative damage in reoxygenated myocardial tissue while adaptive changes which occur in ischemic cells seem to antagonize the oxyradical injury. CONCLUSIONS: In the course of heart surgery the myocardial cell seems to prevent ischemic damage activating some peculiar biomolecular and biochemical adaptive changes which permit the reversibility of the oxidative injury. In contrast it appears evident that massive and rapid reoxygenation of the cardiac tissue leads to peroxidative damage due to oxyradical generation. Nitric oxide seems to play a crucial role in cellular adaptation to ischemia even if further studies will be needed to elucidate these findings. From the data obtained in this work we cannot draw certain conclusions in terms of human cardiac cell adaptation to ischemia whereas it seems convincing that reoxygenation, as actually employed in clinical practice, compromises the integrity of the cells.

Acute Disease↗
PubMedDate not supplied

Deep sedation for magnetic resonance imaging. Personal experience.

AIM: Precision in diagnostic procedure and examination of paediatric patients often requires their absolute immobility. Deep sedation has proven to be an excellent method, allowing optimum technical quality of MRI particularly in younger age groups. The aim of study is to demonstrate the possible application of deep sedation through the use of 2 safe and manageable drugs. METHODS: We carefully evaluated and selected 82 patients (47 males and 35 females; average age 5.4 years): they came from various paediatrics departments. Deep sedation was practiced with: Chloral hydrate (60-80 mg/kg in one oral administration); propofol as intravenous bolus (2-2.5 mg/kg) followed by a maintenance infusion of 75-125 microg/kg/min. This was preceded by midazolam (0.05 mg/kg i.v.) outside the MRI room. Oxygen saturation (SpO2) was monitored in all patients along with heart rate in order to foresee the need for any possible therapeutic intervention. RESULTS: The sedation levels attained permitted the success of MRI assuring the immobilization required. Manually assisted mask ventilation was required for a period of 2-3 min in 5 patients treated with propofol. All other patients breathed autonomously. Complete reawakening occurred within 2 hours of drug administration. Surveillance was prolonged inside their respective units, however, without registering delayed side effects. CONCLUSION: The central point of the success of deep sedation is to define the type and dose of optimum drug for individual patients. This requires a qualified, expert group ready to intervene in the presence of adverse results of drugs administered. Propofol and chloral hydrate are the optimum drugs for diagnostic techniques requiring total immobilization and rapid reawakening.

Child, Preschool↗