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C Guarnieri

Publications and source records attributed to C Guarnieri.

At least 145 records · Page 8Linked to original sources
PubMed1976

[Experimental revascularization of acute myocardial infarction. II: Activity of various oxidoreductive tissutal and serum enzymes (author's transl)].

The behaviour of some enzymatic activities, such as monoamino oxidase (MAO), diamino oxidase (DAO), catalase, peroxidase and creatin chinase (CPK) have been studied both in blood serum and myocardial tissue of acute infarcted dogs (obtained by coronary occlusion). The most significant results are the changes of the DAO activity (--50% from the control) and peroxidase activity (+60%), 6 hours after acute ischemia. The effect of reperfusion was studied 2 hours later. A recovery of DAO activities was shown, while the peroxidase activities stayed elevated. All the enzymatic activities studied were evaluated in the serum, under the same experimental conditions. An increase of all these activities was observed until 6th hour of coronary occlusion. The reperfusion of acute ischemia, after six hours, causes a further increase of CPK and MAO activities and a decrease of catalase peroxidase and particulary evident DAO activities. The results of this experiment show that reoxygenation, under our experimental conditions, increases a further enzymatic release and in part causes a metabolic recovery of heart muscle.

Amino Acid Oxidoreductases↗
PubMed1976

Experimental revascularization of acute myocardial infarction. III: Correlation between the behaviour of the free nucleotide acid solubles and some aliphatic biogenic amines.

Free nucleotide, polyamine and nucleic acid synthesis was studied in myocardial acute ischemia and reperfusion. An early stimulation of biosynthesis of these compounds was observed during ischemia, than later, a remarkable decrease of their specific radioactivity appeared. Reperfusion experiments cause a significant increase of nucleic acids and related compound biosynthesis. The results indicate that the biochemical mechanism of myocardial protein synthesis, under our experimental conditions are not irreversibly damaged by ischemia. In fact, the reperfusion causes a remarkable recovery of nucleic acid, free nucleotide and polyamine specific radioactivity. The changes during the period of infarction and subsequent reperfusion show that polyamines play a key role in myocardial ischemia and reperfusion.

Animals↗
PubMed1975

Polyamine and nucleoprotein correlations in hypertrophied and perfused heart.

A close relationship has been observed between polyamine, as spermine and spermidine, and nucleic acid synthesis during heart hypertrophy, induced in the rats experimentally, by physical exericse (swimming). The role of spermine on RNA synthesis has been studied by perfusion experiments of the heart. Spermine is able to stimulate myocardial RNA synthesis of all subcellular fractions. The biochemical mechanism of this phenomenon may be explained by the results of histone acetylation under the action of spermine, showing an increased radioactivity of F 2aI and F 2a2 arginine-rich histone fractions. This suggests that spermine may act modulating histone acetylation, with a consequence on the gene transcription mechanism.

Animals↗
PubMedDate not supplied

Alpha-tocopherol pretreatment improves endothelium-dependent vasodilation in aortic strips of young and aging rats exposed to oxidative stress.

Acetylcholine-induced, endothelium-dependent relaxation of norepinephrine-precontracted aortic strips, was severely impaired after exposure to a hypoxanthine/xanthine oxidase reaction generating oxygen radicals. This effect was more evident in aortic strips of aging rats (24 months old) in comparison to young rats (3 months old). The addition of authentic .NO (1 microM) completely relaxed aortic strips exposed to oxidative stress both in young and aging rats. In vitro EPR measurements showed that the .NO signal was reduced by enzymatic O2.- generating reaction. The activity of a partial purified preparation of constitutive NO synthase from rat cerebellum was significantly decreased after exposure to exogenous oxygen radicals. Pretreatment of aortic strips with 100 microM alpha-tocopherol-phosphate, produced a significant improvement of acetylcholine-dependent relaxation in the aortic strips exposed to oxidative stress, particularly in the aged vessel. The content of malondialdehyde in aortic tissue did not change after oxidative stress or alpha-tocopherol pretreatment. Alpha-tocopherol was unable to recover the NO synthase activity depressed in vitro by hypoxanthine/xanthine oxidase reaction. This study confirms that an oxidative stress impairs the endothelium-mediated vasodilation. Alpha-tocopherol pretreatment protects the vessel against this damage. The mechanism of action of alpha-tocopherol is unknown, but seems unrelated to an antioxidant activity.

Acetylcholine↗
PubMedDate not supplied

Role of reactive oxygen species in cardiovascular aging.

Biochemical and structural changes occurring in the myocardium with aging are mainly resulting from the association of a general tissue atrophy with the hypertrophy of the remaining myocytes. Whilst hypertrophy seems to be a compensatory process to the loss of cardiomyocytes and to a mild systolic hypertensive condition that accompanies elderly people, atrophy should be the modification more closely related to aging 'per se.' In support to the free radical theory of aging, several signs of oxidative damage have been shown in the aged heart, such as lipofuscin accumulation, decreased phospholipid unsaturation index, greater formation of both hydrogen peroxide and 8-hydroxy-2'deoxyguanosine. As a compensatory reaction, the activities of the main oxygen-radical scavenger enzymes are stimulated in the mitochondria of aged rat heart. Endothelium-mediated vasoregulation is more susceptible to oxidative stress in aged with respect to young rats, suggesting that also the vasculature can be negatively influenced by the oxygen free radicals generated during aging. The possible primary role of oxygen free radicals in the development of myocardial atrophy is also discussed.

Acetylcholine↗
PubMedDate not supplied

Age-dependent production of mitochondrial hydrogen peroxide, lipid peroxides and fluorescent pigments in the rat heart.

Mitochondria were prepared from hearts of 3-, 14-, 18-, and 24-month-old male Wistar rats. Respiratory control ratio (RCR) values did not change with age in the glutamate or succinate-induced respiration except at 24 months in which RCR values significantly increased with both the substrates. Using still glutamate or succinate as substrates the production of H2O2 was measured in the presence of antimycin. A 70% and 25% increase in H2O2 formation was observed at 14 and 18 months of age, respectively, in comparison to the youngest group. Only in the presence of succinate was a 25% elevation in H2O2 found at 24 months of age. These observations parallel with the decrease of the ratio between tissue levels of reduced and oxidized glutathione that was observed at 14 and 18 months of age. The concentration of myocardial malondialdehyde, a secondary product of lipid peroxidation, remained the same at all ages measured, most probably because it is readily metabolized in vivo. On the contrary the myocardial level of lipofuscin, which is not degraded by the cell, progressively increased beginning from 18 months of age.

Aging↗
PubMedDate not supplied

Opioids stimulate sarcolemmal NAD(P)H-vanadate dehydrogenase activity.

The present study demonstrates that the bovine cardiac sarcolemma possesses an NAD(P)H dehydrogenase activity which is able to oxidize both NADH and NAD(P)H in the presence of vanadate as an electron acceptor. The NADH dehydrogenase activity was significantly higher than the NAD(P)H dehydrogenase activity and both of them were almost completely inhibited by superoxide dismutase and atebrin and markedly reduced by the addition of the protonophore 2,4-dinitrophenol. The incubation of the sarcolemma in the presence of 10(-10), 10(-9), 10(-8) M methionine-enkephalin, a prevalent delta-opioid receptor agonist, or dynorphin A (1-17), a prevalent kappa-receptor agonist, produced a dose-dependent increase in the NAD(P)H dehydrogenase activity, with 10(-10) and 10(-9) M dynorphin A (1-17) more effective than the corresponding doses of methionine-enkephalin. The preincubation of the sarcolemma in the presence of superoxide-dismutase, atebrin or 2,4-dinitrophenol strongly inhibited the opioid-stimulated dehydrogenase activity. The stimulatory action elicited by 10(-8) M methionine-enkephalin or dynorphin A (1-17) was completely antagonized by 10(-8) M naloxone or Mr 1452, respectively, whilst 10(-8) M naloxone exerted only a partially antagonistic action against the effect produced by 10(-8) M dynorphin A (1-17), significantly more accentuated than the action of 10(-8) M Mr 1452 versus the same dose of methionine-enkephalin.

Animals↗
PubMedDate not supplied

Activation of lipase by a factor present in the gall-bladder epithelium.

The action of a bovine gall-bladder extract is studied on two lipolytic systems: the pancreas lipase and the plasma lipoproteinlipase. For pancreas lipase the lipolytic activity of pancreas homogenates of different species is evaluated in the presence of different quantities of gall-bladder extract. For plasma lipoproteinlipase, the enzyme is induced by injection of optimal doses of heparin associated with different quantities of gall-bladder extract and the activity is evaluated by measuring the clarifying power of the plasmas of the treated animals. The results confirm that the gall-bladder contains a factor activating the pancreas lipase and put in evidence some differences between lipase activities in different species. For plasma lipolytic activation, the action of the gall-bladder extract is particularly evident in the inductive phase of lipoproteinlipase, according to a typical process of saturation.

Animals↗
PubMedDate not supplied

Inhibitory effect of superoxide radicals on cardiac myofibrillar ATPase activity.

The superoxide radicals generated by the xanthine oxidase reaction reduced the myofibrillar Ca2+-ATPase activity. This negative effect was prevented by superoxide dismutase or by dithiothreitol, a protective thiol compound. Partial protection was achieved by catalase, while mannitol was ineffective. The myofibrillar Ca2+-ATPase exposed to O2-. radicals did not modify the affinity for Ca2+ while it showed a remarkable reduction of Vmax measured at the saturating level of Ca2+. The O2-. inhibited myofibrillar ATPase showed a higher value of Km for the cofactor associated to a reduced value of Vmax when studied in the presence of increasing concentration of ATP. Thus, circumstances that enhance the production of cardiac O2- radicals can be considered a negative metabolic event capable of depressing the myofibrillar Ca2+-ATPase activity.

Actomyosin↗
PubMedDate not supplied

Subcellular localization of alpha-tocopherol and its effect on RNA synthesis in perfused rabbit heart.

3H-tocopherol was administered by perfusion to rabbit hearts and rapidly entered the myocardial cells with an incorporation rate which was more evident inthe alpha-tocopherol deficient hearts than in the control hearts. During perfusion, the labelled alpha-tocopherol was slightly metabolized and 85% of the radioactivity was recovered as authentic alpha-tocopherol. The pattern of alpha-tocopherol distribution showed in both perfused hearts a significant binding of the radioactivity to the nuclei. The vitamin was also retained with high specific labelling in the mitochondria and in a lower degree in the microsomes and soluble fractions. Small amounts of radioactivity was found bound to the myofibrils. The study of the intranuclear distribution of tocopherol has revealed that the tocopherol-binding species were acidic nuclear macromolecules which exhibited characteristics of non-histone chromosomal proteins. Administration of alpha-tocopherol exhibited a positive effect on the stimulation of labelled RNA in the tocopherol-deficient perfused hearts. This was particularly evident at the nuclear level. The intracellular distribution of the vitamin and its ability to stimulate RNA synthesis in heart muscle can suggest a possible role of alpha-tocopherol in the regulation of gene activity.

Animals↗
PubMedDate not supplied

Effect of catecholamines on ornithine decarboxylase activity monitored in the perfused rat heart.

The activity of ornithine decarboxylase was monitored in situ by perfusing rat heart with (1-14COOH)-ornithine. Infusion of isoproterenol or noradrenaline caused after 15-20 min an activation of the ornithine decarboxylation 5 fold above control hearts; less evident was the effect of adrenaline. Isoproterenol induced ornithine decarboxylation was prevented by difluoromethyl-ornithine. Also propranolol produced a significative reduction of the flux of 14CO2 collected from the perfusate. The measurement of the ornithine decarboxylase activity in heart homogenates by confirming the above results, indicated that the in situ monitor of ornithine decarboxylation can represent an accurate method which reveals rapid activation of the enzyme.

Animals↗
PubMedDate not supplied

Inhibitory effect of oxidized glutathione on heart ornithine decarboxylase activity.

Cardiac ODC was prepared from rats after the injection of isoproterenol and was partially purified by thiol-affinity chromatography. This enzymatic preparation incubated with GSSG was inactivated in a concentration dependent process. The inactivated enzyme could be reactivated by the addition of various reducing compounds, including GSH. Kinetic studies on GSSG-inactivated ODC revealed that the enzyme was inhibited by a partially-non competitive mechanism.

Animals↗