Search PubMed⌕ Search

Biomedical subjects

R Raddino

Publications and source records attributed to R Raddino.

At least 55 records · Page 3Linked to original sources
PubMed1986

Myocardial recovery during post-ischaemic reperfusion: effects of nifedipine, calcium and magnesium.

We studied the effects of various interventions introduced at the time of post-ischaemic reperfusion on mechanical activity, tissue and mitochondrial calcium, mitochondrial function and tissue ATP and CP of isolated perfused rabbit hearts. These interventions were: nifedipine, low calcium (0.75 mM, 0.15 mM and 0.05 mM), high magnesium (15 mM) and high magnesium (15 mM) with low calcium (0.75 mM). Ischemia was induced by abolishing coronary flow for 60 min, followed by 30 min of reperfusion. The results indicate that nifedipine when given during reperfusion had no protective effect, whilst it was beneficial when administrated before ischaemia. Lowering calcium content of the perfusate during reperfusion may be advantageous, depending on the degree of calcium reduction. Reperfusion with high magnesium reduced the mitochondrial calcium overload and maintained the mitochondrial ATP-producing capacity but failed to modify the increase of tissue calcium and of diastolic pressure. Lowering calcium content in the presence of high magnesium resulted in better protection. These data suggest that the conditions of reperfusion may influence the capacity of myocardial recovery.

Adenosine Triphosphate↗
PubMed1986

Effects of 17 beta-estradiol on the isolated rabbit heart.

We have studied the effects of 17 beta-estradiol on the left ventricular pressure and on the coronary perfusion pressure in isolated rabbit heart, in order to evaluate the action of this hormone on the myocardial contractility and on the coronary resistances. 17 beta-Estradiol has induced a negative inotropic effect starting from a concentration of 10(-6) M and a vasodilation starting from 10(-7) M when administered on a vasopressin-induced coronary spasm. These effects are not related to sex or to alpha-, beta-adrenergic, histaminergic, anaesthetic-like mechanisms, but seem to interfere with calcium transport.

Animals↗
PubMed1985

Reproducibility of metabolical parameters during successive coronary sinus pacing in patients known to have coronary artery disease.

We have studied the reproducibility of myocardial extraction ratios of lactate, glucose and free fatty acids in patients with stable angina during atrial pacing. Two pacing periods, separated by an interval of 45 min, were imposed. The individual data were highly reproducible for lactate. Mean values for glucose and for free fatty acids were closely similar in the two successive tests, but the individual response was not so highly reproducible. We recommend the demonstration of the reproducibility of events during pacing in studies in which the effects of the therapeutic interventions are being assessed. This is especially so when observations are made in a small number of patients.

Angina Pectoris↗
PubMed1985

Role of oxygen in myocardial ischaemic and reperfusion damage: effect of alpha-tocopherol.

There is evidence that oxygen-derived free radicals may play a role in myocardial ischaemic and reperfusion injury. Major sources of O2 free radicals formation during ischaemia and reperfusion are: the enzyme xanthine oxidase, activated neutrophils and the myocardial mitochondria. However, in the heart there are defense mechanisms against the toxic oxygen metabolites. They include the enzyme superoxide dismutase, catalase and glutathione peroxidase plus endogenous antioxidants like vitamin E, ascorbic acid and cysteine. We have investigated in the isolated rabbit hearts the effects of ischaemia and reperfusion on these defence mechanisms. 90 min of ischaemia and/or hypoxia induced a significant reduction of mitochondrial superoxide dismutase, and of reduced glutathione/oxidized glutathione ratio which was further declined after reperfusion indicating that an oxidative stress has occurred. These alterations are associated with massive tissue and mitochondrial calcium accumulation, loss of mitochondrial function and severe membrane damage. The effects of vitamin E on these parameters have been investigated. Administration of 1.1 mg of dl-alpha-tocopherol acetate showed a protective effect on mitochondrial function but it failed to improve the recovery of mechanical function during reperfusion.

Animals↗
PubMed1984

Action of oxmetidine on the rabbit aorta: comparison with some calcium entry blockers and nitroglycerin.

The novel histamine H2 receptor antagonist, oxmetidine, was tested on isolated rabbit aorta for its activity on calcium ion transport and/or utilization suggested from previous experiments. Its effect was compared with that of some "classical" calcium entry blockers (verapamil, D-600 and nifedipine) and of nitroglycerin which acts predominantly on the intracellular calcium. The effect of all these compounds was evaluated against the contraction elicited by KCl, angiotensin and noradrenaline acting by different spasmogenic mechanisms. Oxmetidine was found to antagonize to approximately the same extent the effect of the three stimulatory substances: however concentrations required for this effect were from 10 to 100 times as high as those required to inhibit histamine H2 receptors. Nitroglycerin behaved quite similarly but was approximately 10.000 times more potent than oxmetidine. Verapamil and D-600 (which were virtually identical) were always more potent (about 10 times) than oxmetidine but less efficacious on the angiotensin-induced contraction. Finally nifedipine was the most active compound on the KCl induced contraction but was almost ineffective against angiotensin. It is concluded that oxmetidine, though with a still unclear mechanism, possesses a weak but definite inhibitory effect on the availability of the intracellular calcium resembling the effect of nitroglycerin. Whether or not an action on the influx of calcium is also present cannot be surely established as long as calcium fluxes are not measured. Differences in the behaviour of the "classical" calcium entry blockers suggest that each of them possesses, together with the main well recognized effect, additional effects responsible for apparently surprising results obtained against different spasmogenic compounds.

Animals↗
PubMed1984

[The ambulatory ECG in the evaluation of coronary insufficiency].

To assess the diagnostic value of continuous ambulatory ECG in exercise angina pectoris, 49 males (mean age 52, 1 years), with exercise ischemic ECG changes and positive coronary angiography were evaluated. Ischemic ST-changes were detected by ambulatory ECG in 47% of those patients; most of these ST segment displacements were asymptomatic and a lot of them occurred at rest. In order to assess the specificity of ambulatory ECG, 90 healthy subjects (47 males and 43 females, mean age 43,6 years), were also evaluated 8.9% of these subjects developed ischemia like episodes of ST segment deviation. We conclude that in exercise angina pectoris the ambulatory ECG allows to recording silent ST segment changes, in spite of a poor diagnostic sensitivity. The low specificity of ST segment depression recorded by ambulatory ECG must be also emphasized.

Adult↗
PubMed1984

Reversible and irreversible ischaemic damage: importance of energy metabolism.

In this study the effects of different degrees and duration of coronary flow reduction on pressure development of the isolated and perfused rabbit hearts has been studied. Three different degrees of ischaemia lasting for 30, 60 and 90 minutes have been investigated, after which the effects of post-ischaemic reperfusion have been followed. The effects of substituting FFA for glucose as myocardial substrate has also been investigated. Reperfusion resulted in a recovery of mechanical function or in a further worsening of mechanical function, depending upon the degree, duration of flow reduction and substrate employed. To establish the causes of reperfusion damage, in a separate series of experiments the effects of reperfusion after 90 minutes of severe ischaemia on lactate, CPK and Mg++ release, tissue and mitochondrial calcium content tissue ATP and CP concentration and mitochondrial function have been determined. The ultrastructural damage of the myocardial cell have also been established. The results obtained suggest that mitochondria play an important role in reperfusion damage.

Adenosine Triphosphate↗
PubMed1980

[Phenoxybenzamine antagonism of ergometrine-induced increase of coronary artery resistance in rabbits].

Ergometrine is currently used as a test for Prinzmetal variant angina, causing specifically a coronary artery spasm in these patients, even if the mechanism of this drug on coronaries is still unclear. In isolated rabbit heart perfused at constant flow the administration of ergometrine at the concentration of 2.2 x 10(-5) M evoked a marked and longlasting increase of coronary resistance which was revealed by a rise in perfusion pressure from 68.2 +/- 12.9 to 124.4 +/- 21.7 (m +/- SD; n=21). This increase appears only with repeated perfusions of the drug and moreover it was not reproducible in the same preparation after its maximal response. The vasoconstriction was not significantly affected either by atropine or mepyramine, but it was strongly reduced by the phenoxybenzamine pretreatment (2.9 x 10(-6) M; n=8). It is evident the role of alpha-adrenergic receptors in ergometrine effect, but our results do not allow to understand its true mechanism, in fact the noradrenaline release can not be completely excluded.

Animals↗
PubMed1980

[Effect and action mechanism of hypothermia to preserve the ischaemic myocardium (author's transl)].

The ability of hypothermia (34 degrees, 28 degrees) to preserve cardiac metabolism and performance during ischemia, was evaluated in the isolated Langendorff perfused rabbit heart. The hearts, isolated and perfused aerobically for 20', were made ischemic for 90' and their wall temperature maintained either at 37 degrees, 34 degrees and 28 degrees. The hearts were consequently reperfused at 37 degrees for 30'. Some of the hearts were frozen and assayed for ATP and CP. Others were homogenized and their mitochondria harvest, using either an EDTA free or an EDTA-containing extraction medium. The oxidative phosphorylating and ATP generating capacity of these mitochondria were established and their Ca++ content determined. The mechanical performance of the hearts, which were paced, was monitored by means of an intra-ventricular balloon filled with water and connected with a pressure transducer. The hearts that were made ischemic and maintained at 37 degrees were severely depleted in ATP and CP content, their mitochondria accumulated Ca++ and their oxidative phosphorylating activity was impaired. During reperfusion mitochondrial Ca++ was substantially increased, the capacity of the mitochondria to use O2 for state III respiration was further impaired and their ATP generating capacity reduced. Diastolic pressure increased and there was no recovery of the ability of the hearts to develop sistolic pressure. The hearts made ischemic and maintained at 28 degrees were protected. There was a less marked rise in mitochondrial Ca++ concentration after ischemia and during reperfusion; the mitochondria recovered the capacity of utilizing O2 and of generating ATP. That was coincident with and almost complete recovery of mechanical performance. Hypothermia at 34 degrees during ischemia provoked only a partial protection. These results are discussed in accordance with the hypothesis that hypothermia protects heart muscle against the deleterious effects of ischemia not only by reducing the metabolic requirement but also by maintaining intracellular homeostasis with respect to Ca++.

Adenosine Triphosphate↗