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R Bugiardini

Publications and source records attributed to R Bugiardini.

At least 73 records · Page 4Linked to original sources
PubMed1982

[Ultrastructural changes in myocardial anoxia and reoxygenation].

The aim of this study is to describe the ultrastructural changes in anoxic rat hearts perfused with Langendorff technique and the effects of reoxygenation on myocardial cells. After 1 h of aerobic perfusion, the hearts were subjected to 30 min of anoxia and then to 5 and 30 min of reoxygenation. The following findings were observed: after 30 min of anoxia, loss of mitochondrial matrix and dilatation of the intracristal spaces. After 5 min of reoxygenation: diffuse mitochondrial swelling, sarcomeres disarranged and out of register, several contraction bands. After 30 min: no evidence of cytoplasmic or mitochondrial swelling. The maximum enzyme release was observed when a wide myofibrillar contraction occurred. These results may suggest that the oxygen availability consequent to myocardium anoxia lead to further cell damage.

Animals↗
PubMed1981

[Markers of necrosis and anoxia in the post-infarct heart failure: determination of infarct size (author's transl)].

28 patients with acute myocardial infarct (AMI), 10 of whom presenting left ventricular failure, have been studied. By serial determinations of alpha-hydroxybutyrate dehydrogenase (HBDH) and creatine kinase (CK), the releasing times (RT) and the total releases (TR) of the two enzymes have been calculated, according to the Shell's method modified by Norris. The RT of HBDH have resulted more prolonged in the decompensated patients (48.1 +/- 16.0 vs 37.3 +/- 9.1 h; t = 2.297; p less 0.05). Highly significant correlations have been demonstrated between the total releases of the two enzymes; r = 0.816, p less than 0.01 (with failure); r = 0.766, p less than 0.001 (without failure). For neither enzyme, instead, significant differences have been shown between the TR of the two patient groups. The following conclusions can be drawn. 1) infarct size probably is not the only factor able to induce heart failure during AMI; 2) infarct size can be equally calculated from both HBDH or CK values, though some considerations may make preferable the choice of CK; 3) the more prolonged release of HBDH during heart failure suggests the hypothesis that lactate accumulation is an important factor influencing the appearance of this compliance.

Adult↗
PubMed1981

[Relationships between the initial area of necrosis and prognosis of acute myocardial infarct].

85 patients with acute myocardial infarction (AMI) have been studied retrospectively. 25 of them died within the 40th day after admission. Serum CK release during AMI can be described by the logistic equation: (formula: see text). We have evaluated for each patient both the final infarct size (calculated at the time of maximal enzyme activity: Tmax) and the initial one (calculated at the inflection time of the curve: Tflex). The total enzyme release in 1 ml of blood has been considered as an indirect index of infarct size. Our results show a good correlation between the initial and the final infarct size. We have considered as limits between survivors and non-survivors the following values: 2.2 IU/ml and 0.6 IU/ml for total CK release at Tmax and at Tflex respectively. The percentage of mortality in those groups is very similar (69% and 75%). However only 38% of non-survivors shows higher values than both 2.2 IU/ml and 0.6 IU/ml. The calculation of infarct size at Tflex allows an early identification of the high risk patients.

Clinical Enzyme Tests↗
PubMed1980

[The protective effects of glucose in ischaemia, anoxia and reoxygenation (author's transl)].

In the present study we used a model of underperfusion or anoxia followed by reperfusion to assess the role of glycolysis by substituting pyruvate or mannitol for glucose as substrate. Hearts were removed from male Sprague-Dawley rats (250-400 g) and perfused by the technique of Langendorff. The perfusate was Krebs-Henseleit bicarbonate buffer gassed with 95% O2, 5% CO2 or with 95% N2, 5% CO2 mixture and containing substrates as can be seen in the figures. The mild ischemia was obtained by reducing the perfusion pressure by 70%, from 60-70 cm H2O to 10-20 cm H2O. The coronary flow was rapidly reduced to 0.8 +/- 0.03 ml/min within the first 5 minutes. After mild ischemia anaerobic glycolysis was accelerated because lactate production in ischemic hearts perfused with glucose (36.2 +/- 15.3 microM/g/min-1) was higher than in the ischemic hearts perfused with mannitol (6.8 +/- 1.9 microM/g/min-1). During mild ischemia or anoxia there was little difference in the rate of release of creatin-kinase for all the substrates tested, but major differences become apparent on reperfusion. In that period the highest values of CK release were found in mannitol perfused hearts, the lowest in glucose perfused hearts. These results suggest that the rate of glycolytic flux during mild ischemia or anoxia may prevent enzyme release. The beneficial effect of glucose has been observed also during reperfusion. In fact enzyme release was higher in hearts reperfused with glucose than with pyruvate. When pyruvate is the only exogenous substrate available for isolated oxigenated hearts, tissue levels of citric acid cycle intermediates are high and oxidation of these substrates can account for 100% of the oxygen consumption. Therefore we suppose that oxidation of noncarbohydrate substrates such as pyruvate in reperfusion is complicated by the high mitochondrial damage. As a consequence anaerobic glycolytic pathway may play a special role in the maintenance of the membrane integrity also in the early phases of reperfusion.

Animals↗
PubMed1980

[Critical analysis of the radioimmunological methods of determining creatine kinase isoenzyme MB (CK-MB), myoglobin (MG) and of LDH (H4) in ischemic cardiopathy].

We have studied 135 subjects of whom 100 were normal individuals; 10 with diagnosis of acute myocardial infarction (AMI); 10 with angina pectoris; 10 undergoing cardiac catheterism; 5 who underwent open heart surgery. To verify the radioimmunoassay usefulness of CPK cardiac isoenzyme (CK-RIA), of lactate dehydrogenase [LDH (H4)], of myoglobin (MG) in the diagnosis of ischemic disease, we have determined for serum samples: LDH (H4) by radioimmunoassay and HBDH by biochemical assay; CK by biochemical assay; CK-MB by biochemical and radioimmunological assay; MG by radioimmunoassay. The results indicate MG as a sensitive marker for the diagnosis of AMI. In fact serial serum determinations in patients with AMI showed myoglobin levels in 60% of the cases within 1 h after the onset of pain. The CK-RIA is the most sensitive test to evaluate infarct size and LDH (H4) conditioned by the amount of intracellular lactate is an useful test to evaluate myocardial anoxia.

Acute Disease↗
PubMed1980

[Prediction of the infarct size by the serum levels of creatin kinase. A new methodological method (author's transl)].

Logistic equation is proposed as a new mathematical model describing the course of the ascending branch of the serum creatine kinase curve: E(t) = K divided by 1 + ea-bt where: E(t) = CK concentration at time t (mU/ml); t = time in hours from the onset of enzyme release; e = natural logarithm base; K = horizontal asymptote of the curve (maximal enzyme activity); a, b = typical variable prameters of the curve. Prediction is based on the identification of the infection point of the ascending branch of the serum CK curve. The enzyme activity corresponding to this point is half of the maximal one. In 14 patients with acute myocardial infarction infarct size (CK-g-Eq) was calculated by the method of Shell et al. In these patients the average differences between observed and predicted parameters were respectively (X +/- SD): -0.64 +/- 2.13 h for the maximal activity time; 16.57 +/- 53.15 mU/ml for the maximal activity and 0.02 +/- 2.44 CK-g-Eq for the infarct size. In detail it can be observed that the average of the per cent differences between observed and predicted infarct size was 1.10 +/- 5.31% and the maximal per cent difference only +10.40%.

Creatine Kinase↗