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Biomedical subjects

R Bugiardini

Publications and source records attributed to R Bugiardini.

At least 55 records · Page 3Linked to original sources
PubMed1985

[Changes in angina threshold induced by administration of ergonovine maleate during pacing in patients with chronic exertional angina].

It is widely accepted that the occurrence of chest pain and/or ST segment elevation during ergonovine testing is a hallmark of abnormal coronary constriction. However, the negativity of this test cannot be considered as an incontrovertible proof of the absence of coronary sensitivity to vasoconstriction. Indeed, it could only indicate that the resulting effect is inadequate to critically reduce coronary blood flow. To test this hypothesis we studied 12 patients with proven coronary artery disease and negative ergonovine test who had complained of chronic exertional angina pectoris and referred variable threshold for the occurrence of pain. They were submitted to atrial pacing (starting from 90 bpm, with 10 bpm increments every 2 min) before (control) and after ergonovine administration (total dose = 0.675 mg). Time, heart rate and rate pressure product were evaluated at the onset of angina and significant ischemia (0.1 mV ST segment depression). After ergonovine, angina was achieved earlier (405 +/- 173 vs 526 +/- 180 sec, p less than 0.005) than during control and at a lower heart rate (116 +/- 15 vs 131 +/- 15 bpm, p less than 0.001) and rate pressure product (15.8 +/- 2.0 vs 18.8 +/- 2.3 X 10(3) U, p less than 0.001). Changes in anginal threshold were widely variable among cases being that the time to onset of pain was dramatically reduced in certain patients but unchanged in one. Similar results were obtained when substituting the ischemic to the anginal threshold. Thus, negativity to ergonovine testing does not imply the absence of coronary constriction which may be revealed when increasing myocardial oxygen demand by atrial pacing.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1984

Evaluation of the effects of catheter sampling for the study of platelet behavior in the pulmonary and coronary circulation.

To study the effects of sampling through cardiac catheters on indices of platelet function, we measured the levels of platelet factor 4 (PF4), beta thromboglobulin (BTG), and platelet aggregate ratio (PAR) in 10 patients with atrioventricular accessory pathway (AVNAP), six patients with primary pulmonary hypertension (PPH), and six patients with critical narrowing of the left anterior descending artery (LAD). In AVNAP and LAD patients samples were drawn simultaneously from a peripheral vein, coronary sinus, and brachial artery; in AVNAP patients samples were also obtained from the axillary vein before the coronary sinus was entered. In PPH patients samples were drawn from pulmonary artery, aorta, and a peripheral vein; in these patients the effects of an intravenous infusion of prostacyclin (PGI2) (2 to 8 ng/kg/min) on PF4, BTG, and PAR were also studied at all sampling sites. In all patients arterial, coronary sinus, pulmonary arterial, and axillary venous levels of PF4, BTG, and PAR significantly exceeded those measured in the peripheral vein. PGI2 infusion resulted in a significant decrease of PF4 at all sampling sites, while no consistent BTG changes were observed and PAR levels did not decrease in the peripheral vein. Although a considerable interpatient variability in PF4 levels was observed, a significant (r = 0.91) correlation was found in patients with AVNAP between simultaneous coronary sinus and arterial PF4 levels. The value of PF4 coronary sinus-arterial difference in LAD patients was consistently higher than that calculated in AVNAP patients (54.5 +/- 28.9 vs 4.2 +/- 3.8 ng/ml).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1984

Myocardial ischemia during ergonovine testing: different susceptibility to coronary vasoconstriction in patients with exertional and variant angina.

Coronary spasm is an accepted cause of transient myocardial ischemia in patients with variant angina; more recently it has been suggested that dynamic stenoses could also play an important role in the pathophysiology of exertional angina. To test this hypothesis we submitted 31 patients with histories typical of exertional angina to ergonovine testing and compared the electrocardiographic and clinical responses to those observed in seven patients with variant angina. All underwent bicycle ergometric exercise testing and coronary angiographic examination. For all tests, ST segment shifts of 0.1 mV or greater were considered to be diagnostic of myocardial ischemia. In patients with exertional angina, exercise testing produced diagnostic ST segment depression in 21 (68%). Ergonovine testing produced diagnostic ST segment depression in nine (29%). All nine had positive exercise test results and two- or three-vessel disease, yet the test was negative in seven other patients with positive exercise test results and similar angiographic findings. Conversely, in the seven patients with variant angina, results of exercise testing were positive in five (ST segment depression in two, ST elevation in three), while ergonovine produced ST segment elevation in all seven. Coronary angiographic examination showed normal arteries in two, one-vessel disease in four, and three-vessel disease in one. Results of all ergonovine tests were positive at values of rate pressure product much lower than those observed during exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1984

Ergonovine-induced myocardial ischemia: no role for serotonergic receptors?

Because ergonovine appears to produce coronary contractions by a serotonergic (5-HT) mechanism, we attempted to prevent ergonovine-induced ischemia in patients with vasospastic angina by pretreatment with ketanserin, a new selective 5-HT blocker. We studied seven patients with consistently positive results of ergonovine testing (ST segment elevation in three and ST segment depression in four). Ergonovine testing was performed before and after a bolus of 10 mg of ketanserin (all patients) and infusion of 2 to 4 mg/hr for 8 hr (six patients). To assess 5-HT blockade during ketanserin infusion, the constrictor response of hand veins to 5-HT was tested before and after ketanserin. Despite evidence of 5-HT blockade in hand veins, ergonovine-induced ischemia was not prevented by ketanserin in any patient, and there was no significant change in the dose of ergonovine required to provoke ischemia. In one patient, four spontaneous episodes of ST segment elevation occurred during infusion of ketanserin. The plasma concentrations of ketanserin at the time of ergonovine testing ranged from 61 to 127 ng/ml (mean 102) and were well above those that completely inhibit canine coronary 5-HT contractions in vitro. Although human coronary arteries may differ in their responsiveness to 5-HT or ketanserin, these data suggest that ischemia from ergonovine-induced coronary vasospasm is not mediated by 5-HT receptors.

Aged↗
PubMed1984

Hypersensitivity of gastric parietal cells to selective H2-receptor stimulation in duodenal ulcer.

According to previous studies, duodenal ulcer patients not only secrete more acid than normal subjects, but are also more sensitive to pentagastrin stimulation. The aim of this study was to investigate whether hypersensitivity of parietal cells also occurs with specific H2-receptor agonists such as impromidine. Twelve duodenal ulcer patients and 12 healthy volunteers were admitted to the study. After 30 minutes of basal secretion, impromidine was infused at increasing doses (2.5; 5.0; 10.0; 20 micrograms/kg-1/h-1) in both groups of subjects. The gastric acid secretion was significantly higher in the duodenal ulcer group. The percentage, for each dose, of the calculated maximal response (CMR) was always higher in the patient group, and the difference with respect to the control group, was always higher in the patient group, and the difference, with respect to the control group, was statistically significant. Also, the average D50 was significantly lower in the duodenal ulcer group. Drug safety evaluation confirmed the presence of reversible dose-dependent pharmacological side effects. This study showed that parietal cells are more sensitive to highly selective H2-receptor agonists such as impromidine. These results add further information to the physiopathological features of duodenal ulcer.

Adult↗
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↗