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Biomedical subjects

M Galvani

Publications and source records attributed to M Galvani.

At least 55 records · Page 3Linked to original sources
PubMed1995

Non-invasive assessment of reperfusion of the infarct-related artery during coronary thrombolysis and its relation with left ventricular function.

We monitored ST segment continuously for at least 3 h after the beginning of lytic treatment in 103 patients undergoing early coronary thrombolysis for acute myocardial infarction in order to ascertain whether this technique, which has been shown to be useful to assess recanalization of the infarct-related artery, is also able to identify the improvement in left ventricular function associated with successful reperfusion. Global left ventricular function (assessed in the 30 degrees right anterior oblique projection with the area/length method) and infarct zone wall motion (studied with the centerline method) were evaluated at least 4 weeks after the event. Reperfusion was thought to be achieved when ST segment elevation dropped > 50% relative to the most abnormal peak documented at any time in the study. Eighty patients (78%) met the criterium for successful reperfusion (group 1), and 23 (22%) did not (group 2). Both groups had similar clinical and angiographic characteristics. All indexes of global left ventricular function were significantly better in group 1 than in group 2 patients (end-diastolic volume: 176 +/- 51 vs. 209 +/- 76 ml, end-systolic volume: 66 +/- 40 vs. 97 +/- 55 ml, ejection fraction: 65 +/- 13 vs. 57 +/- 11%, respectively, all P < 0.02). Also the severity (-1.6 +/- 1.3 vs. -2.6 +/- 1.01 S.D./chord, respectively, P < 0.001) and the extension of hypokinesia in the infarct zone (number of chords with > 2 S.D.: 13 +/- 16 vs. 28 +/- 17, respectively, P < 0.0001) were less in group 1 than in group 2 patients. Furthermore, in reperfused patients, both global left ventricular function and regional wall motion were better in those admitted < 60 min from onset of pain. In conclusion, patients with rapid ( > 50%) decrease of ST segment elevation have smaller infarct size and better global left ventricular function than patients without electrocardiographic signs of reperfusion as assessed by continuous ST segment monitoring. This suggests that this non-invasive technique is a powerful tool able to identify patients most benefiting from thrombolytic therapy.

Cardiac Catheterization↗
PubMed1994

Failure of fixed dose intravenous heparin to suppress increases in thrombin activity after coronary thrombolysis with streptokinase.

OBJECTIVES: This study was designed to define the extent of inhibition of thrombin activity achieved with conjunctive fixed dose intravenous sodium heparin compared with fixed dose subcutaneous calcium heparin in patients receiving intravenous streptokinase for acute myocardial infarction. BACKGROUND: The role of heparin therapy during coronary thrombolysis with streptokinase is controversial, in part because the efficacy of different conjunctive heparin regimens in inhibiting early increases of thrombin activity is not known. METHODS: Twenty-eight patients treated with 1.5 million U of streptokinase and 165 mg of aspirin for acute myocardial infarction were randomly assigned to receive fixed dose subcutaneous heparin therapy (12,500 U every 12 h delayed until 4 h after the end of streptokinase therapy [n = 14]) or fixed dose intravenous heparin (5,000-U bolus followed by 1,000-U/h infusion [n = 14]). Anticoagulation was assessed with serial measurements of activated partial thromboplastin time, and thrombin activity by measuring fibrinopeptide A and thrombin-antithrombin III complex levels. Plasma concentrations of creatine kinase (CK) MM isoforms were measured for 3 h to determine recanalization (increase in activity > 0.18%/min). RESULTS: Recanalization occurred in 27%, 64% and 79% of patients given subcutaneous heparin versus 43%, 76% and 86% of those given intravenous heparin at 1, 2 and 3 h, respectively (p = 0.6). Concentrations of fibrinopeptide A (mean +/- SEM) at 1 h were higher in patients without (n = 5) than in those with (n = 23) CK-MM isoform criteria for recanalization (76.4 +/- 25.7 vs. 25.2 +/- 5.2 nmol/liter, p = 0.02), and at 1, 2 and 3 h were significantly lower with fixed dose intravenous heparin (18.4 +/- 4.8 vs. 46.7 +/- 10.2 nmol/liter at 1 h, p = 0.004) than without heparin. After fixed dose subcutaneous heparin at 4 h, fibrinopeptide A levels were similar in both groups despite lower activated partial thromboplastin times in patients who received fixed dose subcutaneous heparin. However, fibrinopeptide A was not consistently suppressed in either group (fixed dose subcutaneous heparin 8.7 +/- 1.8 nmol/liter vs. fixed dose intravenous heparin 11.8 +/- 5.2 nmol/liter) at 48 h (p = 0.4). No significant changes in the concentration of thrombin-antithrombin III complexes were found between the two groups. CONCLUSIONS: Fixed dose intravenous heparin attenuates increases in fibrinopeptide A early after streptokinase. Subsequent fixed dose intravenous and subcutaneous heparin have similar effects but are relatively ineffective in suppressing thrombin activity, suggesting a role for more potent antithrombin agents during coronary thrombolysis with streptokinase.

Aged↗
PubMed1994

Concurrent nitroglycerin therapy impairs tissue-type plasminogen activator-induced thrombolysis in patients with acute myocardial infarction.

Nitroglycerin given with tissue-type plasminogen activator (t-PA) has been shown to decrease the thrombolytic effect of t-PA in animal models of coronary artery thrombosis. The present study was conducted to determine whether such an interaction between nitroglycerin and t-PA occurs in patients with acute myocardial infarction undergoing thrombolytic treatment. Patients with acute myocardial infarction were treated with t-PA plus saline solution (group 1; n = 11) or t-PA plus nitroglycerin (group 2; n = 36). Stable coronary artery reperfusion assessed by continuous ST-segment monitoring in 2 electrocardiographic leads, and release of creatine kinase occurred in 91% of group 1 patients and in 44% of group 2 patients (95% confidence interval, 14% to 82%; p < 0.02). Plasma levels of t-PA antigen were consistently (p < 0.005) higher in group 1 than in group 2 patients up to 6 hours after t-PA infusion. Conversely, plasminogen activator inhibitor-1 (PAI-1) levels were slightly higher in group 2 than in group 1 patients. These observations indicate that nitroglycerin given with t-PA significantly decreases the plasma t-PA antigen concentrations and impairs the thrombolytic effect of t-PA in patients with acute myocardial infarction.

Aged↗
PubMed1994

[Echocardiographic study of left ventricular function using automated border detection in normal subjects].

BACKGROUND: Two-dimensional (2D) echocardiographic automated border detection (ABD) can provide on-line measurement of left ventricular cavity area and fractional area change. However, this new quantitative method has not been extensively validated. METHODS: Values of manually traced areas on 2D-echo images were compared with those obtained from ABD in 34 consecutive normal subjects (age 16-65 years). Only subjects with more than 70% of endocardial border circumferences clearly seen in both selected imaging planes were included in the study. We evaluated left ventricular end-diastolic and end-systolic area, and fractional area change obtained from mid-left ventricular short axis and apical 4-chamber view. Left ventricular volumes (area/length method) and ejection fraction were manually calculated off-line from apical 4-chamber view. RESULTS: From the short axis view, left ventricular cavity area measurements with ABD were obtained in 85% of subjects. The values closely correlated with off-line measurements: end-diastolic area 15.6 +/- 3.1 vs 14.8 +/- 3.3 cm2, r = 0.88 SEE = 1.58; end-systolic area 7.2 +/- 1.7 vs 6.7 +/- 1.7 cm2, r = 0.88 SEE = 0.80. A good correlation was also found for the apical 4-chamber view; end-diastolic area 25.9 +/- 5.9 vs 25.3 +/- 5.5 cm2, r = 0.97 SEE = 1.36; end-systolic area 16.3 +/- 4.1 vs 15.0 +/- 3.8 cm2, r = 0.92 SEE = 1.51. In this view ABD measurements were obtained in 79% of subjects. A significant correlation was also found between the end-diastolic volume and short axis (r = 0.54, SEE = 2.63; p 0.003) and apical 4-chamber (r = 0.66, SEE = 4.51; p = 0.0002) ABD diastolic area. Similarly, the end-systolic volume was significantly correlated with short axis (r = 0.57, SEE = 1.42; p = 0.001) and apical 4-chamber (r = 0.55, SEE = 3.54; p = 0.003) ABD systolic area. However, the on-line fractional area change correlated with off-line ejection fraction better from short axis view: (r = 0.72 SEE = 3.52) than from apical 4-chamber view (r = 0.45 SEE = 6.84). CONCLUSIONS: These data indicate that: 1) left ventricular areas measured by ABD correlate well with manually measured areas and volumes; 2) short axis ABD fractional area change may be a reliable substitute of off-line manually traced ejection fraction in normal subjects.

Adolescent↗
PubMed1993

Patency of the infarct-related artery and left ventricular function as the major determinants of survival after Q-wave acute myocardial infarction.

One hundred seventy-two patients with 1-vessel disease documented at predischarge angiography who had been followed for 43 +/- 30 months after an initial Q-wave acute myocardial infarction were retrospectively evaluated to investigate the prognostic value of infarct-related artery patency and left ventricular (LV) function. Multiple logistic regression analysis revealed that only infarct artery patency (Thrombolysis in Myocardial Infarction [TIMI] grades 2-3 vs 0-1) (Z = 2.24; p < 0.05) and end-systolic volume index (Z = -2.67; p < 0.01) were independently related to survival. Sixteen cardiac deaths were observed; all 16 patients had LV dysfunction (defined as end-systolic volume index > 40 ml/m2), and 15 had an occluded infarct-related artery. In the subgroup with LV dysfunction, the 10-year percent survival rate was 20% among patients with TIMI grade 0 to 1 versus 96% with grade 2-3 (p < 0.001). Patency of the infarct-related artery was also the only independent predictor of recurrent ischemia (Z = 2.59; p < 0.01). In conclusion, both infarct-related artery patency and LV function are independent predictors of survival after Q-wave acute myocardial infarction. Patients with normal LV function have an excellent long-term prognosis, which is only partially counterbalanced by the tendency toward clinical instability observed in those with an open infarct-related vessel. However, when an occluded infarct-related artery is observed in the setting of LV dysfunction, the long-term outcome appears to be relatively poor.

Cardiac Volume↗
PubMed1988

[Angina of effort with a variable threshold: a unique entity due to different mechanisms?].

Variable threshold during exertion is a common feature in patients with chronic exertional angina. Changes in coronary vasomotor tone, when occurring at sites of critical narrowings, are a plausible explanation for variability of symptoms in these patients. However, the evidence supporting this hypothesis is still uncertain. Accordingly, we performed four computer assisted, multistage bicycle ergometer tests, without drugs, in 30 patients with chronic exertional angina, exercise induced ST depression, and a history of variable anginal threshold during exertion. Significant coronary artery disease was documented in each case by coronary arteriography. Patients were tested at the same time of day within a two week period. Comparison was made between each single test and the average of the remaining three. Time to 0.1 mV ST depression showed significant (+/- 20%) changes in 27 (90%) patients. Variability was shown in two out of four tests in 25 patients (83%), in three tests in 10 (33%), and in four tests in 2 (7%). Rate pressure product at 0.1 mV ST depression was concurrently changed (+/- 20%) in 20 patients (67%). Variability in two, three and four tests was observed in 7 (22%), 2 (7%) and 2 (7%) patients, respectively. Changes in time to 0.1 mV ST depression paralleled those in rate-pressure product at the onset of ischemia in 6 patients (22%) (dynamic ischemic threshold). Rate pressure product at 0.1 mV ST depression was unchanged despite variations in time to 0.1 mV ST depression in 10 patients (37%) (fixed ischemic threshold). The remaining 11 patients (41%) showed variable exercise tolerance associated with fixed (13 tests) and dynamic (13 tests) ischemic threshold.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1987

Myocardial ischemia during intravenous prostacyclin administration: hemodynamic findings and precautionary measures.

This study reports coronary and systemic hemodynamics, and metabolic responses to atrial pacing, prostacyclin (PGI2), and iloprost, its stable analogue, in 16 patients with severe coronary obstruction as well as predominant narrowing in the left anterior descending artery. PGI2 caused ischemia in six patients with low anginal threshold during pacing. In three of them ischemia was also precipitated by iloprost. Drugs were infused at therapeutic doses and were discontinued when pain occurred. Angina disappeared promptly (less than or equal to 3 minutes) and spontaneously after the infusion of PGI2, whereas after the analogue it was long lasting (greater than or equal to 5 minutes) and was relieved by 125 mg intravenous aminophylline, an antagonist of dipyridamole-induced coronary dilation. Ischemia was associated with a drug-induced decrease in arterial blood pressure and reflex tachycardia, and occurred despite increased great cardiac vein (GCV) blood flow and decreased resistance, which is consistent with either a failure of regional flow to increase proportionally to the metabolic demand or a subendocardial-subepicardial steal. However, the following findings favor the latter hypothesis: heart rate and rate-pressure product at the onset of pain were lower with drugs than with pacing, and GCV blood flow, measured at a comparable heart rate, was less with pacing than with drugs. In conclusion, PGI2 and analogues may induce ischemia in patients with advanced coronary artery disease. The mechanism appears to be related to a dipyridamole-like maldistribution of flow. Counteraction of ischemia can be achieved by aminophylline.

Cardiovascular Agents↗
PubMed1986

Effects of iloprost, a stable prostacyclin analog, on exercise capacity and platelet aggregation in stable angina pectoris.

The effects of iloprost, a chemically stable compound with prostacyclin mimetic activity, on exercise capacity and platelet aggregation were assessed in 24 patients with effort angina and proved critical (at least 70% diameter narrowing) coronary artery disease. Upright bicycle ergometer testing (25-W increments every 2 minutes) was performed during drug and placebo infusions using a crossover, randomized, single-blind protocol. Samples for measurements of adenosine diphosphate-induced platelet aggregation in platelet-rich plasma were obtained in all patients before and during the study. Compared with placebo, intravenous iloprost consistently (p less than 0.001) prolonged exercise duration and time to onset of significant (0.1 mV) ST depression. Angina and ST depression occurred at a greater heart rate and rate-pressure product. Benefits were remarkable in some patients (67%) and not in others. Iloprost administration resulted in reduced platelet aggregation at peak exercise in all patients, whether they had consistent or little response to the drug. Thus, iloprost administration may improve exercise capacity in patients with stable exertional angina pectoris. Improvements are independent of changes in the major determinants of myocardial oxygen demand and associated with markedly reduced platelet aggregation, which may account for increased myocardial perfusion in patients with high sensitivity to coronary constriction.

Angina Pectoris↗
PubMed1986

[Opposing effects of propranolol and diltiazem on the angina threshold during an exercise test in patients with syndrome X].

Patients with angina pectoris, exercise induced myocardial ischemia, normal coronary arteries and no evidence of epicardial spasm, i.e. patients with syndrome x, have been suggested to haven inadequate increase in coronary blood flow during tachycardia, possibly due to a functional disorder of small coronary vessels. To evaluate the best medical management of this syndrome we studied 13 patients who showed the above set of findings. Patients were given propranolol (160 mg daily), diltiazem (360 mg daily) and placebo for 2 weeks, using a randomized single blind protocol. Upright bicycle ergometer testing was performed at the end of each period of treatment. Compared to placebo, diltiazem significantly (p less than 0.001) prolonged exercise duration (x +/- SD: 365 +/- 86 vs 303 +/- 89 sec) and time to onset of angina (358 +/- 88 vs 276 +/- 90 sec). Angina appeared in 7 patients with diltiazem vs 13 patients with placebo and occurred at a higher rate pressure product (26.3 +/- 3.5 vs 24.1 +/- 2.8 X 10(-3); p less than 0.02). Conversely, following propranolol exercise duration and time to onset of angina were unchanged and angina appeared in all patients at a lower rate pressure product (18.3 +/- 2.9 vs 24.4 +/- 3.6 X 10(-3); p less than 0.001). The most likely explanations for these findings are: propranolol counteracts beta 2-adrenergic receptors, thus further reducing coronary reserve. This may lower the anginal threshold; Diltiazem reduces smooth muscle tone in small coronary vessels. This may result in increased coronary reserve and exercise duration.

Adult↗
PubMed1985

Myocardial ischemia induced by prostacyclin and iloprost.

Vasodilators of resistive vessels may induce ischemia in patients with coronary artery disease. To evaluate this possibility during prostacyclin (PGI2; scalar doses up to 10 ng/kg/min) and prostacyclin analog (iloprost; scalar doses up to 6 ng/kg/min) infusions, we studied 33 patients with angina pectoris and proved coronary artery disease. Patients were also submitted to dipyridamole (0.15 mg/kg/min for 4 minutes) and exercise stress testing (starting at 25 W and increasing 25 W every 2 minutes). In a preliminary study the hemodynamic and side effects of iloprost were studied in seven healthy subjects. At an iloprost dose of 4 to 6 ng/kg/min, these subjects had a significant decrease in mean arterial pressure and total peripheral and pulmonary vascular resistances. Side effects were limited to facial flushing and slight headache and were readily reversible. PGI2 induced typical chest pain and significant ST segment depression in six patients with severe coronary artery disease (three with left main and three with triple vessel disease) and poor exercise tolerance (means +/- SD = 362 +/- 99 seconds). All six patients had had angina during the dipyridamole infusion. Similar findings were observed after iloprost infusion in four of these. Aminophylline (125 mg iv) completely relieved chest pain. Although the rate-pressure products occasionally rose during PGI2 and iloprost infusions, there were no significant changes between ischemic (11.3 +/- 2.3 and 10.6 +/- 1.4 X 10(-3) U) and preischemic (10.8 +/- 1.5 and 10.7 +/- 1.4 X 10(-3) U) rates of infusion. Our data indicate that PGI2 and iloprost may induce ischemia independently of changes in oxygen demand, and suggest that these drugs dilate small coronary vessels. This may result in decreased subendocardial perfusion pressure and/or "coronary steal."

Adult↗
PubMed1985

[The relation between myocardial oxygen consumption and ischemia during exertion in patients with angina pectoris: effect of propranolol].

Patients with coronary artery disease exhibit a reduced coronary vasodilator reserve in response to exercise testing. Drugs which block coronary beta adrenergic receptors could exacerbate this abnormality leaving the vasoconstrictor alpha tone unopposed and/or counteracting the beta 2-mediated vasodilation elicited by the increase in myocardial oxygen demand. To test this hypothesis we administered propranolol 40 mg qid and placebo, using a cross over randomized single blind protocol, to 14 patients each with effort angina and critical coronary stenosis (greater than or equal to 75%). We performed computer-assisted multistage bicycle ergometer testings (25 W increments at 2 min intervals) after 2 weeks open label placebo (control) and at 2 week intervals following daily administration of propranolol and placebo. Compared to placebo, propranolol reduced significantly (p less than 0.001) peak heart rate (x +/- SD: 114 +/- 6 vs 150 +/- 11 beats/min) and rate pressure product (20.1 +/- 2.1 vs 28.0 +/- 3.9 X 10(-3)) and increased exercise duration (462 +/- 91 vs 355 +/- 85 sec). Conversely 0.1 mV ST segment depression was observed at lower heart rate (106 +/- 9 vs 127 +/- 8 beats/min, p less than 0.001) and rate pressure product (16.9 +/- 3.6 vs 22.4 +/- 2.4 X 10(-3), p less than 0.001). No significant differences were found between placebo and control. Moreover, we assessed the regression lines of the relationship between ST segment depression (ST) and heart rate (HR) during exercise. These have been shown to be shifted to the right after surgical revascularization and are an indirect measure of coronary reserve.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

[Myocardial ischemia induced by the cold pressor test in patients with exertion angina. Case contribution].

The aim of the present study was to assess the incidence of myocardial ischemia during cold pressor test in patients with stable exertional angina pectoris. Thirty-seven patients with proven coronary artery disease were submitted to cold pressor and exercise stress testing; computer assisted electrocardiographic recordings were obtained throughout the examinations. Cold stimulation provoked electrocardiographic signs of subendocardial ischemia only in 3 patients. They had suffered of a previous myocardial infarction and showed low exercise tolerance and severe coronary lesions (one with triple vessel and 2 with left main disease). Interestingly, only one of these patients gave an history of angina during cold exposure. Thus these data indicate that chest pain and electrocardiographic signs of ischemia are an uncommon event during cold pressor stimulation which occurs more likely in patients with fairly severe coronary narrowings. More sensitive markers of ischemia and/or different modalities of cold application are required for studies concerning the relationship between cold exposure and angina pectoris.

Angina Pectoris↗
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↗
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↗