Biomedical subjects

D Garcia-Dorado

Publications and source records attributed to D Garcia-Dorado.

36 records · Page 2Linked to original sources

PubMed1996

Intimal injury in a transiently occluded coronary artery increases myocardial necrosis. Effect of aspirin.

This study tested the hypothesis that intimal injury in a transiently occluded coronary artery limits myocardial salvage. The effect of intimal injury on reactive hyperaemia was investigated in 17 pigs submitted to a 30-min occlusion of the left anterior descending coronary artery (LAD), not resulting in myocardial infarction. Catheter-induced intimal damage increased local platelet deposition (99mTc) and reduced hyperaemia, but did not modify myocardial platelet or polymorphonuclear leucocyte content (myeloperoxidase activity) after 6 h reperfusion. To investigate the influence of intimal injury on the extent of myocardial necrosis secondary to a more prolonged coronary occlusion, and the role of platelets on this influence, 52 pigs were submitted to a double randomization (2x2 factorial design) to 250 mg i.v. aspirin vs. placebo and to coronary intimal injury vs. no coronary damage before a 48-min occlusion of the LAD and 6 h of reperfusion. After excluding 12 animals with reocclusion, coronary intimal injury was associated with larger infarcts (triphenyltetrazolium reaction) in animals receiving placebo (36.2+/-7.0% of the area at risk in animals with intimal injury vs. 10.8+/-3.9% in animals without coronary injury, P=0.006) but not in those receiving aspirin (20.3+/-6.5 vs. 21.7+/-6.5% of the area at risk in animals with and without intimal injury respectively). These results suggest that coronary intimal injury in the reperfused artery may have adverse effects on myocardial salvage by mechanisms other than reocclusion or embolization of platelet aggregates.

Animals↗

PubMed1996

Pre-treatment with trimetazidine increases sarcolemmal mechanical resistance in reoxygenated myocytes.

OBJECTIVE: Cytoskeletal and sarcolemmal fragility secondary to anoxia may contribute to sarcolemmal rupture and cell death during reoxygenation of cardiomyocytes. This study investigated the influence of trimetazidine (TMZ), a drug with effects on lipid metabolism and cell membranes, on reoxygenation-induced sarcolemmal rupture. METHODS: Isolated adult rat myocytes were submitted to 60 min of metabolic inhibition and 5 min of hypo-osmotic reoxygenation to simulate reperfusion edema in situ. Cells were allocated to 3 groups of treatment: in one group, TMZ 100 mumol/l was added to both the metabolic inhibition and reoxygenation buffers (group TMZ); another group was submitted to the same treatment but cells had previously been incubated with TMZ 100 mumol/l for 3 h (group TMZ-Pre); a control group underwent metabolic inhibition and hypo-osmotic reoxygenation without any treatment. Cell morphology was monitored throughout the experiment and sarcolemmal integrity was assessed by quantification of LDH activity and trypan blue exclusion test. RESULTS: After 60 min of metabolic inhibition most cells (83.1 +/- 2%) presented rigor contracture without between-group differences. Reoxygenation resulted in hypercontracture of 84.2 +/- 2.3, 91.2 +/- 1.4 and 84.1 +/- 2.1% of cells in TMZ, TMZ-Pre and control groups, P = NS. The trypan blue exclusion test revealed a higher proportion of cells with sarcolemmal integrity in TMZ and TMZ-Pre groups than in controls (12.7 +/- 2.0, 10.0 +/- 1.5 and 6.3 +/- 0.8%, respectively, P = 0.002). No between-group differences in LDH activity in the extracellular medium were observed at the onset or at the end of metabolic inhibition. However, LDH release was significantly lower (P = 0.002) in the TMZ-Pre group (1.6 +/- 0.1 IU/1000 cells) than in the TMZ and control groups (1.9 +/- 0.2 and 2.2 +/- 0.1 IU/1000 cells). CONCLUSION: Preincubation of cardiomyocytes with TMZ does not prevent rigor contracture induced by metabolic inhibition or hypercontracture during subsequent reoxygenation, but does improve sarcolemmal resistance to reoxygenation-induced mechanical stress. This could help to explain the beneficial effect of TMZ on infarct size.

Animals↗

PubMed1996

Protection of reoxygenated cardiomyocytes against osmotic fragility by nitric oxide donors.

In ischemic-reperfused myocardium, myocardial cells are jeopardized not only by reoxygenation-induced hypercontracture but also by the development of a transsarcolemmal osmotic gradient. Here the question of whether osmotic fragility of cardiomyocytes can be reduced by interventions during reoxygenation was addressed. Isolated ventricular cardiomyocytes (from adult rats), exposed to 120 min of hypoxia and subsequent reoxygenation, were used as model. With reoxygenation, medium osmolarity was reduced from 270 to 80 mosM. Loss of sarcolemmal integrity was characterized by enzyme loss from cells (creatine kinase and lactate dehydrogenase). Cardiomyocytes reoxygenated after 120 min of hypoxia hypercontracted, but enhanced enzyme loss was observed only at 80 mosM. The nitric oxide (NO) donors 3-morpholinosydnonimine (10 mM), sodium nitroprusside (10 mM), S-nitroso-N-acetyl-DL-penicillamine (100 microM), and the antilipid peroxidant diphenylphenylenediamine (DPPD, 2.5 microM) reduced enzyme loss with hyposmolar reoxygenation. Agents activating guanosine 3',5'-cyclic monophosphate (cGMP)-dependent pathways [atrial natriuretic peptide (1 microM), urodilatin (1 microM), and 8-bromo-cGMP (10 mM)], the contractile inhibitor 2,3-butanedione monoxime (10 mM), and the SIN-1 metabolite SIN-1C (10 mM) did not protect cardiomyocytes against osmotic fragility. The results show that increased osmotic fragility of isolated adult rat cardiomyocytes can be prevented at the time of reoxygenation by NO donors and DPPD in a cGMP-independent way.

Animals↗

PubMed1995

Previous aspirin use may attenuate the severity of the manifestation of acute ischemic syndromes.

BACKGROUND: The present study was designed to investigate whether the prior use of aspirin could influence the severity of the manifestation of acute coronary artery syndromes, given the well-documented observations that aspirin can prevent myocardial infarction, stroke, and death in cardiovascular disease. METHODS AND RESULTS: A series of 539 consecutive patients admitted to the Coronary Care Unit of a General Hospital was carefully characterized in a study with an ambidirectional design, with regard to previous medical history, aspirin use, and subsequent hospital diagnosis. Among the 214 patients previously taking aspirin, the hospital diagnosis was myocardial infarction in 24% and unstable angina in 76% compared with 54% and 46%, respectively, among the 325 not taking aspirin (P < .0001), for a reduction in the odds ratio of myocardial infarction with aspirin of 72% (95% CI, 59% to 90%). The decrease in odds was homogeneous in all subsets studied and independent of age, sex, previous angina, or previous myocardial infarction. The myocardial infarction was of a Q-wave type in 62% of aspirin users compared with 76% of nonusers (P < .05). By multivariate analysis, previous aspirin use was a strong predictor of unstable angina versus myocardial infarction and the only independent predictor of non-Q-wave versus Q-wave myocardial infarction. CONCLUSIONS: This study, thus, suggests a shift to less severe manifestation of acute coronary syndromes with aspirin use, implying that the failure of the drug in many patients with an acute coronary syndrome is only partial and that aspirin has the potential of attenuating the severity of the underlying acute thrombotic disease process.

Angina, Unstable↗

PubMed1995

Cardiac index quantification by Doppler ultrasound in patients without left ventricular outflow tract abnormalities.

OBJECTIVES: We attempted to ascertain whether cardiac index can be directly estimated from Doppler mean velocity. BACKGROUND: Although diverse Doppler echocardiographic methods have been described for cardiac output quantification, they are not widely used in clinical practice. Cross-sectional area measurement has been identified as the main source of error in flow volume quantification. METHODS: A three-phase study by Doppler echocardiography was conducted in 306 patients. In phase I, the normal mean velocity ratio of the left and right ventricular outflow tracts was established in 170 normal subjects. In phase II, cardiac index, calculated as the product of aortic annular area index by mean velocity (conventional method), and mean velocity determined in the left ventricular outflow tract and ascending aorta by pulsed and continuous wave Doppler, respectively, were correlated with thermodilution cardiac index in 66 patients. In phase III, the accuracy of the regression equations obtained was prospectively assessed in an additional 70 patients. RESULTS: The normal left/right ventricular outflow tract mean velocity ratio by pulsed wave Doppler was 1.1 +/- 0.1. Cardiac index (CI) calculated by the conventional method and thermodilution (TD) showed acceptable correlation (r = 0.90, CITD = 1.20 CIPWD + 357; r = 0.86, CITD = 0.90 CICWD + 262) for pulsed (PWD) and continuous wave (CWD) Doppler, respectively, but with systematic underestimation (-28 +/- 13%, p < 0.01) by pulsed wave Doppler. Mean velocity (MV) showed excellent correlation with the thermodilution cardiac index (r = 0.97, CITD = 172 MVPWD - 172; r = 0.93, CITD = 129 MVCWD - 255). When these regression equations were prospectively applied, better agreement with the thermodilution cardiac index was obtained by pulsed wave Doppler directly from mean velocity (SD 240 ml/min per m2) than when aortic annular area was considered in the calculation (SD 428 ml/min per m2). Similar results were obtained by continuous wave Doppler (SD 433 vs. 599 ml/min per m2) but with less accuracy. CONCLUSIONS: Left ventricular outflow tract mean velocity determined by pulsed wave Doppler permits easy, accurate cardiac index quantification in the absence of left ventricular outflow abnormalities. The simplicity of this method enhances its clinical applicability in noninvasive monitoring of cardiac index.

Adolescent↗

PubMed1995

Contraction band necrosis at the lateral borders of the area at risk in reperfused infarcts. Observations in a pig model of in situ coronary occlusion.

The aim of this study was to test the hypothesis that increased mechanical stress at the lateral borders of the area at risk may render this area more susceptible to ischaemia/reperfusion injury in the absence of collateral flow. The spatial distribution of myocardial necrosis within the territory of a transiently occluded left anterior descending coronary artery was investigated in 31 porcine hearts submitted to 48 min of coronary occlusion and 6 h of reperfusion. Immediately before excising the heart, the left anterior descending coronary artery was re-occluded and 10% fluorescein was injected in the left atrium. The area at risk was imaged by ultraviolet illumination of the myocardial slices, and the area of necrosis by incubation in triphenyltetrazolium chloride. The area at risk was divided in four sectors and an index of eccentricity was calculated as the percent of the area of necrosis located in the two lateral sectors of the area at risk. The area of contraction band necrosis was measured in whole heart histological sections. Infarcts were generally small, and were composed almost exclusively of contraction band necrosis. There was a good correlation between the extent of the area of contraction band necrosis and infarct size (r = 0.831, P < 0.0005). The area of necrosis had a patchy appearance and was predominantly distributed along the lateral borders of the area at risk. This eccentric distribution was more prominent in smaller infarcts, and the eccentricity index was inversely correlated with infarct size (r = -0.471, P = 0.007), suggesting that contraction band necrosis occurs first at the interface between control and reperfused myocardium in this model. These results are in agreement with a prominent role of mechanical factors in the genesis of myocardial necrosis during transient coronary occlusion.

Animals↗

PubMed1993

Myocardial oedema: a preventable cause of reperfusion injury?

Myocardial ischaemia increases cellular and extracellular osmolarity, alters membrane permeability to ions and causes moderate cell swelling and interstitial oedema. Ischaemia also reduces the mechanical resistance of the sarcolemma of myocytes, probably as a result of proteolytic digestion of the connections between cell membrane and the cellular scaffold. During reperfusion, the abrupt normalisation of extracellular osmotic pressure results in marked osmotic cell swelling. In the clinical situation, the ability of mechanical stress imposed by cell swelling to disrupt the weakened sarcolemma of viable myocytes during reperfusion has not been definitively established. Observations demonstrating the important role of mechanical stress caused by contraction and cell to cell interaction in myocyte necrosis support the hypothesis that osmotic cell swelling may actually produce lethal reperfusion injury. This hypothesis has been investigated by analysing the effect of hyperosmotic reperfusion with mannitol on final infarct size after coronary occlusion. Studies using highly hyperosmotic reperfusion after relatively short periods of ischaemia have yielded positive results, while studies using intravenous mannitol at the time of reperfusion, and more closely resembling clinical situations, have failed to detect any beneficial effect. Myocardial oedema could also contribute to postischaemic functional derangements, such as reperfusion arrhythmias and stunning, and could modify the passive mechanical properties of the infarcts and alter ventricular remodelling. Interventions aimed to limit myocardial oedema will probably not play a role as a co-adjuvant therapy in patients with acute myocardial infarction receiving thrombolytic treatment. However, they should probably form part of controlled reperfusion strategies to be evaluated in patients with acute myocardial infarction in whom reperfusion is accomplished by percutaneous transcoronary angioplasty or surgery.

Cardiomyopathies↗

PubMed1992

Favorable effects of hyperosmotic reperfusion on myocardial edema and infarct size.

Myocardial water content and infarct size were studied in 39 pigs randomly assigned to a nonintervention group, a group with an intracoronary infusion of a control solution, and a group with a hyperosmotic infusion to 450 mosM by the addition of D-mannitol. The intracoronary solutions were selectively infused into the left anterior descending coronary artery just distal to the occlusion site starting 48 min after occlusion. Reperfusion was performed 3 min later and the infusion rate progressively tapered off over the following 33 min. Multiple myocardial fragments were then obtained in nine pigs, from endocardial, mesocardial, and epicardial regions of the ischemic and control myocardium. Water content measured after 48 h of dessication was significantly greater in the reperfused [530 +/- 7 ml/100 (mean +/- SE) g dry wt] compared with control myocardium (374 +/- 3; P less than 0.0001) and similar in reperfused control and isotonic infusion groups (556 +/- 7 and 543 +/- 8 ml/100 g dry wt); it was 491 +/- 11 with intracoronary D-mannitol infusion, representing 35% less increase (P less than 0.001). In the 30 remaining pigs, area at risk and infarct size were measured 24 h later by in vivo fluorescein and in vitro triphenyltetrazolium chloride. Infarct size was similar in control and in the isotonic reperfused hearts, 6.80 +/- 1.05 and 6.22 +/- 0.76% of ventricular weight, and smaller with D-mannitol, 4.46 +/- 0.46 (P less than 0.05). The ratio of infarct size to area at risk was also smaller [0.415 +/- 0.029 vs. 0.543 +/- 0.052 and 0.547 +/- 0.045 (P less than 0.02)].(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1992

Selective inhibition of the contractile apparatus. A new approach to modification of infarct size, infarct composition, and infarct geometry during coronary artery occlusion and reperfusion.

BACKGROUND: Myocardial reperfusion is associated with calcium overload and cell contracture, mechanisms that may precipitate cell death. In this study, we tested the hypothesis that in vivo inhibition of this contracture could lead to cell preservation in an open-chest large animal model. METHODS AND RESULTS: Regional myocardium function was measured during a selective intracoronary infusion of 2,3-butanedione monoxime (BDM), a specific inhibitor of actin-myosin coupling, in the control state (10 pigs) and in a protocol of a 51-minute coronary occlusion followed by reperfusion (40 pigs). The effects on coronary artery blood flow in the basal state were also studied (seven pigs). Intramyocardial distribution of the infusate during coronary occlusion, myocardial water content after 30 minutes of reperfusion and area at risk, infarct size, type of histological necrosis, and infarct geometry after 24 hours of reperfusion were assessed. Methods used included electromagnetic flowmeter, radiolabeled microspheres, subendocardial sonomicrometers, fluorescein, triphenyl tetrazolium chloride and Masson's trichrome staining, and computer quantification of infarct edges. In the absence of ischemia, BDM infusion inhibited regional shortening in a dose-dependent manner up to full systolic bulging while producing marked regional increase in coronary blood flow. During early reperfusion, BDM reduced end-diastolic length 76% more than the control infusion (p less than 0.05) and increased systolic bulging by 420% compared with no change in control animals. The ratio of infarct size/area at risk was reduced by 31% with BDM (p less than 0.05), with striking modifications of infarct histology and infarct geometry; specifically, the extent of contraction band necrosis was reduced by 63% from 105.5 +/- 18.2 to 39.2 +/- 13.6 mm2 (p less than 0.02), and more patches of necrosis (6.5 +/- 2.1 versus 1.6 +/- 0.4, p less than 0.05) and higher contour (7.7 +/- 1.2 versus 5.03 +/- 0.2, p less than 0.05) and fractal (12.1 +/- 1.3 versus 7.8 +/- 0.2, p less than 0.05) indexes were found. CONCLUSIONS: Selective intracoronary infusion of BDM at doses inhibiting regional wall motion decreased infarct size after reperfusion. The effects of BDM on regional function, the reduction in contraction band necrosis at histology, and the peculiar configuration of these infarcts all suggest that inhibition of contracture can interfere with cell-to-cell progression of myocardial necrosis, supporting a role for contracture in reperfusion-induced cell death.

Actins↗

PubMed1990

Determinants of hemorrhagic infarcts. Histologic observations from experiments involving coronary occlusion, coronary reperfusion, and reocclusion.

Quantification of intramyocardial hemorrhage was performed in 69 pigs submitted to various protocols of coronary artery occlusion and reperfusion. The study groups include 1) permanent occlusion; 2) reperfusion after periods of coronary occlusion of 30, 45, 60, 90, and 120 minutes; 3) reperfusion with diltiazem and with 4) methoxamine after a 60-minute occlusion period; and 5) permanent reocclusion after a 30-minute period of reperfusion. Red blood cell counts were directly assessed by visual examination of histologic slices of myocardium and in a subgroup of animals by counts of red blood cells labeled with 99m-technetium pertechnetate. Hemorrhage occurs in infarcts reperfused after a duration of 45 minutes or more of coronary occlusion and after a period of reperfusion maintained for at least 30 minutes. Red blood cell counts were maximal in the mid portions of transmural sections of the infarcts, with decreasing values toward epicardium and endocardium. Diltiazem decreased total red blood cell counts, whereas methoxamine increased it and also caused subendocardial hemorrhage. The most powerful predictors of the severity of hemorrhage after sustained reperfusion were infarct size and higher blood pressure.

Animals↗

PubMed1988

Influence of tachycardia and arterial hypertension on infarct size in the pig.

To investigate the clinically important but controversial question of how hypertension during coronary occlusion affects infarct size 24 pigs underwent 1 h occlusion of the mid left anterior descending coronary artery and 24 h reperfusion and were randomised to one of three treatment groups. In group 1 blood pressure was increased during the occlusion period by an infusion of methoxamine; in group 2 tachycardia was induced by atrial pacing; and in group 3 no intervention was performed. The area at risk and infarct size were quantified by digital planimetry of slices of myocardium previously marked with fluorescein and with triphenyl-tetrazolium. Methoxamine maintained mean aortic blood pressure at 117 (SEM8) mmHg during occlusion, whereas the values were 80(6) mmHg in group 2 and 67(9) mmHg in group 3. Pacing increased heart rate to 146(1) beats.min-1 in group 2; it was 103(5) in group 1 and 99(8) in group 3. The pressure-rate product achieved was similar in groups 1 and 2 and significantly higher than in group 3. The pathological studies showed infarct size to be moderately but significantly larger in group 1 (14[3.5]% of the left ventricle) and similar in groups 2 (10.5[3.9]%) and 3 (10.1[2.2]%). The ratio of infarct size to area at risk was also significantly higher (0.743[0.057]) in group 1 with no differences between group 2 (0.604[0.055]) and group 3 (0.613[0.027]). At similar pressure-rate product, infarct size was thus greater with hypertension but not with pacing alone, showing a deleterious effect of increasing blood pressure in this experimental model with negligible collateral blood flow.

Animals↗

PubMed1987

Diltiazem and progression of myocardial ischemic damage during coronary artery occlusion and reperfusion in porcine hearts.

This study was designed to investigate whether a cardioprotective intervention could delay the completion of necrosis so that subsequent reperfusion would be more useful. Thirty-six pigs were randomly allocated to treatment with diltiazem (15 micrograms/kg per min) or saline solution and to a 60 or 120 minute coronary occlusion period followed by reperfusion. The treatment was begun 15 minutes before coronary occlusion and terminated 75 minutes after reperfusion. Twenty-four hours after the procedure, the heart was sliced and incubated in triphenyltetrazolium chloride. The infarct area and the maximal transmural area of extension of the infarct were calculated by planimetry. The total number of red blood cells in a transmural section was also counted. In the pigs with a 60 minute coronary occlusion, diltiazem (compared with saline solution) significantly reduced infarct size from 9.7 +/- 1.5% of left ventricular mass to 5.9 +/- 0.6% (p less than 0.05) and the percent transmural extension from 0.72 +/- 0.05 to 0.61 +/- 0.05% (p less than 0.05). Red blood cell extravasation in the infarcted area was reduced from 161,934 +/- 59,905 to 78,525 +/- 46,484 cells/mm3 (p less than 0.05) with diltiazem and the percent transmural extension of the hemorrhagic necrosis from 70 +/- 10 to 36 +/- 15% (p less than 0.05). No such differences were observed in the 120 minute coronary occlusion groups. Mean red blood cell counts and the extent of hemorrhagic necrosis did not correlate with either infarct size or transmural extension.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1987

Myocardial reperfusion in the pig heart model: infarct size and duration of coronary occlusion.

The effect of coronary artery reperfusion on infarct size was studied in a pig heart model. Forty four open chest pigs underwent occlusion of the mid-left anterior descending artery. Fifteen minutes after occlusion the animals were randomised to one of five groups: reperfusion at 30, 45, 60, or 90 min after occlusion (groups 1-4) or permanent occlusion (group 5). Twenty four hours after coronary occlusion the pigs were killed. The heart was sectioned in slices, which were incubated in triphenyl-tetrazolium. Mean(SEM) infarct sizes calculated by planimetry were 0.46(0.42), 2.85(1.14), 9.74(1.65), 8.93(1.37), and 13.17(1.17)% of left ventricular mass in the five groups. The transmural extension of the infarct was 14.6(11.4), 42.1(12.9), 87.4(6.6), 96.2(3.2), and 100(0)% and a transmurality index used as an estimate of the mean extension of the infarct relative to wall thickness was calculated to be 0.08(0.06), 0.32(0.10), 0.72(0.06), 0.79(0.04), and 0.92(0.02) respectively. Infarct size was similar in groups 3-5, but significantly smaller in groups 1 and 2 (p less than 0.05). Infarct size and the transmurality index correlated exponentially with the duration of the occlusion (r = 0.80, p less than 0.01; and r = 0.95, p less than 0.001 respectively). These results indicate that in the pig heart model submitted to an acute coronary occlusion cell viability may be less than that suggested by previous canine studies. This observation is probably related to a less well developed collateral blood flow in the pig heart and may provide an experimental model that better resembles certain clinical conditions.

Acute Disease↗

PubMed1986

Fracture of the Carpentier-Edwards ring in tricuspid position: a report of three cases.

Three cases of fracture of a Carpentier-Edwards ring in tricuspid position are presented. In all three cases the shape of the ring was shown to be abnormal by roentgenogram examination; there was an abrupt bend in the middle portion of each ring. At the time of operation, fracture of the ring skeleton at this midpoint was found in all three instances. Roentgenogram examination seems to be a reliable method of diagnosing this uncommon entity, and tricuspid valve replacement is required for its correction.

Adult↗

PubMed1983

An epidemic of pulmonary hypertension after toxic rapeseed oil ingestion in Spain.

The cardiac profile of 38 patients readmitted to the hospital with the clinical and radiologic findings of pulmonary artery hypertension and right ventricular failure 2 months after ingestion of toxic rapeseed oil was determined with M-mode and two-dimensional echocardiography, pulsed Doppler flow studies and right and left heart catheterization and ventriculography. The echocardiogram and pulsed Doppler recordings revealed right ventricular enlargement in 84% of the patients, indirect evidence of pulmonary artery hypertension in 76% and tricuspid insufficiency in 13%. At cardiac catheterization (n = 11) the mean (+/- standard deviation) pulmonary artery pressure was 40 +/- 9 mm Hg, mean pulmonary systemic vascular resistance ratio was 0.45 +/- 0.12 and mean right ventricular end-diastolic pressure was 13 +/- 4 mm Hg. Pulmonary artery hypertension was sustained after the acute administration of 100% oxygen and persisted in six patients who were restudied within 6 months. Cardiac index and left heart pressures were normal in all but one patient. The contrast ventriculographic studies revealed right ventricular dilation in all patients, tricuspid regurgitation in three patients and a normal left ventricular contraction pattern in all but one patient. The data confirm that symptomatic pulmonary artery hypertension and associated right ventricular dysfunction can complicate toxic rapeseed oil ingestion and that these findings persist for at least 6 months.

Acetanilides↗

PubMed1982

Hemodynamic evaluation of the Angell-Shiley porcine xenograft.

The Angell-Shiley porcine xenograft was evaluated in 48 asymptomatic subjects who underwent cardiac catheterization an average of 14 months after operation. Nineteen patients had mitral and 29 had aortic valve replacement. The average mitral valve gradient was 8 +/- 3 mm Hg and the average effective orifice area was 1.8 +/- 0.6 cm2. The average aortic valve gradient was 22 +/- 7 mm Hg and the average effective orifice area was 1.2 +/- 0.3 cm2. During supine leg exercise, the average mitral valve gradient increased to 12 +/- 4 mm Hg (p less than 0.001) and the average aortic valve gradient increased to 27 +/- 8 mm Hg (p less than 0.001) compared to findings at rest. On the basis of data obtained with a regression analysis model, there is a high probability that an Angell-Shiley aortic xenograft with a stent diameter less than 25 mm will have a postoperative effective orifice area of less than 1 cm2, and that an Angell-Shiley mitral xenograft with a stent diameter less than 30 mm will have a postoperative effective orifice area of less than 1.5 cm2. Our data suggest that the Angell-Shiley xenograft has suboptimal hemodynamic performance in stent sizes less than 30 mm in the mitral position and less than 25 mm in the aortic position.

Adult↗

PubMedDate not supplied

The role of Na+/H+ exchange in ischemia-reperfusion.

In ischemia the cytosol of cardiomyocytes acidifies; this is reversed upon reperfusion. One of the major pH(i)-regulating transport systems involved is the Na+/H+ exchanger. Inhibitors of the Na+/H+ exchanger have been found to more effectively protect ischemic-reperfused myocardium when administered before and during ischemia than during reperfusion alone. It has been hypothesized that the protection provided by pre-ischemic administration is due to a reduction in Na+ and secondary Ca2+ influx. Under reperfusion conditions Na+/H/ exchange inhibition also seems protective since it prolongs intracellular acidosis which can prevent hypercontracture. In detail, however, the mechanisms by which Na+/H+ exchange inhibition provides protection in ischemic-reperfused myocardium are still not fully identified.

Acidosis↗

PubMedDate not supplied

Intracoronary infusion of superoxide dismutase and reperfusion injury in the pig heart.

The effects of an intracoronary infusion of superoxide dismutase on infarct size were studied in 16 pigs submitted to a 48-min coronary occlusion of the mid left anterior descending coronary artery followed by reperfusion for 24 h. Areas at risk marked with fluorescein and infarct sizes calculated with triphenyl tetrazolium chloride staining 24 h after the occlusion were similar in the five control animals with coronary reperfusion alone, in the five animals with an intracoronary infusion of lactate Ringer initiated 3 min before reperfusion and maintained for 33 min and in the six animals with superoxide dismutase added to the solution of lactate Ringer and infused at a rate of 2500 units/min. The ratios infarct size/area at risk were respectively 0.50 +/- 0.10, 0.65 +/- 0.04 in the three study groups (NS). The extent of intramyocardial hemorrhage, evaluated by morphometric analysis was also similar 0.90 +/- 0.29 x 10(6), 0.70 +/- 0.14 and 1.62 +/- 0.42 red blood cells/mm3 of tissue (NS). The superoxide dismutase infusion, however, resulted in significantly fewer early reperfusion arrhythmias which involved 23 +/- 15 s of each minute electrocardiographic recording in the superoxide dismutase group, compared to 37 +/- 13 s in the lactate Ringer group and 45 +/- 14 s in the control group (p = 0.004). The lack of an effect of intracoronary infusion of superoxide dismutase on infarct size suggests that in this experimental model, extracellular superoxide radicals generated during early reperfusion have no major role on myocardial cell necrosis and microvascular damage. Reperfusion arrhythmias were, however, reduced.

Animals↗