Thyroxine-induced partial complex status epilepticus.
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Epilepsy, Complex Partial↗
Biomedical subjects
J Elizaga
Publications and source records attributed to J Elizaga.
Q fever mimicking herpetic encephalitis.
We describe a patient with temporal lobe encephalitis associated with primary Coxiella burnetii infection who presented with CT and MRI findings suggestive of herpes simplex encephalitis and an initial improvement during treatment with acyclovir. Q fever should be considered in the differential diagnosis of patients whose manifestations suggest herpes encephalitis.
Coxiella burnetii↗
[Balloon angioplasty in the nineties: the lessons of a decade and the future prospects].
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Angina, Unstable↗
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↗
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↗
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↗
Cell-to-cell interaction: a mechanism to explain wave-front progression of myocardial necrosis.
Histological sections performed 24 h after coronary occlusion in eight pigs displayed compact infarcts extending transmurally with well-defined edges; reconstruction and inspection of the area of necrosis showed a geometric distribution of the infarcts with very irregular, interdigitating edges always in continuity with the main mass of necrosis. Reperfusion in 32 pigs after periods of coronary occlusion of 90, 60, 45, and 30 min exponentially reduced infarct size and transmural extension of the infarct but did not modify its geometry. The two-dimensional size, progression, and geometry of the infarcts could be reproduced by a computer model. In the simulated infarcts, each myocardial cell within the area at risk was represented by a pixel. The algorithm included an inner loop, which determined at random at each iteration a status of reversible or irreversible damage to all pixels. The number of iterations could reproduce infarct of various sizes. With the addition of an index of transmural sensitivity to ischemia, progression of the infarct area could also be reproduced. The only possible means of reproducing the geometry of the infarct was to enter into the program a contiguity condition requiring a direct contact between irreversibly damaged pixels. These observations suggest that the physical interaction between cells is an important determinant of progression of necrosis during coronary occlusion.
Animals↗
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↗
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↗
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↗
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↗