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PubMed1998

Assessment of left ventricular wall motion and delineation of the endocardial border after intravenous injection of Infoson during dobutamine stress echocardiography.

OBJECTIVES: To investigate whether intravenous injection of Infoson facilitates the assessment of left ventricular wall motion and definition of endocardial border and thereby reduces inter- and intra-observer variability during dobutamine stress echocardiography. BACKGROUND: Clear detection of the endocardial border is essential during dobutamine stress echocardiography. Although several contrast agents have been tested for their efficacy in enhancing definition of left ventricular endocardium, their usefulness during dobutamine stress echocardiography has not been evaluated. METHODS: Thirty coronary artery disease patients underwent dobutamine stress echocardiography. Infoson was injected at 0.2 ml/kg in both apical four- and two-chamber views. Detection of the left ventricular endocardial borders was scored from 0 (undetectable) to 10 (best) and expressed as a percentage of image quality at rest and peak stress by two independent observers. Regional wall motion was also evaluated and the total wall motion score index calculated each time. RESULTS: Delineation of the left ventricular endocardium improved from 76 +/- 4% to 84 +/- 2% at rest (P < 0.01) and from 75 +/- 4% to 89 +/- 1% at peak stress (P < 0.01) after administration of Infoson. The greatest improvement was seen in the basal and middle regions of the lateral and anterior walls. Inter- and intra-observer variability was reduced after administration of Infoson. At rest, the probability of concordance between two observers increased from 0.86 (0.82-0.89) to 0.91 (0.88-0.94) (P < 0.05) and at peak stress from 0.86 (0.82-0.9) to 0.90 (0.86-0.92) after administration of Infoson (P < 0.05). The probability of concordance between on- and off-line assessment by one observer also increased from 0.84 (0.8-0.88) to 0.90 (0.86-0.93) (P < 0.01) at rest and from 0.90 to 0.92 (NS) at peak stress. Overall, a change in wall motion score index occurred in 16 of 30 (53%) patients after administration of Infoson, thus improving the accuracy of the stress test compared with coronary angiography. The wall motion score index was overestimated in 11 of 16 (37%) patients without Infoson while the detection of new wall motion abnormalities increased in 5 of 16 (17%) (P < 0.01). CONCLUSIONS: Intravenous administration of Infoson facilitates the assessment of wall motion, particularly of the basal lateral and anterior walls where endocardial border drop-out frequently occurs during dobutamine stress echocardiography; it thus reduces the inter- and intra-observer variability.

Adult↗
PubMed1978

Endocardial fibrosis in apparently normal infant hearts.

A classification of the histological appearance of the endocardium in infants, and observers' reproducibility tests have been carried out. In a retrospective survey of 262 overtly normal hearts, what is considered to be abnormal thickening of the endocardium was found in 3.4%, and probably significant thickening in 20%. The changes occurred in unexpected home deaths as well as in hospital deaths and the lesions may be a contributing factor in some cot deaths, but a prospective study is required to confirm this.

Endocardial Fibroelastosis↗
PubMed1993

Laser induced fluorescence identification of sinoatrial and atrioventricular nodal conduction tissue.

UNLABELLED: Transcatheter ablation of nodal tissue is used for the treatment of arrhythmia resistant to medical therapy. We have investigated the use of laser induced fluorescence spectroscopy for the in vitro recognition of nodal conduction tissue. Twelve fresh human necropsy specimens (< 48 hours) were obtained from sinoatrial node and atrioventricular node areas. Spectra were recorded during excitation at 308 nm (XeCl excimer laser, 1.5-2.0 mJ/pulse, 10 Hz). Ech area examined was marked for subsequent histologic examination. Four hundred eleven spectra were obtained, of which 37 contained nodal conduction tissue (21 sinoatrial, 16 atrioventricular node). Normalized fluorescence emission intensity from these areas was compared with that of surrounding endomyocardial tissue at 18 wavelengths and 35 ratios of fluorescence intensity at selected wavelengths. Spectra recorded from nodal tissue could be clearly distinguished by a visible decrease in fluorescence emission intensity at wavelengths from 440 to 500 nm (P < 0.0006 at 450 nm), peak area, and peak width when compared to that of adjacent atrial endomyocardial tissue. Nodal conduction tissue was also distinguished from ventricular endocardium (14 spectra) by an increase in fluorescence emission at 430 to 550 nm (P < 0.0001). The specificity was 73% and 88% and the sensitivity was 73% and 60% for sinus nodal and atrioventricular nodal conduction tissue identification, respectively. A ratio of fluorescence emission intensity > 1.3 for 380/475 nm was able to detect nodal conduction tissue (P < 0.001). CONCLUSION: Laser induced fluorescence can differentiate nodal conduction tissue from atrial and ventricular endocardium and may provide a new diagnostic tool for the recognition and subsequent ablation of nodal conduction tissue.

Adolescent↗
PubMed1997

Temperature guided radiofrequency catheter ablation of myocardium: comparison of catheter tip and tissue temperatures in vitro.

Temperature monitoring during RF ablation has been proposed as a means of controlling the creation of the lesion. However, in vivo studies have shown poor correlation between lesion size and catheter tip temperature. Thus, we hypothesized a difference between catheter tip and tissue temperatures during RF catheter ablation, and that this difference may depend on flow passing the ablation site, tip electrode length, and catheter-tissue orientation. In vitro studies were performed using four different ablation catheters (tip electrode length: 2, 4, or 6 mm) with a thermistor or a thermocouple as temperature sensor. Set temperature was 70 degrees C and pulse duration was 30 seconds. Pieces of porcine left ventricle were immersed in a bath of isotonic saline-dextrose solution at 37 degrees C. The ablation catheters were positioned perpendicularly, obliquely, or parallel to the endocardium. A temperature sensor was inserted from the epicardial side and positioned 1 mm beneath the catheter-tissue interface. Experiments were made with a flow of 200 mL/min passing the ablation site or with no flow. The catheter tip and tissue temperatures differed significantly (P < 0.0001) during ablation. This difference increased with time, with flow passing the ablation site, with the length of the tip electrode, and when the catheter was positioned perpendicularly or obliquely to the endocardium as compared to the parallel catheter-tissue orientation (P < 0.05). In conclusion, the tissue temperature may far exceed the catheter tip temperature, and intramyocardial superheating resulting in steam formation and popping may occur despite a relatively low catheter tip temperature.

Animals↗
PubMed1993

Drug-induced afterdepolarizations and triggered activity occur in a discrete subpopulation of ventricular muscle cells (M cells) in the canine heart: quinidine and digitalis.

INTRODUCTION: Oscillations of membrane potential that attend or follow the cardiac action potential and depend on preceding transmembrane activity for their manifestation are known as afterdepolarizations. Early afterdepolarizations (EADs) interrupt or retard repolarization of the cardiac action potential, whereas delayed afterdepolarizations (DADs) arise after full repolarization. EADs and DADs can give rise to spontaneous action potentials or triggered activity believed to be responsible for a variety of cardiac arrhythmias. Recent studies from our laboratory have highlighted differences in the electrophysiology and pharmacology of three functionally distinct myocardial cell types found in the canine ventricle. Epicardial, M region, and endocardial tissues and cells show distinct, sometimes opposite, responses to a variety of drugs, including those capable of inducing EADs and DADs. METHODS AND RESULTS: In the present study, we used standard microelectrode techniques to examine the pharmacologic response of these cellular subtypes to therapeutic levels of quinidine and toxic levels of digitalis. Quinidine readily produced prominent EADs and EAD-induced triggered activity in tissue preparations from the M region (deep subepicardium), but not in those from epicardium, endocardium, or deep subendocardium of the canine ventricle. Acetylstrophanthidin produced prominent DADs in M cell preparations and subendocardial Purkinje fibers but only minute DADs, if any, in epicardium, endocardium, or deep subendocardium. DAD-induced triggered activity was observed to arise only in Purkinje and M cells and never in myocardial tissues from the epicardial, endocardial, or deep subendocardial regions of the ventricular wall. CONCLUSION: We conclude that EADs, DADs, and triggered activity caused by therapeutic levels of quinidine and toxic levels of digitalis are limited to or much more readily induced in a select population of cells in the deep subepicardial (M cell) region of the canine ventricle in addition to the Purkinje system of the heart.

Animals↗
PubMed1997

Noncontact endocardial mapping: reconstruction of electrograms and isochrones from intracavitary probe potentials.

INTRODUCTION: Mapping endocardial activation and repolarization processes is critical to the study of arrhythmias and selection of therapeutic procedures. Previously, we developed methodology for reconstructing endocardial potentials from potentials measured with a noncontact, intracavitary probe. This study further develops and evaluates the ability of the approach to provide detailed information on the spatiotemporal characteristics of the activation process. Specifically, we reconstructed endocardial electrograms and isochrones throughout the activation process over the entire endocardium during a single beat. METHODS AND RESULTS: Cavity potentials were measured with a 65-electrode probe placed inside an isolated canine left ventricle. Endocardial potentials were measured simultaneously using 52 electrodes. Potentials were acquired during subendocardial pacing from different locations. Computed electrograms at various sites closely resemble the measured electrograms (correlation coefficient > 0.9 at 60% of the electrodes). Computed isochrones locate subendocardial pacing sites with 10-mm accuracy. Two pacing sites, 17 mm apart, were resolved. Critical regions, such as areas of isochrone crowding, were accurately reconstructed. CONCLUSIONS: Results indicate the applicability of the approach to mapping the cardiac excitation process on a beat-by-beat basis without occluding the ventricle. The ability of locating electrical events (e.g., single or multiple initiation sites) is demonstrated. Importantly, the method is shown to be capable of reconstructing electrograms over the entire endocardium and determining nonuniformities of activation spread (e.g., areas of slow conduction). These capabilities are important to clinical application in the electrophysiology laboratory and experimental studies of arrhythmias in the intact animal.

Animals↗
PubMed1998

Lead fixation in dogs achieved with RF energy.

INTRODUCTION: The purpose of this study was to test whether radiofrequency (RF) energy could be used to fixate leads to the endocardium. METHODS AND RESULTS: In six dogs we measured the dislodgment force and pacing threshold before and after RF fixation in the coronary sinus (CS) and right ventricle (RV). RF fixation was achieved with a CardioRhythm Atakr ablation unit. The dislodgment force of CS leads fixed with RF energy was 1.63+/-0.65 oz, compared with < 0.1 oz for similar leads placed in the CS of six separate dogs. In the RV, leads fixed with RF energy had a dislodgment force of 1.29+/-0.27 oz, compared with 0.48+/-0.28 oz. for urethane (P < 0.01) and 1.01+/-0.21 oz for silicone (P = 0.41) tined leads. In the CS, the pacing threshold for RF fixed leads increased significantly from 2.2+/-1.1 V (0.5 msec) before fixation to 4.2+/-1.3 V after fixation (P < 0.01), while in the RV, the pacing threshold increased from 0.41+/-0.05 V (0.5 msec) before fixation to a mean of 2.03+/-0.44 V after fixation (P < 0.01). In another group of six dogs studied for 12 weeks, 5 of 6 RF fixed CS leads remained attached, as did 8 of 10 RF fixed RV leads. For the RV leads, the mean pacing threshold was 0.90+/-0.35 V, compared with 0.53+/-0.18 V (0.5 msec) for similar tined leads (P = 0.02) and 1.2+/-0.30 V (0.5 msec) for screw leads (P = 0.18) in the RV. CONCLUSION: We conclude that RF energy can be used to attach leads to the RV and CS endocardium. While the RV pacing thresholds increased acutely, the mean chronic thresholds were not significantly different for RF fixed leads and standard tined or screw leads.

Animals↗
PubMed1998

Repair of septal and posterior tricuspid leaflets in Ebstein's anomaly.

BACKGROUND AND AIM: In Ebstein's anomaly, the septal and posterior tricuspid leaflets are plastered to the endocardium. We postulated that tricuspid valve function could be corrected by restoring mobility of these leaflets. (Feasibility of such repair was explored by anatomical and clinical studies.) METHODS: Ten heart specimens with Ebstein's anomaly were examined to investigate the size of the tricuspid leaflets. We operated on four patients with Ebstein's anomaly: the plastered septal and posterior leaflets were mobilized from the endocardium, the atrialized right ventricle was longitudinally plicated, and the basal attachment of the mobilized leaflets was sutured (reattached) to the valve annulus. RESULTS: In heart specimens, approximately 40% of the total surface of the tricuspid leaflets was comprised of the septal and posterior leaflets. Clinically, all patients operated on returned to normal functional status after surgery. The mean cardiothoracic ratio on chest X-rays decreased from 0.70 to 0.55 (after surgery). Echocardiographic tricuspid regurgitation, graded from 0 to 4, decreased from 3.5 to 1.0, and tricuspid annular diameter ratio to the normal value reduced from 1.88 to 0.66. Angiographic right ventricular ejection fraction increased from 0.36 to 0.50, and end-diastolic volume ratio to the normal value decreased from 3.65 to 1.19. CONCLUSIONS: Repair of the septal and posterior tricuspid leaflets was found to be feasible and effective as tricuspid valvuloplasty for Ebstein's anomaly.

Adolescent↗
PubMed1976

Atrial receptors in the cat.

Action potentials were recorded from slips of the cervical vagi in anaesthetized cats. Single functional units with atrial patterns of discharge (type A, B and Intermediate) were first obtained and then attempts were made to alter (i.e. convert) their patterns of discharge. Finally the points of origin of their action potentials were located. The investigations were done in five stages. 2. In the first series, thirty unselected units were investigated in thirty cats. Twenty-five of these were located in the endocardium of vein-atrial system and consisted of two type A, fifteen type B and eight Intermediate type units. The remaining five units were located elsewhere in the chest Conversion of the pattern of discharge was achieved in sixteen of the twenty-five atrial units. Both atrial type A units were converted. 3. In the second series, eight type A units were selectively studied in twelve cats. Five were located in the atrial endocardium and all were converted. Of the other three units which were located at other sites in the chest, one could not be converted. 4. In the third series, four type A units which could not be converted were selectively studied in twenty cats. All were located outside the atria. 5. In the fourth series, three type B units which could not be converted were selectively studied in six cats. These units were located in the pulmonary veins and in the lateral walls of the atria. 6. In the fifth series, fifty-five units were investigated in three anaesthetized spontaneously breathing cats. The proportion of the types of units were similar to that obtained in the artificially respired cats (first series). 7. The present study has shown that atrial receptors with a type A pattern of discharge are relatively rare in the cat and that conversion of the patterns of discharge is a common phenomenon. Evidence is presented which suggests that there is one basic type of atrial receptor whose pattern of discharge is determined by their precise location in the vein-atrial system.

Action Potentials↗
PubMed1991

Regional variations in action potentials and transient outward current in myocytes isolated from rabbit left ventricle.

1. Regional variations in the shape of early repolarization of the action potential have been correlated to differences in transient outward K+ current, I(t), in myocytes isolated from the epicardial surface, the endocardial trabeculae and the papillary muscles of rabbit left ventricles. Temperature was 35 degrees C during whole-cell, and 22-23 degrees C during cell-attached experiments. 2. Membrane resting potentials were very similar regionally. At 0.1 Hz stimulation the action potential plateau amplitude in papillary muscle cells was significantly higher (104.7 mV) than in epicardial cells (96.47 mV). Exposure to 4-aminopyridine or increases in the rate of stimulation from 0.1 Hz to 3.3 Hz increased plateau height and diminished the initial notch on repolarization. These effects were correlated to the magnitude of I(t) in these cells. At low rates of stimulation I(t) caused a 'spike and dome' morphology of the action potential. 3. Voltage clamp experiments confirmed a higher current density of I(t) in epicardial cells (7.66 pA/pF at +20 mV) than in endocardial (6.45 pA/pF) or papillary muscle cells (3.69 pA/pF). I(t) at 35 degrees C was faster and larger than previously reported and individual currents inactivated almost completely during 100 ms pulses to plateau potentials. No differences in the kinetics or voltage dependence of whole-cell currents were found. Thus, the half-inactivation potential was -37.8 mV in cells from all three regions. 4. Cell-attached recordings from endocardial and epicardial cells showed very similar single-channel amplitudes, burst open probabilities and ensemble averages. The peak channel open probability soon after the start of depolarizing voltage clamp pulses did not change between cell types (P approximately 0.8). The slope conductance of I(t) channels was 13.0 pS with an intercept near the resting potential of the cell. 5. We conclude that regional variations in the shape of initial repolarization in cells from rabbit left ventricle are caused by variations in the magnitude of the transient outward K+ current, I(t). Epicardial cells have the largest, and papillary muscle cells the smallest I(t). The differences are not explained by alterations in the whole-cell kinetics or single-channel kinetics and conductance. The most likely explanation for variations in whole-cell current density is therefore a decrease in channel density in endocardium and papillary muscle compared with epicardial tissue. We estimate the density of I(t) channels per cell to be 1495 (one per 3-4 micron2) in epicardium, 1175 (one per 4-5 micron2) in endocardium, and 875 (one per 6 micron2) in papillary muscle cells.

Action Potentials↗
PubMed2003

Myocardial infarction causes increased expression but decreased activity of the myocardial Na+-Ca2+ exchanger in the rabbit.

Na+-Ca2+ exchanger (NCX) protein levels and activity were measured in myocardium from the basal region of the left ventricle of rabbit hearts with significant left ventricular dysfunction (LVD), 8-9 weeks after an apical infarction. NCX protein abundance was higher in the tissue homogenates (121 +/- 11%) and purified membrane fractions (143 +/- 12%) in the LVD compared to the sham-operated (sham) group. NCX mRNA was also higher in the LVD group (126%). Lower NCX protein expression was observed in the membrane fractions from the epicardium compared to the endocardium in both the sham and LVD groups. Transmembrane currents were recorded in isolated cardiomyocytes by single-electrode voltage clamp; [Ca2+]i was measured using Fura-2. Rapid application of 10 mmol l-1 caffeine was used to induce Ca2+ release from the sarcoplasmic reticulum. The subsequent NCX-mediated Ca2+ efflux rate constant was lower (70% of sham) in the LVD group. NCX currents were measured in cardiomyocytes dialysed with 250 nM Ca2+ (50 mmol l-1 EGTA). A lower NCX current (75% of sham) was observed in the LVD group. Lower NCX activity was also observed in cardiomyocytes isolated from the epicardium compared to the endocardium; a transmural difference that was also seen in the LVD group. Reduced activity despite increased protein expression may result from reduced Ca2+ sensitivity of the allosteric regulation of NCX. However, measurements indicated increased Ca2+ sensitivity in the LVD group. Cardiomyocytes from LVD hearts displayed a marked reduction in the transverse tubule area (59% of sham) and the surface area/volume ratio (80% of sham). Disrupted transverse tubule structure may contribute to the decrease in NCX activity despite increased protein expression in LVD.

Algorithms↗
PubMed1970

Endocardial lesion in a case of Takayasu's arteriopathy.

The clinical findings and the necropsy report of a 14-year-old girl suffering from Takayasu's arteriopathy have been presented. In addition to the typical arterial changes, thickening and puckering of the aortic valve and a patch of thickening in the left atrial endocardium were shown at necropsy. The histology of this lesion was found to be identical with the arterial intimal changes. It has been postulated that Takayasu's arteriopathy may rarely extend to the valvular and mural endocardium of the heart, producing cardiac murmurs. Similar cases with cardiac murmurs reported earlier and attributed to associated rheumatic endocarditis were probably due to the same pathological process extending to the endocarditis.

Adolescent↗
PubMedDate not supplied

Modification of excitation-contraction coupling in cat ventricular myocardium following endocardial damage.

Damage to endocardial endothelium (denudation of the superficial tissue) by brief exposure to a 100-microL bolus of detergent (Triton X-100, 1% by volume stock) decreased the twitch force of papillary muscle (and trabeculae) by approximately 30% to a new but steady level without changes in resting tension. The decline in twitch force was evident immediately after the addition of Triton. Modification of the action potential measured from the contracting tissue appeared only later, when the change in contraction was already well established (i.e., after approximately 2 min). Action potential shortened in duration at 50% repolarization by approximately 100 ms and increased in plateau amplitude, although the latter increase was not always observed. A similar treatment procedure applied to strips of ventricular wall with the endocardium exposed to the superfusion solution resulted in a substantial decrease in action potential duration (approximately 110 ms). In contrast, treatment of strips of epicardial layers of ventricular walls (with epicardial side facing the superfusion solution) did not produce a similar result. In beta-stimulated (1 microM isoproterenol) and partially depolarized preparations (with 20 mM KCl), with intact endocardium, electrically evoked contractions were followed by aftercontractions, which were suppressed following Triton treatment. Action potentials in a depolarizing medium also shortened in duration (approximately 50 ms), although following a delay (2-3 min). The decay to steady state of postextrasystolic potentiated beat was slower after endocardial damage than under control conditions. This suggests an increased Ca2+ recirculation through the sarcoplasmic reticulum between two consecutive beats (35% before Triton vs. 45% after Triton).(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1984

Transmural DC electrograms after coronary artery occlusion and latex embolization in pigs.

Changes in epicardial and endocardial direct current (DC) electrograms and ventricular arrhythmias observed during 60 min of left anterior descending coronary artery (LAD) occlusion in nine anesthetized pigs were compared with those observed in eight other pigs after embolization of the LAD with latex, a procedure able to block collateral blood flow to the ischemic area. After LAD occlusion 1) T-Q segment depression and S-T segment elevation showed a faster rate of development, and monophasic potentials occurred earlier in the endocardium than in the epicardium; 2) T-Q segment depression was greater at the center than at the periphery of the ischemic area during the first 20-30 min, and later it become greater at the periphery than at the center; and 3) a period of transient recovery in the local activation beginning after 8-15 min and lasting for 10-20 min occurred in all cases, commonly associated with T-wave alternans. LAD embolization with latex induced greater T-Q and S-T segment changes in the epicardium than in the endocardium, increased the incidence of ventricular fibrillation, and failed to impede the appearance of the period of transient electrical recovery. Thus, within an acutely ischemic area in the in situ pig heart, there are inhomogeneities in the magnitude and time course of the electrical changes, which are not prevented by procedures able to block collateral blood flow to the ischemic area. Ventricular fibrillation was also not prevented by such a procedure.

Animals↗
PubMed1995

Effect of erythrocyte deformability on myocardial hematocrit gradient.

Myocardial hematocrit gradient was determined between epicardium and endocardium of the left ventricular wall in rat heart under the influence of erythrocyte deformability alterations. Hematocrit determinations were performed by measuring two different radionuclides labeling plasma (125I-labeled albumin) and erythrocytes (99mTc) in 100-microns-thick left ventricular myocardium slices. Myocardial hematocrit gradient calculated after exchange transfusions with partially hardened red blood cell suspensions was compared with the results of the control group, in which the exchange transfusions were done using normal, hematocrit-matched blood. In the control group, the hematocrit value in the myocardium adjacent to epicardium was 0.331 +/- 0.076 l/l and decreased to 0.232 +/- 0.054 l/l near the endocardium. Myocardial hematocrit between these two was represented by a linear gradient. In the group with impaired erythrocyte deformability, the hematocrit value was 0.359 +/- 0.074 l/l in the epicardial myocardium and remained at 0.341 +/- 0.082 l/l in the endocardial layer. These results indicate that tissue hematocrit gradient in the left ventricular myocardium may be disturbed if erythrocyte deformability is altered.

Animals↗
PubMed1995

Effects of chemical subendocardial ablation on activation rate gradient during ventricular fibrillation.

The mechanism by which an endocardial-epicardial activation rate gradient develops after 1 or 2 min of sustained ventricular fibrillation is unknown. We recorded from electrodes on the epicardium and from hook electrodes in the endocardium in three open-chest control dogs during prolonged ventricular fibrillation. The same recordings were also made in seven dogs after right ventricular subendocardial ablation with Lugol solution and in three dogs after substitution of air for the cavitary blood. The effects of these interventions, i.e., Lugol ablation (n = 2) and the exposure to air (n = 2), on the subendocardial Purkinje fiber transmembrane action potential properties were also evaluated in vitro using microelectrode recording techniques. The in vivo studies showed a significant endocardial-epicardial rate gradient in the control dogs and in dogs that had air substituted for the cavitary blood. In comparison, in dogs that underwent chemical subendocardial ablation, the activation cycle lengths for the endocardium and epicardium were not significantly different. The in vitro studies showed that subendocardial Purkinje fiber action potentials could still be recorded for up to 10 min of exposure to air. In comparison, in the tissues subjected to chemical ablation, no transmembrane action potentials could be recorded from either the Purkinje fibers or superficial ventricular muscle cells. We conclude that the development of an endocardial-epicardial activation rate gradient during prolonged ventricular fibrillation depends on the presence of intact subendocardial Purkinje fibers and ventricular myocytes. The retained cavitary blood is not responsible for the development of the rate gradient.

Animals↗
PubMed2000

Cardiac interstitial bradykinin release during ischemia is enhanced by ischemic preconditioning.

Ischemic preconditioning is known to protect the myocardium from ischemia-reperfusion injury. We examined the transmural release of bradykinin during myocardial ischemia and the influence of ischemic preconditioning on bradykinin release during subsequent myocardial ischemia. Myocardial ischemia was induced by occlusion of the left anterior descending coronary artery in anesthetized cats. Cardiac microdialysis was performed by implantation and perfusion of dialysis probes in the epicardium and endocardium. In eight animals, bradykinin release was greater in the endocardium than in the epicardium (14.4 +/- 2.8 vs. 7.3 +/- 1.7 ng/ml, P < 0.05) during 30 min of ischemia. In seven animals subjected to preconditioning, myocardial bradykinin release was potentiated significantly from 2.4 +/- 0.6 ng/ml during the control period to 23.1 +/- 2.5 ng/ml during 30 min of myocardial ischemia compared with the non-preconditioning group (from 2.7 +/- 0.6 to 13.4 +/- 1.9 ng/ml, P < 0.05, n = 6). Thus this study provides further evidence that transmural gradients of bradykinin are produced during ischemia. The results also suggest that ischemic preconditioning enhances bradykinin release in the myocardial interstitial fluid during subsequent ischemia, which is likely one of the mechanisms of cardioprotection of ischemic preconditioning.

Animals↗
PubMed1998

Identification of an autocrine signaling pathway that amplifies induction of endocardial cushion tissue in the avian heart.

Endocardial cushion tissue is formed by an epithelial-mesenchymal transformation of endocardial cells, a process which results from an inductive interaction between the myocardium and endocardium within the atrioventricular (AV) and outflow tract (OT) regions of the heart. We report here that a protein previously found to be required for myocardially induced transformation of endocardial cells in vitro, ES/130, is highly expressed within the AV and OT regions not only by myocardial cells, but also by the endocardium and its mesenchymal progeny. Given these findings and others, we have tested the hypothesis that endocardial cushion tissue secretes factors which autoregulate its transformation to mesenchyme. Endocardial cushion tissue was cultured and its conditioned growth medium was harvested and applied to nontransformed endocardial cells maintained in the absence of the inductive myocardium. This treatment resulted in endocardial cell invasion into three-dimensional collagen gels plus increased expression of proteins associated with endocardial cell transformation in vivo. Whereas endocardial cushion tissue was found to express ES/130 protein in vivo and in vitro, minimal detection of ES/130 in its conditioned growth medium was observed in immunoblots. Attempts to inhibit the mesenchyme-promoting activity of the conditioned medium with ES/130 antisense were unsuccessful. However, strong intracellular ES/130 expression was detected in endocardial cells, and this expression correlated with the ability of endocardial cells to transform. For example, the minority of endocardial cultures that failed to transform in response to conditioned medium treatment also failed to undergo increased expression of ES/130. These observations are interpreted to suggest that (i) endocardial cushion tissue secretes factors that promote its transformation to mesenchyme, and (ii) while endocardial cushion tissue appears to signal through secretion of factors other than or in addition to ES/130, intracellular ES/130 expression nevertheless may be a target endocardial cell response required for endocardial cell transformation.

Animals↗