AbstractBackground:Development of pulmonary arteriovenous fistulas in patients with cavopulmonary anastomosis may result in a significant morbidity. Although the use of bubble contrast echocardiography with selective injection into both the branch pulmonary arteries in identifying pulmonary arteriovenous fistulas has been increasing, the actual efficacy of this diagnostic modality has not been properly evaluated. Thus, this study aimed to assess the efficacy of bubble contrast echocardiography in detecting pulmonary arteriovenous fistulas in children with total cavopulmonary connection.Methods:A total of 140 patients were included. All patients underwent cardiac catheterisation. Bubble contrast echocardiographic studies were performed by injecting agitated saline solution into the branch pulmonary arteries. Transthoracic echocardiograms that use an apical view were conducted to assess the appearance of bubble contrast in the systemic ventricles. Then, the contrast echocardiogram results and other cardiac parameters were compared.Results:No correlation was found between contrast echocardiogram grade and other cardiac parameters, such as pulmonary capillary wedge saturation and pulmonary artery resistance. Moreover, only 13 patients had negative results on both the right and left contrast echocardiograms, and 127 of the 140 patients had positive results on contrast echocardiograms even though they had normal pulmonary capillary wedge saturation. Results showed that bubble contrast echocardiography was a highly sensitive method and was likely to obtain false-positive results.Conclusions:Bubble contrast echocardiography might be highly false positive in detecting pulmonary arteriovenous fistulas in patients with cavopulmonary anastomosis. We have to consider how we make use of this method. Further standardisation of techniques is required.
Ca
2+
overload is a cardinal feature of cardiomyocyte injury, and its progression to irreversible state leads to cell death. However, unknowns are the precise spatiotemporal changes in the myocyte Ca
2+
dynamics and the relevant cell morphology of irreversibly injured hearts. On the hypothesis that myocytes exhibit high-frequency Ca
2+
waves and contraction band necrosis in saponin-permeabilized injured heart, we observed changes in the Ca
2+
dynamics and the relevant morphological changes in the subepicardial myocardium of the Fluo4-loaded rat hearts (n = 14) by rapid-scanning confocal microscopy (100 frames/s) under Langendorff perfusion with 0.3 mM Ca
2+
-Tyrode solution including 0.4 % saponin at 30°C. Also performed was confocal imaging of tetramethylrhodamine methyl ester (TMRM) fluorescence of the myocardium. Under quasi-quiescence of the heart after dissection of the SA node, individual myocytes barely exhibited spontaneous Ca
2+
waves, whereas after commencement of saponin perfusion high-frequency (118 ± 9.7 /min/cell, mean ± SEM) Ca
2+
waves (hereafter, “agonal waves”) emerged within 1 min, showing asynchronous, oscillatory contractions in the individual myocytes with a V
prop
of 124 ± 2.5 μm/s (n = 60). Subsequently, the waves gradually decreased in frequency with concomitant slowing of its decay time course, and eventually, disappeared in 6 min; myocytes exhibited high, static Fluo4-fluorescence intensity. Along with the progression of Ca
2+
overload by saponin, the TMRM fluorescence intensity was discretely lost in individual myocytes. The myocytes showing the agonal waves exhibited contraction bands, i.e., band-like aggregations of the actin fibers. Under mechanical arrest of the heart by 2,3-butanedione monoxime (20 mM), saponin still induced the agonal waves with a frequency of 253 ± 10.6 /cell/min and V
prop
of 118 ± 2.1 μm/s (n = 60); however, contraction bands were barely seen.In conclusion, irreversible myocyte injury by saponin provoked agonal Ca
2+
waves and oscillatory contractions indicating progressive Ca
2+
overload and the following mitochondrial damage, which may provide deeper insights into understanding the mechanism of contraction band necrosis.
The reaction of Ca(OH) 2 with hydrogen chloride was studied using single crystals to elucidate the reaction mechanism under simulated bag filter conditions. The Xray diffraction patterns of the chlorinated single crystals indicated that products at both surfaces (( 1010) and ( 0001) planes on the side and top faces, respectively) were CaCl 2 anhydrate and CaOHCl anhydrate. The observed chlorination product layer on the singlecrystal surface was only several micrometers thick, even after 24 h. Comparing the thickness of the chlorinated product layer on the (1010) side face and (0001) top face of the Ca(OH) 2 crystals revealed that the reaction proceeded more rapidly on the former than on the latter. H 2 O strongly promoted the chlorination reaction.
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