Effect of electrical activity of the diaphragm waveform patterns on SpO₂ for extremely preterm infants ventilated with neurally adjusted ventilatory assist

[Objective] This study aimed to evaluate the association between electrical activity of the diaphragm (Edi) waveform patterns and peripheral oxygen saturation (SpO2) in extremely preterm infants who are ventilated with neurally adjusted ventilatory assist (NAVA). [Study Design] We conducted a retrospective cohort study at a level III neonatal intensive care unit. Extremely preterm infants born at our hospital between November 2019 and November 2020 and ventilated with NAVA were included. We collected Edi waveform data and classified them into four Edi waveform patterns, including the phasic pattern, central apnea pattern, irregular low-voltage pattern, and tonic burst pattern. We analyzed the Edi waveform pattern for the first 15 h of collectable data in each patient. To investigate the association between Edi waveform patterns and SpO2, we analyzed the dataset every 5 min as one data unit. We compared the proportion of each waveform pattern between the desaturation (Desat [+]) and non-desaturation (Desat [–]) groups. [Results] We analyzed collected data for 105 h (1260 data units). The proportion of the phasic pattern in the Desat (+) group was significantly lower than that in the Desat (–) group (p < .001). However, the proportions of the central apnea, irregular low-voltage, and tonic burst patterns in the Desat (+) group were significantly higher than those in the Desat (–) group (all p < .05). [Conclusion] Our results indicate that proportions of Edi waveform patterns have an effect on desaturation of SpO2 in extremely preterm infants who are ventilated with NAVA

Possible involvement of ATP-purinoceptor signalling in the intercellular synchronization of intracellular Ca2+ oscillation in cultured cardiac myocytes.

Isolated and cultured neonatal cardiac myocytes contract spontaneously and cyclically. The contraction rhythms of two isolated cardiac myocytes, each of which beats at different frequencies at first, become synchronized after the establishment of mutual contacts, suggesting that mutual entrainment occurs due to electrical and/or mechanical interactions between two myocytes. The intracellular concentration of free Ca2+ also changes rhythmically in association with the rhythmic contraction of myocytes (Ca2+ oscillation), and such a Ca2+ oscillation was also synchronized among cultured cardiac myocytes. In this study, we investigated whether intercellular communication other than via gap junctions was involved in the intercellular synchronization of intracellular Ca2+ oscillation in spontaneously beating cultured cardiac myocytes. Treatment with either blockers of gap junction channels or an un-coupler of E–C coupling did not affect the intercellular synchronization of Ca2+ oscillation. In contrast, treatment with a blocker of P2 purinoceptors resulted in the asynchronization of Ca2+ oscillatory rhythms among cardiac myocytes. The present study suggested that the extracellular ATP-purinoceptor system was responsible for the intercellular synchronization of Ca2+ oscillation among cardiac myocytes

Changes in the fluctuation of the contraction rhythm of spontaneously beating cardiac myocytes in cultures with and without cardiac fibroblasts.

The heart functions as a syncytium of cardiac myocytes and surrounding supportive non-myocytes such as fibroblasts. There is a possibility that a variety of non-myocyte-derived factors affect the maturation of cardiac myocytes in the development of the heart. Cultured neonatal cardiac myocytes contract spontaneously and cyclically. The fluctuation of beating rhythm varies depending on the strength of coupling through gap junctions among cardiac myocytes, indicating that the development of intercellular communication via gap junctions is crucial to the stability of contraction rhythm in cardiac myocytes. In this study, we aimed at elucidating whether and how cardiac fibroblasts affect the development of cardiac myocytes from the point of view of the changes in the fluctuation of the contraction rhythm of cardiac myocytes in cardiac myocyte-fibroblast co-cultures. The present study suggested that cardiac fibroblasts co-cultured with cardiac myocytes enhanced the intercellular communication among myocytes via gap junctions, thereby stabilizing the spontaneous contraction rhythm of cultured cardiac myocytes

Ischemia/reperfusion-induced death of cardiac myocytes: possible involvement of nitric oxide in the coordination of ATP supply and demand during ischemia.

Nitric oxide (NO) has been known to play various functional and pathological roles as an intracellular or intercellular messenger in the heart. In this study, we investigated whether NO produced during ischemia was involved in the coordination of ATP supply and demand, and also in protection from cell death using cultured cardiac myocytes. Unexpectedly, the survival rate of myocytes for 3 h simulated ischemia (SI) was increased as compared with that for 2 h SI at 24 h after reperfusion. The cellular ATP level at 3 h after the start of SI was increased compared with that at 2 h, and was almost the same as that before the start of SI. The cellular ATP level at 3 h SI was significantly reduced by either the inhibition of nitric oxide synthase (NOS) or scavenging of NO. Either the inhibition of NOS or the scavenging of NO during SI for 3 h also resulted in a significant decrease in the survival rate of myocytes. Immunocytochemical and Western blot analyses revealed that the expression of nNOS was most evident in cardiac myocytes, but no significant change was observed in the expression of all three NOS isoforms at 2 h SI and at 3 h SI. The fluorescent intensity of DAF-FM was significantly increased at 3 h SI as compared with that at 2 h SI, and the increase in DAF fluorescence during SI was almost completely suppressed by treatment with vinyl-l-NIO (l-VNIO), a potent specific inhibitor of nNOS. In addition, treatment with l-VNIO decreased the cellular ATP level and survival rate. This study suggested that the enhanced production of NO was critical in balancing ATP supply and demand during ischemia, and also in protecting cells from ischemia/reperfusion injury