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Articles by N Lai
Total Records ( 2 ) for N Lai
  N Lai , H Zhou , G. M Saidel , M Wolf , K McCully , L. B Gladden and M. E. Cabrera
 

Noninvasive, continuous measurements in vivo are commonly used to make inferences about mechanisms controlling internal and external respiration during exercise. In particular, the dynamic response of muscle oxygenation (SmO2) measured by near-infrared spectroscopy (NIRS) is assumed to be correlated to that of venous oxygen saturation (SvO2) measured invasively. However, there are situations where the dynamics of SmO2 and SvO2 do not follow the same pattern. A quantitative analysis of venous and muscle oxygenation dynamics during exercise is necessary to explain the links between different patterns observed experimentally. For this purpose, a mathematical model of oxygen transport and utilization that accounts for the relative contribution of hemoglobin (Hb) and myoglobin (Mb) to the NIRS signal was developed. This model includes changes in microvascular composition within skeletal muscle during exercise and integrates experimental data in a consistent and mechanistic manner. Three subjects (age 25.6 ± 0.6 yr) performed square-wave moderate exercise on a cycle ergometer under normoxic and hypoxic conditions while muscle oxygenation (Coxy) and deoxygenation (Cdeoxy) were measured by NIRS. Under normoxia, the oxygenated Hb/Mb concentration (Coxy) drops rapidly at the onset of exercise and then increases monotonically. Under hypoxia, Coxy decreases exponentially to a steady state within ~2 min. In contrast, model simulations of venous oxygen concentration show an exponential decrease under both conditions due to the imbalance between oxygen delivery and consumption at the onset of exercise. Also, model simulations that distinguish the dynamic responses of oxy-and deoxygenated Hb (HbO2, HHb) and Mb (MbO2, HMb) concentrations (Coxy = HbO2 + MbO2; Cdeoxy = HHb + HMb) show that Hb and Mb contributions to the NIRS signal are comparable. Analysis of NIRS signal components during exercise with a mechanistic model of oxygen transport and metabolism indicates that changes in oxygenated Hb and Mb are responsible for different patterns of SmO2 and SvO2 dynamics observed under normoxia and hypoxia.

  W Lu , P Ran , D Zhang , N Lai , N Zhong and J. Wang
 

Recent advances have identified an important role of bone morphogenetic protein 4 (BMP4) in pulmonary vascular remodeling, yet the underlying mechanisms remain largely unexplored. We have previously found that Ca2+ influx through store-operated calcium channels (SOCC), which are mainly thought to be composed of canonical transient receptor potential (TRPC) proteins, likely contribute to the pathogenic development of chronic hypoxic pulmonary hypertension. In this study, we investigated the effect of BMP4 on expression of TRPC and store-operated Ca2+ entry (SOCE) in pulmonary arterial smooth muscle cells (PASMCs). Real-time quantitative PCR and Western blotting revealed that treatment with BMP4 (50 ng/ml, 60 h) increased TRPC1, TRPC4, and TRPC6 mRNA and protein expression in growth-arrested rat distal PASMCs. Moreover, in comparison to vehicle control, cells treated with BMP4 also exhibited enhanced SOCE, and elevated basal intracellular calcium concentration ([Ca2+]i) as determined by fluorescent microscopy using the Ca2+ indicator Fura-2 AM. Perfusing cells with Ca2+-free Krebs-Ringer bicarbonate solution (KRBS) or KRBS containing SOCC antagonists SKF-96365 or NiCl2 attenuated the increases in basal [Ca2+]i caused by BMP4. Specific knockdown of BMP4 by small interference RNA significantly decreased the mRNA and protein expression of TRPC1, TRPC4, and TRPC6 and reduced SOCE and basal [Ca2+]i in serum-stimulated PASMCs. We conclude that BMP4 regulates calcium signaling in PASMCs likely via upregulation of TRPC expression, leading to enhanced SOCE and basal [Ca2+]i in PASMCs, and by this mechanism contributes to pulmonary vascular remodeling during pulmonary arterial hypertension.

 
 
 
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