Impact factor 0.175

Signa Vitae

Journal of Intensive Care and Emergency Medicine

The role of nitric oxide in apoptosis modulation in newborns with pneumonia

Abstract

Introduction. Nitric oxide (NO) is an important diagnostic marker and mediator in the inflammatory process, which plays a key role in the mechanism of programmed cell death, thus, forming the basis of many pathological diseases.

Methods. The study involved 73 newborns with pneumonia (moderate severity in 44 neonates (group 1), severe pneumonia in 29 (group 2)). The intensity of neutrophil apoptosis and necrosis was determined by flow cytometry, whereas nitric oxide metabolites were measured by spectrophotometry.

Results. The level of nitric oxide metabolites (NO2+NO3) in newborns with pneumonia was higher than in healthy children (16.93 (15.82; 17.79) μmol/ml) and correlated with disease severity (in group 1 – 22.65 (21.42; 23.40) μmol/ml in group 2 – 26.82 (25.81; 27.91) μmol/ml). The level of NO3 increased moderately, while NO2 generation was more intense, exceeding control indexes in both groups (рc1<0.001; рc2<0.001; р12<0.001).

The occurrence of intensive neutrophil apoptosis was revealed in newborns with pneumonia of moderate severity (рc1<0.001), while necrosis prevailed in severe pneumonia (рc2<0.001).

Inverse correlation (R=-0.63; р<0.05) was found between the level of nitric oxide metabolites and neutrophil apoptosis; and direct correlation (R=0.68; р<0.05) was revealed between NO metabolites and neutrophil necrosis indices.

Conclusions. Increased generation of nitric oxide metabolites, that directly correlated with disease severity in newborns with pneumonia, was found. NO2 has multidirectional effects on neutrophil apoptosis and necrosis, leading to toxic accumulation of neutrophils in the organism, thus enhancing the inflammatory and intoxication process that impact disease severity.

Key words: nitric oxide, apoptosis, necrosis, neutrophils, pneumonia, newborn

Read More

Myocardial effects of cardiac arrest and resuscitation with especial reference to mitochondrial injury

Abstract

The underlying mechanism of cell injury during ischemia and reperfusion is complex and timesesnsitive. Some processess develop coincidentally with the onset of ischemia and during reperfusion leading to abnormalities in energy metabolism, acid base status, and intracellular ion homeostasis. Other processes develop later and encompass activation of various signalling pathways that have deleterious or beneficial effects on specific effectors, but associated with sustained disruption of energy production contractile dysfunction and activation of apoptotic pathways. Discussion on the various cell mechanisms resposible for cell injury is beyond the scope of this review. However, pertinent to our discussion is the mounting evidence pointing to mitochondria as key target organelles of reperfusion injury.

Key words: cardiac arrest, mito-chondrial injury, cardiopulmonary resuscitation, apoptosis

Read More

© 2019. Signa Vitae. Except where otherwise noted, content on this site is licensed under a Creative Commons Attribution 4.0 International license.