nitrogen-dioxide and Ischemia

Short-term exposure to ambient air pollution has been linked to increased risk of stroke mortality, but its adverse effects on mortality from specific types of stroke including ischemic stroke and hemorrhagic stroke remain poorly understood.. Using the China National Mortality Surveillance System, we conducted a time-stratified case-crossover study among 412,567 stroke deaths in Jiangsu province, China during 2015-2019. Residential daily PM. Each 10 μg/m. Short-term exposure to ambient air pollution was significantly associated with increased risk of both ischemic and hemorrhagic stroke mortality and posed considerable excess mortality. Our results suggest that air pollution exposure may lead to substantially greater adverse effects on mortality from ischemic stroke than that from hemorrhagic stroke.

Topics: Air Pollutants; Air Pollution; China; Cross-Over Studies; Environmental Exposure; Hemorrhagic Stroke; Humans; Ischemia; Ischemic Stroke; Nitrogen Dioxide; Particulate Matter; Stroke

We report a mitochondria-targeted nitroreductase (NTR)-activated near-infrared fluorescent probe: CS-NO2. Overexpressed NTR in mitochondria was measured with high sensitivity. More importantly, the probe CS-NO2 successfully monitored NTR activity in solid tumors and a hind-limb model of ischemia in mice. This novel finding indicates the promising function of our probe for the diagnosis of solid tumors and hypoxia-associated diseases.

Topics: Animals; Fluorescent Dyes; Ischemia; Mice; Mitochondria; Neoplasms; Nitrogen Dioxide; Nitroreductases

Increasing ozone concentrations have been known to damage human health and ecosystems. Although ozone tends to display diurnal variation, most studies have reported only on the association between daily ozone concentrations and ischemic stroke occurrence on the same day, or with a 1-day lag. We investigated the effect of the diurnal variation of ozone on ischemic stroke occurrence during the same day.. We included a consecutive series of 1,734 patients from January 1, 2008, to December 31, 2014, at a single tertiary hospital in Seoul, South Korea. We evaluated differences between temperature and pollutants at the time of stroke onset for each time interval and averaged those parameters across the 7-year study period.. During the interval from 13:00 to 16:59, we found a positive association between ischemic stroke occurrence and ozone concentration relative to other time periods. Upper median ozone levels from 13:00 to 16:59 were positively correlated with ischemic stroke (odds ratio, 1.550; 95% confidence intervals, 1.220 to 1.970; P = <0.001) when compared with lower median levels.. The results show diurnal patterns of ischemic stroke occurrence based on upper and lower median ozone levels for a 24-hour period, which extends understanding of the association between stroke occurrence and environmental influences.

Topics: Aged; Air Pollutants; Circadian Rhythm; Female; Humans; Ischemia; Male; Middle Aged; Nitrogen Dioxide; Odds Ratio; Ozone; Republic of Korea; Retrospective Studies; Stroke; Temperature

Blockade of the T-type calcium channel (TCC), which is expressed in the renal efferent arterioles of the juxtamedullary nephron and vasa recta, has been shown to protect against renal injury. Studies were designed to determine the effects of a specific TCC blocker, R(-) efonidipine [R(-)EFO], on the regulation of renal circulation.. Renal medullary blood flux (MBF) and cortical blood flux (CBF) were simultaneously monitored using laser-Doppler flowmetry in Sprague-Dawley rats. Responses were also determined in rats with angiotensin II (AngII) induced renal ischemia. Intravenous (i.v.) or renal interstitial (r.i.) infusion of R(-)EFO (0.25 mg/h, i.v. or r.i.) significantly increased MBF by 24.0 ± 7.0 and 21.0 ± 4.4%, respectively, but without changing CBF or mean arterial pressure. The nitric oxide (NO) synthase inhibitor NG-nitro-L-argininemethylester (L-NAME, 1 μg/kg per min, i.v. or r.i.) significantly attenuated R(-)EFO-induced increase in MBF. R(-)EFO inhibited the AngII-mediated (50 ng/kg per min, i.v.) reduction of MBF (28.4 ± 1.7%), which was associated with increased urinary NO(2) + NO(3) excretion and decreased urinary hydrogen peroxide (H(2)O(2)) excretion. Intracellular H(2)O(2) fluorescence (real-time fluorescence imaging) in the epithelial cells of isolated medullary thick ascending limb (mTAL) significantly increased following AngII stimulation (1 μmol/L, 235 ± 52 units), which was significantly inhibited by pre and coincubation with R(-)EFO. R(-)EFO stimulation also increased the intracellular NO concentration in the epithelial cells of mTAL (220 ± 62 units).. These results suggest that TCC blockade with R(-)EFO selectively increases MBF, an effect that appears to be mediated by changes in renal NO and oxidative stress balance, which may protect against ischemic renal injury in the renal medullary region.

Topics: Angiotensin II; Animals; Blood Flow Velocity; Calcium Channel Blockers; Calcium Channels, T-Type; Dihydropyridines; Disease Models, Animal; Drug Antagonism; Infusions, Intravenous; Ischemia; Kidney Medulla; Laser-Doppler Flowmetry; NG-Nitroarginine Methyl Ester; Nitrogen Dioxide; Nitrogen Oxides; Nitrophenols; Organophosphorus Compounds; Rats; Rats, Sprague-Dawley; Renal Circulation; Vasoconstrictor Agents