[Litter storage and water-holding capacity of typical forests in mountainous area of Southwest China]. / è¥¿å—å±±åŒºå ¸åž‹æ£®æž—æž¯è½ç‰©å‚¨é‡åŠæŒæ°´èƒ½åŠ›.

Current studies on water conservation capacity of litter in the mountainous area of Southwest China (MASC) mainly focus on local scale. Such results are difficult to evaluate the storage and water-holding capacity of litter in the whole MASC. In this study, the results of site-scale research in the MASC from 2004 to 2021 were collated (a total of 16 research sites and 70 data), as well as the storage and water-holding characteristics of litters of three typical forests in the MASC were compared and analyzed. The results showed that the water-holding processes of litter in coniferous forest, broadleaved forest and mixed forest were similar, which could be divided into three stages: rapid water absorption, gradual slowing, and stable. The absorption rate and duration of different forests were different in each stage. The broadleaved forest had the fastest water absorption rate, while coniferous forest had the slowest with the longest duration to reach stability. There was no significant difference in litter storage among diffe-rent forest types. The total litter storage of coniferous forest, broadleaved forest and mixed forest ranged from 8.26 to 8.82 t·hm-2. The significant spatial variations of litter storage in semi-decomposed layer resulted in that of total litter storage. The total maximum water-holding capacity of litters of the three forests ranged from 17.85 t·hm-2 to 19.87 t·hm-2, and the maximum water-holding rate of litter ranged from 200.6% to 228.0%. There was a positive correlation between the maximum water-holding capacity and litter storage in different forests. The total effective retention capacity of three forest litters ranged from 11.66 to 12.29 t·hm-2, while the total effective retention rate of three forests ranged from 128.1% to 145.2%. There were no significant differences in litter storage and water holding capacity among three forest types with two decomposition degrees in MASC.

Prostaglandins mediate the cardioprotective effects of atorvastatin against ischemia-reperfusion injury.

OBJECTIVES: Statins attenuate myocardial ischemic injury by activating nitric oxide synthase (NOS). It is unknown whether cyclooxygenase-2 (COX2), which mediates late ischemic preconditioning, also mediates statins-induced cardioprotection. We investigated the involvement of the prostaglandins and NOS in the cardioprotective effect of atorvastatin (ATV) in the rat. METHODS: Sprague-Dawley rats were randomized to a 3-day oral treatment with ATV 10 mg/kg, valdecoxib, a selective COX2 inhibitor (VAL) 3 mg/kg, ATV+VAL or water alone. Rats underwent 30-min myocardial ischemia followed by 4-h reperfusion. RESULTS: Infarct size was smaller in the ATV group (31.3+/-1.9%) than controls (44.5+/-3.1%; p=0.011) and VAL (44.5+/-3.1%; p=0.008). VAL attenuated the protective effect of ATV when administered together (40.2+/-2.5%). ATV pretreatment increased myocardial content of 6-keto-PGF(1alpha) (69.5+/-1.5 pg/mg) and PGE2 (57.9+/-0.6 pg/mg) compared with controls (16.2+/-0.2 and 42.1+/-2.0 pg/mg, respectively) and ATV+VAL (15.8+/-0.3 and 39.9+/-1.9 pg/mg, respectively). ATV increased myocardial content of cytosolic phospholipase A2 (cPLA2) (174.8+/-0.5%), COX2 (446.2+/-0.9%), PGI2 synthase (201.8+/-1.1%) and PGE2 synthase (122+/-0.7%), whereas ATV+VAL did not (123.0+/-7.9%, 93.8+/-8.5%, 103.0+/-1.6% and 99.0+/-0%, respectively). ATV did not change the myocardial content of eNOS and nNOS, but increased the concentration of phosphorylated eNOS (231.8+/-2.4%) and iNOS (154.5+/-1.2%). This effect was not blocked by coadministration of VAL (231.5+/-3.0% and 154.5+/-1.8%, respectively). CONCLUSIONS: Our results suggest that the prostaglandins are essential for mediating the myocardial protective effects of ATV and their production is downstream to eNOS phosphorylation and iNOS.

Simvastatin-induced myocardial protection against ischemia-reperfusion injury is mediated by activation of ATP-sensitive K+ channels.

OBJECTIVES: Previous studies have suggested that the 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors attenuate ischemia-reperfusion injury. We investigated whether pretreatment with simvastatin reduces myocardial infarct size and whether glyburide, a non-selective inhibitor of the ATP-sensitive K channels, abrogates this infarct size-limiting effect. METHODS: Sprague-Dawley rats were treated with either simvastatin (20 mg/kg per day) or saline alone for 3 days. Additional groups of rats were treated as above and on the fourth day they received intravenous glyburide (0.3 mg/kg). All rats underwent 30 min of coronary artery occlusion followed by 180 min of reperfusion. Ischemic myocardium at risk was assessed with blue dye and infarct size with triphenyltetrazolium chloride. RESULTS: Infarct size, expressed as a percentage of the myocardium at risk, was significantly smaller in the simvastatin group (n = 8, 20.8 +/- 3.4%) than in the placebo group (n = 6, 40.1 +/- 2.7%) (P = 0.001). Glyburide abolished the protective effect of simvastatin with infarct size being 34.2 +/- 6.9% and 29.7 +/- 3.9% of the area at risk in the simvastatin group (n = 7) and placebo (n = 7) group, respectively (P = 0.58). CONCLUSIONS: Simvastatin significantly reduced myocardial infarct size. The protective effect was completely abrogated by glyburide, strongly suggesting that this protective effect is mediated via activation of the ATP-sensitive K channels.

Cigarette smoke exposure and hypercholesterolemia increase mitochondrial damage in cardiovascular tissues.

BACKGROUND: A shared feature among cardiovascular disease risk factors is increased oxidative stress. Because mitochondria are susceptible to damage mediated by oxidative stress, we hypothesized that risk factors (secondhand smoke and hypercholesterolemia) are associated with increased mitochondrial damage in cardiovascular tissues. METHODS AND RESULTS: Atherosclerotic lesion formation, mitochondrial DNA damage, protein nitration, and specific activities of mitochondrial proteins in cardiovascular tissues from age-matched C57 and apoE(-/-) mice exposed to filtered air or secondhand smoke were quantified. Both secondhand smoke and hypercholesterolemia were associated with significantly increased mitochondrial DNA damage and protein nitration. Tobacco smoke exposure also resulted in significantly decreased specific activities of mitochondrial enzymes. The combination of secondhand smoke and hypercholesterolemia resulted in increased atherosclerotic lesion formation and even greater levels of mitochondrial damage. CONCLUSIONS: These data are consistent with the hypothesis that cardiovascular disease risk factors cause mitochondrial damage and dysfunction.