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- Bulhak, AA, et al.
(författare)
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PPAR-alpha activation protects the type 2 diabetic myocardium against ischemia-reperfusion injury: involvement of the PI3-Kinase/Akt and NO pathway
- 2009
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Ingår i: American journal of physiology. Heart and circulatory physiology. - : American Physiological Society. - 0363-6135 .- 1522-1539. ; 296:3, s. H719-H727
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Tidskriftsartikel (refereegranskat)abstract
- Several clinical studies have shown the beneficial cardiovascular effects of fibrates in patients with diabetes and insulin resistance. The ligands of peroxisome proliferator-activated receptor-α (PPAR-α) reduce ischemia-reperfusion injury in nondiabetic animals. We hypothesized that the activation of PPAR-α would exert cardioprotection in type 2 diabetic Goto-Kakizaki (GK) rats, involving mechanisms related to nitric oxide (NO) production via the phosphatidylinositol 3-kinase (PI3K)/Akt pathway. GK rats and age-matched Wistar rats (n ≥ 7) were given either 1) the PPAR-α agonist WY-14643 (WY), 2) dimethyl sulfoxide (DMSO), 3) WY and the NO synthase inhibitor NG-nitro-l-arginine (l-NNA), 4) l-NNA, 5) WY and the PI3K inhibitor wortmannin, or 6) wortmannin alone intravenously before a 35-min period of coronary artery occlusion followed by 2 h of reperfusion. Infarct size (IS), expression of endothelial NO synthase (eNOS), inducible NO synthase, and Akt as well as nitrite/nitrate were determined. The IS was 75 ± 3% and 72 ± 4% of the area at risk in the Wistar and GK DMSO groups, respectively. WY reduced IS to 56 ± 3% in Wistar ( P < 0.05) and to 46 ± 5% in GK rats ( P < 0.001). The addition of either l-NNA or wortmannin reversed the cardioprotective effect of WY in both Wistar (IS, 70 ± 5% and 65 ± 5%, respectively) and GK (IS, 66 ± 4% and 64 ± 4%, P < 0.05, respectively) rats. The expression of eNOS and eNOS Ser1177 in the ischemic myocardium from both strains was increased after WY. The expression of Akt, Akt Ser473, and Akt Thr308 was also increased in the ischemic myocardium from GK rats following WY. Myocardial nitrite/nitrate levels were reduced in GK rats ( P < 0.05). The results suggest that PPAR-α activation protects the type 2 diabetic rat myocardium against ischemia-reperfusion injury via the activation of the PI3K/Akt and NO pathway.
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- Gladwin, MT, et al.
(författare)
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The emerging biology of the nitrite anion
- 2005
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Ingår i: Nature chemical biology. - : Springer Science and Business Media LLC. - 1552-4450 .- 1552-4469. ; 1:6, s. 308-314
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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- Lundberg, JO
(författare)
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Cardiovascular prevention by dietary nitrate and nitrite
- 2009
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Ingår i: American journal of physiology. Heart and circulatory physiology. - : American Physiological Society. - 0363-6135 .- 1522-1539. ; 296:5, s. H1221-H1223
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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- Lundberg, JO
(författare)
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Nitric oxide and the paranasal sinuses
- 2008
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Ingår i: Anatomical record (Hoboken, N.J. : 2007). - : Wiley. - 1932-8494. ; 291:11, s. 1479-1484
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Tidskriftsartikel (refereegranskat)
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- Lundberg, JO, et al.
(författare)
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Nitrite reduction to nitric oxide in the vasculature
- 2008
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Ingår i: American journal of physiology. Heart and circulatory physiology. - : American Physiological Society. - 0363-6135 .- 1522-1539. ; 295:2, s. H477-H478
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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- Lundberg, JO
(författare)
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No kidding! Hemoglobin makes NO
- 2006
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Ingår i: BLOOD. - : American Society of Hematology. - 0006-4971 .- 1528-0020. ; 107:2, s. 414-414
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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| 30. |
- Lundberg, JO
(författare)
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Rectal NO and fecal calprotectin in IBD
- 2009
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Ingår i: Scandinavian journal of gastroenterology. - : Informa UK Limited. - 1502-7708 .- 0036-5521. ; 44:1, s. 128-128
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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- Sobko, T, et al.
(författare)
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Intestinal hydrogen and nitric oxide gases in preterm infants--effects of antibiotic therapy
- 2009
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Ingår i: Neonatology. - : S. Karger AG. - 1661-7819 .- 1661-7800. ; 95:1, s. 68-73
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Tidskriftsartikel (refereegranskat)abstract
- <i>Objective:</i> Measurements of hydrogen (H<sub>2</sub>) and nitric oxide (NO) levels in intestinal gas have recently been shown to be useful to monitor bacterial colonization in healthy term newborn infants. The significance of preterm birth and antibiotic therapy for intestinal gas production is not known and was the subject of this study. <i>Methods:</i> A minimally invasive tonometric technique was used for repeated measurements (44 samples) of luminal colonic H<sub>2</sub> and NO in 23 preterm infants with gestational age 27–35 weeks, birth weight 1,170–2,996 g and postnatal age 2–31 days. <i>Results:</i> The measuring procedure was well tolerated in all infants. Intestinal H<sub>2</sub> was 300 (4–1,990) ppm and NO was 34 (11–82) ppb. Intestinal H<sub>2</sub> and NO increased during the first week (p < 0.05) to average levels that in the case of H<sub>2</sub>, exceeded those of healthy, term infants. In preterm infants treated with antibiotics (n = 12), H<sub>2</sub> and NO levels were significantly lower than in those without such therapy (p < 0.05). <i>Conclusion:</i> These observations suggest that intestinal measurements of H<sub>2</sub> and NO may be used to monitor birth-related bacterial colonization in relation to postnatal age, maturation and antibiotic therapy. In preterm infants, gaseous distension of the gut is common and may signal bacterial overgrowth. The potential role of intestinal gas measurements as a diagnostic tool for intestinal disorders remains to be clarified.
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