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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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- Cermak, NM, et al.
(författare)
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No improvement in endurance performance after a single dose of beetroot juice
- 2012
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Ingår i: International journal of sport nutrition and exercise metabolism. - : Human Kinetics. - 1543-2742 .- 1526-484X. ; 22:6, s. 470-478
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Tidskriftsartikel (refereegranskat)abstract
- Dietary nitrate supplementation has received much attention in the literature due to its proposed ergogenic properties. Recently, the ingestion of a single bolus of nitrate-rich beetroot juice (500 ml, ~6.2 mmol NO3−) was reported to improve subsequent time-trial performance. However, this large volume of ingested beetroot juice does not represent a realistic dietary strategy for athletes to follow in a practical, performancebased setting. Therefore, we investigated the impact of ingesting a single bolus of concentrated nitrate-rich beetroot juice (140 ml, ~8.7 mmol NO3−) on subsequent 1-hr time-trial performance in well-trained cyclists.Methods:Using a double-blind, repeated-measures crossover design (1-wk washout period), 20 trained male cyclists (26 ± 1 yr, VO2peak 60 ± 1 ml · kg−1 · min−1, Wmax 398 ± 7.7 W) ingested 140 ml of concentrated beetroot juice (8.7 mmol NO3−; BEET) or a placebo (nitrate-depleted beetroot juice; PLAC) with breakfast 2.5 hr before an ~1-hr cycling time trial (1,073 ± 21 kJ). Resting blood samples were collected every 30 min after BEET or PLAC ingestion and immediately after the time trial.Results:Plasma nitrite concentration was higher in BEET than PLAC before the onset of the time trial (532 ± 32 vs. 271 ± 13 nM, respectively; p < .001), but subsequent time-trial performance (65.5 ± 1.1 vs. 65 ± 1.1 s), power output (275 ± 7 vs. 278 ± 7 W), and heart rate (170 ± 2 vs. 170 ± 2 beats/min) did not differ between BEET and PLAC treatments (all p > .05).Conclusion:Ingestion of a single bolus of concentrated (140 ml) beetroot juice (8.7 mmol NO3−) does not improve subsequent 1-hr time-trial performance in well-trained cyclists.
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| 29. |
- Checa, A, et al.
(författare)
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Hexosylceramides as intrathecal markers of worsening disability in multiple sclerosis
- 2015
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Ingår i: Multiple sclerosis (Houndmills, Basingstoke, England). - : SAGE Publications. - 1477-0970 .- 1352-4585. ; 21:10, s. 1271-1279
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Tidskriftsartikel (refereegranskat)abstract
- Sphingolipids are important components of neurons and the myelin sheath whose levels are altered in multiple sclerosis (MS). Objectives: We aimed to determine if cerebrospinal fluid (CSF) sphingolipids can be used as markers of MS disease progression. Methods: Using liquid chromatography tandem mass spectrometry, we analysed sphingolipids in CSF from 134 individuals. The MS group included 65 patients divided into 41 relapsing–remitting MS (RRMS) and 24 progressive MS (ProgMS). In addition, a group of 13 early MS/clinically isolated syndrome (EarlyMS) and two control groups consisting of 38 individuals with other neurological diseases (OND) and 18 OND with signs of inflammation (iOND) were analysed. A follow-up study included 17 additional RRMS patients sampled at two time points 4.7±1.7 years apart. Results: Levels of sphingomyelin (SM)- and hexosylceramide (HexCer)-derived sphingolipids increased in the CSF of patients with MS independently of the fatty acid chain length in RRMS ( p<0.05). Levels of palmitic acid (16:0)-containing HexCer (HexCer16:0) increased significantly in ProgMS compared with the OND ( p<0.001), iOND ( p<0.05) and EarlyMS ( p<0.01) groups and correlated with Expanded Disability Status Scale in RRMS in both studies ( p=0.048; p=0.027). Conclusion: HexCer16:0 is a promising candidate marker of disease progression in MS, especially in RRMS.
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| 32. |
- Crespo, AS, et al.
(författare)
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Nasal nitric oxide and regulation of human pulmonary blood flow in the upright position
- 2010
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Ingår i: Journal of applied physiology (Bethesda, Md. : 1985). - : American Physiological Society. - 1522-1601 .- 8750-7587. ; 108:1, s. 181-188
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Tidskriftsartikel (refereegranskat)abstract
- There are a number of evidences suggesting that lung perfusion distribution is under active regulation and determined by several factors in addition to gravity. In this work, we hypothesised that autoinhalation of nitric oxide (NO), produced in the human nasal airways, may be one important factor regulating human lung perfusion distribution in the upright position. In 15 healthy volunteers, we used single-photon emission computed tomography technique and two tracers (99mTc and 113mIn) labeled with human macroaggregated albumin to assess pulmonary blood flow distribution. In the sitting upright position, subjects first breathed NO free air through the mouth followed by the administration of the first tracer. Subjects then switched to either nasal breathing or oral breathing with the addition of exogenous NO-enriched air followed by the administration of the second tracer. Compared with oral breathing, nasal breathing induced a blood flow redistribution of ∼4% of the total perfusion in the caudal to cranial and dorsal to ventral directions. For low perfused lung regions like the apical region, this represents a net increase of 24% in blood flow. Similar effects were obtained with the addition of exogenous NO during oral breathing, indicating that NO and not the breathing condition was responsible for the blood flow redistribution. In conclusion, these results provide evidence that autoinhalation of endogenous NO from the nasal airways may ameliorate the influence of gravity on pulmonary blood flow distribution in the upright position. The presence of nasal NO only in humans and higher primates suggest that it may be an important part of the adaptation to bipedalism.
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| 36. |
- Feelisch, M, et al.
(författare)
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Is sunlight good for our heart?
- 2010
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Ingår i: European heart journal. - : Oxford University Press (OUP). - 1522-9645 .- 0195-668X. ; 31:9, s. 1041-1045
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Tidskriftsartikel (refereegranskat)
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| 41. |
- 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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| 48. |
- Gronros, J, et al.
(författare)
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Arginase inhibition restores in vivo coronary microvascular function in type 2 diabetic rats
- 2011
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Ingår i: American journal of physiology. Heart and circulatory physiology. - : American Physiological Society. - 1522-1539 .- 0363-6135. ; 300:4, s. H1174-H1181
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Tidskriftsartikel (refereegranskat)abstract
- Nitric oxide (NO) is crucial for maintaining normal endothelial function and vascular integrity. Increased arginase activity in diabetes might compete with NO synthase (NOS) for their common substrate arginine, resulting in diminished production of NO. The aim of this study was to evaluate coronary microvascular function in type 2 diabetic Goto-Kakizaki (GK) rats using in vivo coronary flow velocity reserve (CFVR) and the effect of arginase inhibition to restore vascular function. Different groups of GK and Wistar rats were given vehicle, the arginase inhibitor Nω-hydroxy-nor-l-arginine (nor-NOHA), l-arginine, and the NOS inhibitor NG-monomethyl -l-arginine (l-NMMA). GK rats had impaired CFVR compared with Wistar rats (1.31 ± 0.09 vs. 1.87 ± 0.05, P < 0.001). CFVR was restored by nor-NOHA treatment compared with vehicle in GK rats (1.71 ± 0.13 vs. 1.23 ± 0.12, P < 0.05) but remained unchanged in Wistar rats (1.88 ± 0.10 vs. 1.79 ± 0.16). The beneficial effect of nor-NOHA in GK rats was abolished after NOS inhibition. CFVR was not affected by arginine compared with vehicle. Arginase II expression was increased in the aorta and myocardium from GK rats compared with Wistar rats. Citrulline-to-ornithine and citrulline-to-arginine ratios measured in plasma increased significantly more in GK rats than in Wistar rats after nor-NOHA treatment, suggesting a shift of arginine utilization from arginase to NOS. In conclusion, coronary artery microvascular function is impaired in the type 2 diabetic GK rat. Treatment with nor-NOHA restores the microvascular function by a mechanism related to increased utilization of arginine by NOS and increased NO availability.
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| 49. |
- Hansen, MN, et al.
(författare)
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The roles of tissue nitrate reductase activity and myoglobin in securing nitric oxide availability in deeply hypoxic crucian carp
- 2016
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Ingår i: The Journal of experimental biology. - : The Company of Biologists. - 1477-9145 .- 0022-0949. ; 219:24Pt 24, s. 3875-3883
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Tidskriftsartikel (refereegranskat)abstract
- In mammals, treatment with low doses of nitrite have cytoprotective effects in ischemia/reperfusion events, due to nitric oxide formation and S-nitrosation of proteins. Interestingly, anoxia-tolerant lower vertebrates possess an intrinsic ability to increase intracellular [nitrite] during anoxia in tissues with high myoglobin and mitochondria contents, such as the heart. Here we test the hypothesis that red and white skeletal muscle develops different nitrite levels in crucian carp exposed to deep hypoxia and whether this correlates with myoglobin concentration. We also tested if liver, muscle, and heart tissue possess nitrate reductase activity that supply nitrite to the tissues during severe hypoxia. Crucian carp exposed to deep hypoxia (1<Po2<3mmHg) for one day increased nitrite in red musculature to more than double the value in normoxic fish, while nitrite was unchanged in white musculature. There was a highly significant positive correlation between tissue concentrations of nitrite and nitros(yl)ated compounds. Myoglobin levels were 7 times higher in red than white musculature, but there was no clear correlation between [nitrite] and [Mb]. Finally, we found a low but significant nitrate reductase activity in liver and white muscle, but not in cardiomyocytes. Nitrate reduction was inhibited by allopurinol, showing that it was partly catalyzed by xanthine oxidoreductase.
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