4 articles - 08.09.10
1: Klin Med (Mosk). 2009;87(4):37-41.
[Article in Russian]
Vasil'ev AP, Strel'tsova NN, Sekisova MA.
The aim of the study was to assess effect of omega-3 polyunsaturated fatty acids (PUFAs) on clinical manifestations of metabolic syndrome (MS) and microcirculation in patients with arterial hypertension (AH). 22 patients of the 32 with grade 2 AH and MC symptoms (by ATP III criteria) were given 1.5 mg of omega-3 PUFAs for 1 months. The control group comprised 10 patients. Serum lipid profile was detected and forearm skin microcirculation evaluated by laser Doppler flowmetry. Therapy with omega-3 PUFAs resulted in a significant decrease of serum triglycerides from 3.04 +/- 0.39 to 1.91 +/- 0.15 mmol/l (-37.2%). Its combination with hypotensive therapy reduced mean AP from 114.5 +/- 2.4 to 106.3 +/- 1.8 mm Hg (p < 0.01). Also, omega-3 PUFAs increased amplitude fluctuations in LDF-grams in endothelial and neurogenic ranges by 33.3 and 30.8% respectively, tissue hemoperfusion rate from 4.9 +/- 0.13 to 5.3 +/- 0.15 U (p < 0.05), capillary blood flow reserve by 13.7% (p < 0.05), maximum tissue hemoperfusion by 18.8% (p < 0.01), and coefficient of variation of tissue blood flow by 26.9%. Blood C-reactive protein level dropped by 40.7%. These changes were absent in control patients. It is concluded that correction of omega-3 PUFAs deficiency in patients with HA and MS reduces hyperlipidemia, has moderate antihypertensive effect, improves endothelial function and microcirculation. Multifunctional action of omega-3 PUFAs gives reason to recommend them for the treatment of MS.
Publication Types: English Abstract
Links http://www.ncbi.nlm.nih.gov/entrez/queryd.fcgi?cmd=Retrieve&db=PubMed&list_uids=19514319&dopt=ExternalLink
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PMID: 19514319 [PubMed - indexed for MEDLINE]2: Hepatology. 2007 Apr;45(4):855-63.
El-Badry AM, Moritz W, Contaldo C, Tian Y, Graf R, Clavien PA.
Swiss HPB (Hepato-Pancreatico-Biliary) Centre, Department of Visceral and Transplant Surgery, University Hospital Zurich, Zurich, Switzerland.
Macrovesicular hepatic steatosis has a lower tolerance to reperfusion injury than microvesicular steatosis with an abnormally high ratio of omega-6 (n-6): omega-3 (n-3) polyunsaturated fatty acids (PUFAs). We investigated the influence of PUFAs on microcirculation in steatotic livers and the potential to minimize reperfusion injury in the macrosteatotic liver by normalization of PUFAs. Ob/ob mice were used as a model of macrovesicular hepatic steatosis and C57/Bl6 mice fed a choline-deficient diet for microvesicular steatosis. Steatotic and lean livers were subjected to 45 minutes of ischemia and 3 hours of reperfusion. Hepatic content of omega-3 and omega-6 PUFAs was determined. Microcirculation was investigated using intravital fluorescence microscopy. A second group of ob/ob mice was supplemented with dietary omega-3 PUFAs and compared with the control diet-fed group. Microcirculation, AST, and Kupffer cell activity were assessed. Macrosteatotic livers had significant microcirculatory dysfunction correlating with high omega-6: omega-3 PUFA ratio. Dietary omega-3 PUFA resulted in normalization of this ratio, reduction of intrahepatic lipids, and decrease in the extent of macrosteatosis. Defective microcirculation was dramatically ameliorated with significant reduction in Kupffer cell activity and protection against hepatocellular injury both before ischemia and after reperfusion. CONCLUSION: Macrosteatotic livers disclosed an abnormal omega-6: omega-3 PUFA ratio that correlates with a microcirculatory defect that enhanced reperfusion injury. Thus, protective strategies applied during or after ischemia are unlikely to be useful. Preoperative dietary omega-3 PUFAs protect macrosteatotic livers against reperfusion injury and might represent a valuable method to expand the live liver donor pool.
Publication Types: Research Support, Non-U.S. Gov't
Links http://www.ncbi.nlm.nih.gov/entrez/queryd.fcgi?cmd=Retrieve&db=PubMed&list_uids=17393510&dopt=ExternalLink
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PMID: 17393510 [PubMed - indexed for MEDLINE]3: Adv Exp Med Biol. 1997;415:195-208.
Bruckner G.
Department of Clinical Sciences/Division Clinical Nutrition, University of Kentucky, Lexington 40506-0080, USA.
We have observed significant increases in LDF and similar trends for CBV after FO supplementation in younger subjects (both normolipidemic and hyperlipidemic). In elderly subjects, this trend appears to be reversed unless subjects are supplemented with higher doses of vit. E (100 IU/10 KG/day). Our mouse data suggest that dietary vit. E at 100 IU/Kg does not adequately protect against lipid oxidation in vivo or in vitro following an oxidative insult when mice are fed an 8% FO & 2% linoleic acid containing diet. It has been reported that FO significantly lowers triglycerides and VLDL-cholesterol (especially where subjects have higher initial triglyceride values) and tends to increase LDL-cholesterol and Apo-B100. These findings are all the more important because the oxidation of LDL from FO-supplemented subjects caused a time-dependent increase in the ability to facilitate albumin transfer which was not diminished following a 2 month washout (WO). Addition of vit. E to the FO supplement prevented this change. These data suggest that FO supplementation without sufficient vit. E may be deleterious to the vascular endothelium. The western fat blend supplement appeared to be protective with increased length of supplementation most likely due to increased MONO fatty acids which are resistant to oxidation; vit. E supplementation appeared to have little additional effect. Our combined studies, and those reported by others, suggest that in humans, increased peripheral microcirculatory flow is most likely due to changes in precapillary vascular tone i.e., vasodilation. It is also possible that subtle changes in each of the three variables i.e. blood pressure, blood viscosity and vascular tone when combined may contribute to the significant changes which we have noted as increased LDF or CBV after intervention with dietary n-3 fatty acids. We hypothesize that interactions between dietary fatty acids and vit. E alters the ratios of vasoconstrictive-platelet aggegatory/vasodilatory-antiplatelet aggregatory agents (TXA2 and endothelin/PGI2 and nitric oxide), the expression of adhesion molecules (P-selectin and E-selectin) and thereby directly influences the modulation of free radical mediated events between blood elements and the vascular endothelium. Fatty acids of the n3 series may alter these events by favoring the production of vasodilatory compounds and decreased expression of P and/or E-selectins, provided that these highly oxidizable lipids are protected by adequate antioxidants.
Publication Types: Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S. Review
Links http://www.ncbi.nlm.nih.gov/entrez/queryd.fcgi?cmd=Retrieve&db=PubMed&list_uids=9131193&dopt=ExternalLink
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PMID: 9131193 [PubMed - indexed for MEDLINE]4: Am J Physiol. 1993 May;264(5 Pt 1):G828-34.
Miura S, Imaeda H, Shiozaki H, Kurose I, Fukumura D, Tashiro H, Serizawa H, Suematsu M, Sekizuka E, Tsuchiya M.
Department of Internal Medicine, School of Medicine, Keio University, Tokyo, Japan.
The major objective of this study is to investigate whether oral administration of eicosapentanoic acid (EPA) has any preventive effect on endotoxin-induced microcirculatory damage of rat small intestine. EPA in a daily dose of 300 mg/kg was orally given to male Wistar rats for 3 wk. Submucosal microvessels of the ileum were observed by intravital microscopy equipped with a high-speed video camera system after the intra-arterial infusion of endotoxin at a dose of 2 mg.kg-1.h-1. The number of sticking leukocytes was significantly increased at 30 min after the treatment of endotoxin especially along the smaller branch of intestinal venules. It reached the maximal plateau at 45 min after treatment. The pretreatment of EPA significantly attenuated the increase in sticking leukocytes induced by endotoxin. A platelet-activating factor (PAF) antagonist 2-[N-acetyl-N-(2-methoxy-3-octadecylcarbamoyloxy propoxycarbonyl) aminomethyl]-1-ethylpyridinium chloride (CV-6209) significantly prevented the increased leukocyte sticking to the same extent as EPA treatment. Thirty minutes after endotoxin infusion, red blood cell (RBC) velocity was significantly decreased in both arterioles and venules. RBC velocity appeared to be continuously decreased thereafter and reached its minimum value at approximately 60 min. EPA treatment was revealed to prevent the decrease in RBC velocity of microvessels induced by endotoxin. CV-6209 also significantly attenuated the decreased RBC velocity. The remarkable elevation of PAF content in the ileal mucosa as observed by endotoxin infusion was also significantly attenuated by administration of EPA.(ABSTRACT TRUNCATED AT 250 WORDS)
Publication Types: Research Support, Non-U.S. Gov't
Links http://www.ncbi.nlm.nih.gov/entrez/queryd.fcgi?cmd=Retrieve&db=PubMed&list_uids=8498509&dopt=ExternalLink
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PMID: 8498509 [PubMed - indexed for MEDLINE]