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Dietary saturated fat (SF) has adverse effects on cardiac and vascular smooth muscle (VSM) contractility. Furthermore, VSM of spontaneously hypertensive rats (SHR) is overreactive to various biological stimuli. The aim of this study was to investigate the effects of increasing dietary fat as lard on gut contractility in SHR. Control Wistar-Kyoto (WKY) rats and SHR (13 wk old) were fed for 12 wk a diet containing 3% sunflower oil [low fat (LF), 3% total fat] or diets supplemented with 7% lard [medium fat (MF), 10% total fat] or 27% lard [high fat (HF), 30% total fat]. For ileal and colonic tissues (WKY and SHR), there was a lower total phospholipid PUFA (n-6)/(n-3) ratio with increased dietary SF (P < 0.003). For WKY, increasing SF led to lower levels of the major SCFA and lower total SCFA levels in cecal digesta (P < 0.01). This trend was evident in SHR but significant only for butyrate (P < 0.01). Contractility responses were unaltered in ileum. In colon, there was a change of sensitivity (50% effective concentration) to angiotensin II in WKY (P < 0.05) due to increased SF and a change of sensitivity to prostaglandin (PG)[E.sub.2] and carbachol in SHR (P < 0.05). When the 3 dietary groups were combined, there was lower sensitivity (P < 0.01) and lower maximal, contraction (P < 0.05) in ileum and lower maximal contraction in colon of SHR in response to PG[F.sub.2[alpha]] (P < 0.05) and PG[E.sub.2] (P < 0.01) compared with WKY. Unlike (n-3) PUFA, dietary SF had little overall effect on gut contractility. However, this is the first report of a defect in PG responsiveness from gut tissue from hypertensive rats. J. Nutr. 134: 2924-2929, 2004. KEY WORDS: * hypertensive rats * saturated fat * gut contractility * prostanoid defect

Previous research showed that dietary fish oil was potently antiarrhythmic in rats but olive oil was not. This study was designed to test the hypothesis that canola oil, another major dietary source of oleic acid additionally containing the (n-3) polyunsaturated fatty acid [Alpha]-linolenic acid [18:3(n-3)], can reduce vulnerability to cardiac arrhythmia in rats. Rats were randomly assigned to one of four experimental diet groups for 12 wk. The fat source in the diets was 12% olive (63% oleic acid), canola (55% oleic, 8% [Alpha]-linolenic acid), soybean [50% linoleic 18:2(n-6), 7% [Alpha]-linolenic acid] or sunflower seed oil (64% linoleic acid). Arrhythmias were induced by coronary artery occlusion and reperfusion. Incidence of ventricular fibrillation, mortality and arrhythmia score during reperfusion were significantly lower in rats fed the diet containing canola oil than in those fed the olive oil diet. No difference in the severity of arrhythmias was seen in groups fed diets containing soybean or sunflower seed oils. Analysis of myocardial phospholipid fatty acids showed that consumption of canola oil decreased the ratio of (n-6)/(n-3) polyunsaturated fatty acids relative to the other diets, as does dietary fish oil. These results suggest that regular substitution of canola oil for other dietary lipid sources may assist in reducing the likelihood of a transient ischemic event leading to life-threatening cardiac arrhythmias, but the effectiveness of [Alpha]-linolenic acid is reduced by high levels of linoleic acid. INDEXING KEY WORDS: reperfusion; (n-3) fatty acids; canola; arrhythmia; [Alpha]-linolenic acid; rats

Regular fish or fish oil intake is associated with a low incidence of heart failure clinically, and fish oil-induced reduction in cardiac remodelling seen in hypertrophy models may contribute. We investigated whether improved cardiac energy efficiency in non-hypertrophied hearts translates into attenuation of cardiac dysfunction in hypertrophied hearts. Male Wistar rats (n 33) at 8 weeks of age were sham-operated or subjected to abdominal aortic stenosis to produce pressure-overload cardiac hypertrophy. Starting 3 weeks post-operatively to follow initiation of hypertrophy, rats were fed a diet containing 10 % olive oil (control) or 5 % fish oil (ROPUFA® 30 (17 % EPA, 10 % DHA))+5 % olive oil (FO diet). At 15 weeks post-operatively, ventricular haemodynamics and oxygen consumption were evaluated in the blood-perfused, isolated working heart. Resting and maximally stimulated cardiac output and external work were >60 % depressed in hypertrophied control hearts but this was prevented by FO feeding, without attenuating hypertrophy. Cardiac energy efficiency was lower in hypertrophy, but greater in FO hearts for any given cardiac mass. Coronary blood flow, restricted in hypertrophied control hearts, increased with increasing work in hypertrophied FO hearts, revealing a significant coronary vasodilator reserve. Pronounced cardiac dysfunction in hypertrophied hearts across low and high workloads, indicative of heart failure, was attenuated by FO feeding in association with membrane incorporation of n-3 PUFA, principally DHA. Dietary fish oil may offer a new approach to balancing the high oxygen demand and haemodynamic requirements of the failing hypertrophied heart independently of attenuating hypertrophy. [ABSTRACT FROM PUBLISHER]

We have reported that dietary fish oil (FO) leads to the incorporation of long-chain n-3 PUFA into the gut tissue of small animal models, affecting contractility, particularly of rat ileum. This study examined the FO dose response for the incorporation of n-3 PUFA into ileal tissue and how this correlated with in vitro contractility. Groups of ten to twelve 13-wk-old Wistar-Kyoto rats were fed 0, 1, 2.5, and 5% FO-supplemented diets balanced with sunflower seed oil for 4 wk, after which ileal total phospholipid FA were determined and in vitro contractility assessed. For the total phospholipid fraction, increasing the dietary FO levels led to a significant increase first evident at 1% FO, with a stepwise, nonsaturating six-fold increase in n-3 PUFA as EPA (20:5n-3), DPA (docosapentaenoic acid, 22:5n-3), and DHA, but mainly as DHA (22:6n-3), replacing the n-6 PUFA linoleic acid (18:2n-6) and arachidonic acid (20:4n-6) over the dosage range. There was no difference in KCl-induced depolarization-driven contractility. However, a significant increase in receptor-dependent maximal contractility occurred at 1% FO for carbachol and at 2.5% FO for prostaglandin E2, with a concomitant increase in sensitivity for prostaglandin E2 at 2.5 and 5% FO. These results demonstrate that significant increases in ileal membrane n-3 PUFA occurred at relatively low doses of dietary FO, with differential receptor-dependent increases in contractility observed for muscarinic and prostanoid agonists.