The presence of an active and functioning endocannabinoid (EC) system within cardiovascular tissues implies that this system has either a physiological or pathophysiological role (or both), and there is a substantial literature to support the notion that, in the main, they are protective in the setting of various CVD states. Moreover, there is an equally extensive literature to demonstrate the cardio- and vasculo-protective effects of n-3 long-chain (LC)-PUFA. It is now becoming evident that there appears to be a close relationship between dietary intervention with n-3 LC-PUFA and changes in tissue levels of EC, raising the question as to whether or not EC may, at least in part, play a role in mediating the cardio-and vasculo-protective effects of n-3 LC-PUFA. This brief review summarises the current understanding of how both EC and n-3 LC-PUFA exert their protective effects in three major cardiovascular disorders (hypertension, atherosclerosis and acute myocardial infarction) and attempts to identify the similarities and differences that may indicate common or integrated mechanisms. From the data available, it is unlikely that in hypertension EC mediate any beneficial effects of n-3 LC-PUFA, since they do not share common mechanisms of blood pressure reduction. However, inhibition of inflammation is an effect shared by EC and n-3 LC-PUFA in the setting of both atherosclerosis and myocardial reperfusion injury, while blockade of L-type Ca2+ channels is one of the possible common mechanisms for their antiarrhythmic effects. Although both EC and n-3 LC-PUFA demonstrate vasculo- and cardio-protection, the literature overwhelmingly shows that n-3 LC-PUFA decrease tissue levels of EC through formation of EC–n-3 LC-PUFA conjugates, which is counter-intuitive to an argument that EC may mediate the effects of n-3 LC-PUFA. However, the discovery that these conjugates have a greater affinity for cannabinoid receptors than the native EC provides a fascinating avenue for further research into novel approaches for the treatment and prevention of atherosclerosis and myocardial injury following ischaemia/reperfusion.
Objectives Lowering dietary intakes of free sugars is currently promoted by several authorities worldwide. However, the free sugars’ content of food is today not readily available on food packaging or food composition tables. The aim of this work was to develop and test the reproducibility of a new methodology to evaluate the free sugars’ content of packaged foods sold in the European market. Methods The new methodology is an 8-step algorithm, consisting of a series of sequential questions based on the information available on packaging. This includes nutrition declaration and list of ingredients, both of which are mandatory on any pre-packaged food sold in the European Union. This method has been tested by eight trained nutritionists on a selection of 37 packaged food products, twice with a 6-week interval. Inter-and intra-individual variability in the estimated free sugar values were studied by linear regression, analysis of variance and principal component analysis. Results Correlation coefficients between users and sessions for estimated free sugar contents of the 37 selected products were highly significant and above 0.965. When available, the free sugar values provided by the manufacturer, considered to be the true values, were always lower than the estimates generated with the algorithm, in line with the prerequisite of maximizing the free sugars’ content in case of uncertainties. In terms of amounts of free sugars, the algorithm performed better than the World Health Organization's method (i.e., provided a value closer to the true value) in 50% of cases; performance was equal in 20% and worse in 30% of cases. Variation coefficients were not dependent on the mean value of estimated free sugars or on the session, but were higher for mixed dishes and composite products (0.942 and 0.193 on average for pooled sessions, respectively) than for other food categories (below 0.09 on average). Finally, there was a user effect, which may come from selecting different steps in the algorithm, a situation that may be limited by improving instructions or training to users. Conclusions With optimization, this new method shows potential to inform about free sugars’ content of individual food products, even those closely related, and could be used for monitoring at the product level. Funding Sources No funding has been received from external sources for this study.
We previously reported that Angeli's salt (AS) simultaneously increases cardiac contractility and coronary flow (CF) in normal rat hearts. In this study, we tested the hypothesis that the cardiac contractile and vasodilator actions of AS will be preserved after myocardial ischaemia‐reperfusion (I/R). Isolated hearts from male rats were Langendorff‐perfused for 90 min (sham) or subjected to 30 min equilibration followed by 30 min global ischaemia and 30 min reperfusion. Haemodynamic responses to AS (1 nmol ‐ 10 μmol), the nitric oxide donor, diethylamine NONOate (DEA/NO, 1 nmol – 1 μmol) and the clinically used inotrope for heart failure, dobutamine (DOB, 0.1 nmol – 0.1 μmol) were determined. I/R reduced the cardiac contractile action of AS [change (Δ) in left ventricular (LV) +dP/dt (% baseline) by 10 μmol: sham 77 ± 13%, I/R‐treated hearts 17 ± 5%, p<0.0001] however, I/R had no effect on the AS‐induced increase in heart rate (HR) [Δ HR (% baseline) by 10 μmol: sham 11 ± 3%, I/R‐treated hearts 14 ± 6%] or CF [Δ CF (% baseline) by 1 μmol: sham 72 ± 13%, I/R‐treated hearts 76 ± 15%]. In contrast, the DEA/NO‐induced vasodilatation was reduced by I/R [Δ CF (% baseline) by 1 μmol: sham 78 ± 12%, I/R‐treated hearts 37 ± 8%, p<0.05]. I/R also significantly reduced the DOB‐induced increase in contractility [Δ LV+dP/dt (% baseline) by 10 nmol: sham 71 ± 13%, I/R‐treated hearts 22 ± 4%, p<0.0001] while I/R aggravated DOB‐induced tachycardia [Δ HR (% baseline) by 0.1 μmol: sham 11 ± 4%, I/R‐treated hearts 36 ± 8%, p<0.01], which increases the risk of arrhythmias. These data suggest that AS has superior coronary vasodilator capacity after I/R.
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