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Changes in AP duration (APD) measured to 50% (above left) and 90% repolarization (below left) of epicardial muscle fibers with increasing time after coronary artery occlusion [5] . Mean values±S.D. are shown by columns for the first layer of muscle fibers beneath the epicardial surface in normal noninfarcted preparations (striped columns) and in each group of infarcted preparations (solid columns) studied at the times indicated on the abscissa. Asterisks denote values significantly different from control. At the right are shown representative transmembrane potential recordings; (A) normal; (B) 1 day; (C) 5 days; (D) 2 weeks; (E) 2 months. Note that APs in the 1- and 5-day-old infarcts show loss of the plateau phase during repolarization. Action potential duration is decreased more in 5-day-old than in 1-day-old infarcts. Reproduced from [5] .

Fig. 1
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Changes in AP duration (APD) measured to 50% (above left) and 90% repolarization (below left) of epicardial muscle fibers with increasing time after coronary artery occlusion [5] . Mean values±S.D. are shown by columns for the first layer of muscle fibers beneath the epicardial surface in normal noninfarcted preparations (striped columns) and in each group of infarcted preparations (solid columns) studied at the times indicated on the abscissa. Asterisks denote values significantly different from control. At the right are shown representative transmembrane potential recordings; (A) normal; (B) 1 day; (C) 5 days; (D) 2 weeks; (E) 2 months. Note that APs in the 1- and 5-day-old infarcts show loss of the plateau phase during repolarization. Action potential duration is decreased more in 5-day-old than in 1-day-old infarcts. Reproduced from [5] .

The origin of the delayed phase of spontaneous arrhythmias secondary to coronary artery occlusion in canine and porcine hearts is most likely in the depolarized and abnormally automatic subendocardial Purkinje fibers that survive. The loss of resting potential is significant and dramatic in the multicellular preparations of these fibers. Concomitant with this dramatic loss is a reduction in intracellular K + ion concentration ( a K i ). However, a decrease in K + equilibrium potential ( E K ) (average change 16 mV) cannot fully account for the loss in resting potential (average change 35 mV) [6] .

Abnormalities in the resting potentials of subendocardial Purkinje fibers surviving in the infarcted heart persist even after they are enzymatically disaggregated and studied as single myocytes [7] . In the myocyte, a reduction in a K i could not provide the basis for the reduced resting potential. Rather, Purkinje myocytes isolated from the infarcted myocardium show an increase in the ratio of the membrane permeability of Na + to K + ions ( P Na / P K ) as compared to control. The larger value of P Na / P K in these cells could be due to an increase in P Na or a decrease in P K or both. Input resistance measurements suggest that the subendocardial Purkinje myocytes from the infarcted myocardium have higher input resistances than control cells. This is in agreement with a multicellular study on these fiber bundles [8] . Combined with the P Na / P K measurements in the myocytes, it is likely that there is a net decrease in P K in the cells with reduced resting potentials. Finally, this is consistent with a decrease in the density of both the outward K + current and inward rectifying K + current, I K1 , recently described for the Purkinje myocytes surviving in the 48-h infarcted heart [9] .

Because two double carbon bonds in an 18-carbon fatty acid were so effective, then what about fatty acids with five or six double bonds in 20- or 22-carbon atoms? What about shifting the series of double bonds from omega-6 to omega-3? Unfortunately, neither more carbons, more double bonds, nor the omega-3 isomer improve blood cholesterol reduction. In fact, eicosapentaenoic acid (EPA) (20 carbons, 5 double bonds, omega-3) or docosahexaenoic acid (DHA)(22 carbons, 6 double bonds, omega-3), found in fish oils, given in doses less than 6 g/d (equivalent to 12–20 1-g fish oil capsules per day) increase low-density lipoprotein (LDL) cholesterol levels ( 3 , 4 ). When large amounts of fish oil (containing 24 g of omega-3 fatty acid per day) replace saturated fat, lower LDL cholesterol levels are observed, similar to the effects of vegetable oil ( 5 ). In contrast, EPA and DHA are much more potent than linoleic acid for lowering plasma triglycerides ( 6 ). The molecular mechanisms mediating these effects of PUFAs on serum cholesterol and CVD are still not fully understood. Thus, linoleic acid remains the most effective PUFA for lowering serum cholesterol and the fatty acid most well established to prevent CVD.

Readers may find themselves surprised at this last statement in view of the dominance of the omega-3 PUFA theory in basic and clinical research. In the early 1980s, two lines of evidence coalesced to engender widespread excitement on the potentially cardioprotective effects of omega-3 fatty acids, particularly those from fish oil (EPA and DHA). Populations eating large amounts of fatty fish had low rates of CVD, and in many epidemiological studies, n-3 PUFA intake or blood levels are inversely related to CVD ( 7 ). Omega-3 fatty acids are metabolized to prostaglandins and leukotrienes that are antithrombotic, antiinflammatory, and vasodilating.

The omega-3-cyclooxygenase-lipoxygenase paradigm came to include a negative view of omega-6 PUFA ( 8 ). The theory considered the fact that dietary linoleic acid can be metabolized to arachidonic acid that can be metabolized further to prostaglandins and leukotrienes that are relatively prothrombotic, proinflammatory, and vasoconstricting. Also, n-6 PUFAs may reduce by competition for cyclooxygenase the formation of antiinflammatory mediators from n-3 PUFAs. Carried to its extreme, the theory called for the ideal fatty acid balance to be high in omega-3 and low in omega-6, producing a high omega-3 to omega-6 ratio. This vision was restricted because it did not recognize the known benefits of linoleic acid on LDL cholesterol and CVD.

The established benefits of omega-6 PUFAs raise the question that if omega-6 PUFAs are capable of being metabolized to undesirable prostaglandins and leukotrienes, why should they protect against CVD? One explanation is that LDL cholesterol is such a dominant force in atherosclerosis, effects on prostanoids are not completely offsetting. Another explanation is that omega-6 dietary PUFAs ordinarily in vivo may be minimally involved in cyclooxygenase reactions and do not stimulate appreciably the production of vasoactive and prothrombotic molecules. A third explanation is that omega-6 PUFAs operate in antiinflammatory metabolic pathways that do not involve cyclooxygenase, and that these pathways have a protective influence on CVD.

It is true that LSMPAs are presently not fully ecologically representative or well connected at the global scale. Nor, on their own, are they likely to provide enough protection to highly mobile species, although they could offer substantial benefits to more resident elements of populations (e.g., White et al. 2017 ). Even if considered with all existing smaller MPAs, these broader goals would still not be met because of our current inability to protect and represent species and habitats in areas beyond national jurisdiction, including the deep-sea and pelagic realms. However, we are only at the start of the process for developing effective large-scale ocean management, and it takes time to enact ambition. In addition, although LSMPAs offer rapid progress toward meeting global targets, a fully representative global MPA network cannot be constructed by protecting only 10% of the seas. To reach goals of ecological representation and connectivity, it will be necessary to increase coverage ambition and extend protection beyond EEZs (O’Leary et al. 2016 ). Moreover, the 10% coverage target does not differentiate between the level of protection afforded to different MPAs despite this being a key driver of ecological benefits (Edgar et al. 2014 ). Expanding the coverage of strongly or fully protected MPAs across all seascapes must therefore also be an aspiration. Finally, strong fisheries management outside of protected areas is required to support LSMPAs, and likewise, well-managed LSMPAs can help reinforce the goals of managers in fishing zones (Ban et al. 2017 ).

The crux of this criticism is that conservation close to population centers suffers because of protection given to remote areas. However, eight nations, including small island developing states, have made or are in the process of making critically important contributions to local domestic conservation via the establishment of ambitious LSMPAs (figure 4 b). Nations such as Palau and Kiribati, for example, have established LSMPAs in their coastal waters that are approximately 500 and 1000 times larger, respectively, than their own land masses. Although 17 of the 35 LSMPAs we identified are in the remote waters of seven countries (table 2 ; figure 4 b), marine conservation efforts began in their local domestic waters and are ongoing there (table 2 ). LSMPAs are complementary to those efforts, not substitutes. It is often the case, however, that MPAs in local domestic waters are subject to much weaker protection than those in distant waters. For example, the United Kingdom currently has strongly or fully protected approximately 1,495,000 km 2 in its overseas territories but only 7.5 km 2 (less than 0.001%) within the EEZ of the British Isles. Likewise, the United States has less than 1% of seas in continental US waters under strong or full protection compared with approximately 43% (approximately 2.6 million km 2 ) of remote waters. Similarly, Chile has protected less than 1% of their mainland EEZ in strongly or fully protected MPAs versus 27% (approximately 450,000 km 2 ) of their EEZ around remote oceanic islands. Given the contingency of beneficial outcomes on high-level protection (Edgar et al. 2014 ), local domestic waters of these countries clearly need much stronger protection. Nonetheless, lessons regarding MPA effectiveness must also be applied to LSMPAs. Currently, 47.9% of the area within designated LSMPAs (7,991,520 km 2 out of 16,670,988 km 2 ) is strongly or fully protected (table S1). However, this falls to 19.8% for promised LSMPAs (1,609,641 km 2 out of 8,137,596 km 2 ; table S1). To ensure that LSMPAs deliver anticipated benefits, adequate levels of protection will be key.

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