Comparison of Cod-Liver Oil and Aspirin-Dipyridamole for the Prevention of Intimal Hyperplasia in Autologous Vein Grafts

Landymore, R.W.; Macaulay, Malcolm; Sheridan, B.; Cameron, C.

doi:10.1016/s0003-4975(10)64496-7

Cited by 54 publications

(14 citation statements)

References 13 publications

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“…Administration of dipyridamole to cholesterol-fed dogs with autologous vein-to-artery grafts significantly reduced the intimal thickening measured 6 weeks later. 192 There was no effect on the plasma concentrations of the major metabolites of thromboxane A 2 and prostacyclin. Dipyridamole treatment significantly reduced the accumulation of smooth muscle cells in the intimas of rabbit ear arteries subjected to repeated mechanical injury, as did the structurally related compound AH-P719.…”

Section: Drugs That Modify Vascular Smooth Muscle Cell Proliferation mentioning

confidence: 91%

Pharmacology of smooth muscle cell replication.

1992

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The suggestion that smooth muscle cell proliferation contributes to hypertension, atherosclerosis, and restenosis after angioplasty has led to a growing interest in the use of drugs to inhibit this process. This review summarizes pharmacological studies of smooth muscle cell proliferation in vitro and in vivo and identifies specific mediators of proliferation that are implicated by drugs binding with high affinity to enzymes or receptors. (Hypertension 1992^0:713-736) KEY WORDS • atherosclerosis • growth substances • hypertension, essential • muscle, smooth, vascular T his review emphasizes agents that influence smooth muscle proliferation. Four overlapping categories of agents that could be discussed are growth factors, drugs with known pharmacological effects, endocrine hormones with growth regulatory properties, and intracellular mediators of replication. This review will concentrate on the last three categories. A great deal has already been written in other reviews about the growth factors, but the much longer list of possible targets discussed here has not been reviewed systematically. Moreover, a great deal is known about the pharmacology of some of the molecules in our review, so their therapeutic value in the treatment of conditions arising from smooth muscle replication is likely to be realized more quickly in a clinical sense than treatments based on the still very poorly understood pharmacology of growth factors. Pathology of Smooth Muscle ProliferationSmooth muscle proliferation has been implicated as playing a central role in atherosclerosis and hypertension.1 The evidence that smooth muscle cell proliferation occurs in these diseases is clear. As we will briefly review, however, evidence for a causal connection is not well established. Smooth Muscle Replication in HypertensionThe argument for a role of smooth muscle cell replication in hypertension is an outgrowth of the structural hypothesis of hypertension proposed by Folkow.2 Folkow explained that the ability of a resistance artery to restrict blood flow depends on the thickness of the vessel wall as well as on the size of the vessel lumen, the responsiveness of the wall to vasoactive stimuli, and the level of stimulation by vasoconstrictors. Folkow's idea is based on the simple physical fact that a thicker vessel wall will act as an amplifier, so that an equal vasoconstrictor stimulus will produce greater narrowing of the lumen in a hypotensive vessel than in a normotensive vessel. Studies of essential and secondary hypertension have confirmed that hypertensive vessel walls are thickened.3 Indeed, there is evidence that such structural changes precede any elevation in blood pressure,*-5 and, at least for the spontaneously hypertensive rat, wall thickening may depend on the increased sympathetic innervation that develops in the spontaneously hypertensive rat vessel wall within the first month of life. 5 -6 A correlation exists between the development of sympathetic innervation and the development of arterial medial hypertrophy in normotensive...

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Section: Drugs That Modify Vascular Smooth Muscle Cell Proliferation mentioning

confidence: 91%

Pharmacology of smooth muscle cell replication.

1992

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“…Thus long-chain n-3 fatty acids exert effects at many steps involved in the process of atherosclerosis and so they might be expected to decrease or slow this disease. Indeed, including long-chain n-3 PUFAs in the diet has been demonstrated to decrease atherosclerosis in a variety of animal models [69][70][71][72][73][74]. Despite the potential for protection against atherosclerosis, much interest has been focussed on the potent protective effect of n-3 fatty acids towards fatal MI [25,27,46,47], and particularly towards sudden death [28,34,35,47], suggesting that they influence acute events.…”

Section: N-3 Fatty Acids and Lower Cardiovascular Disease Risk: Mechamentioning

confidence: 99%

n–3 Fatty acids and cardiovascular disease: evidence explained and mechanisms explored

2004

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Long chain n-3 PUFAs (polyunsaturated fatty acids) are found in fatty fish and in fish oils. Substantial evidence from epidemiological and case-control studies indicates that consumption of fish, fatty fish and long-chain n-3 PUFAs reduces the risk of cardiovascular mortality. Secondary prevention studies using long-chain n-3 PUFAs in patients post-myocardial infarction have shown a reduction in total and cardiovascular mortality, with an especially potent effect on sudden death. Long-chain n-3 PUFAs have been shown to decrease blood triacylglycerol (triglyceride) concentrations, to decrease production of chemoattractants, growth factors, adhesion molecules, inflammatory eicosanoids and inflammatory cytokines, to lower blood pressure, to increase nitric oxide production, endothelial relaxation and vascular compliance, to decrease thrombosis and cardiac arrhythmias and to increase heart rate variability. These mechanisms most likely explain the primary and secondary cardiovascular protection afforded by long-chain n-3 PUFA consumption. A recent study suggests that long-chain n-3 PUFAs might also act to stabilize advanced atherosclerotic plaques, perhaps through their anti-inflammatory effects. As a result of the robust evidence in their favour, a number of recommendations to increase intake of long-chain n-3 PUFAs have been made.

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“…45 Other factors believed to be involved in the pathogenesis of atherosclerosis also appear to be affected by (0-3 fatty acids. These include the inhibition of intimal hyperplasia in canine autologous vein grafts, 6 -7 decreased endothelial cell production of a platelet-derived growth factor-like protein, 8 increased activity of endothelium-derived relaxing factor, and a potential reduction in the intensity of the inflammatory response. 1011 Furthermore, fish oil has prevented the development of experimental atherosclerosis in pigs and rhesus monkeys.…”

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Dietary eicosapentaenoic acid and docosahexaenoic acid from fish oil. Their incorporation into advanced human atherosclerotic plaques.

Rapp

Connor

Lin

et al. 1991

Arterioscler Thromb

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The incorporation of fatty acids from dietary fish oil was measured in obstructive atherosclerotic plaques removed from 11 patients fed fish oil, rich in &>-3 fatty acids, for 6-120 days before a planned arterial endarterectomy. The fatty acids of plasma and atheroma were analyzed with special reference to docosahexaenoic acid (DHA, 22:6) and eicosapentaenoic acid (EPA, 20:5), the principal &>-3 fatty acids offish oil. The o>-3 fatty acid content increased greatly in plasma from 0.9% of fatty acids to 14.8% in cholesteryl esters, from 3.8% to 22.1% in phospholipids, and from 1.3% to 21.9% in triglycerides. The to-3 fatty acid content of the atherosclerotic plaques was also greater when compared with that of plaques removed from 18 non-fish oil-fed controls. The &>-3 fatty acid in cholesteryl esters of the plaques was 4.9% in the experimental group versus 1.4% in control plaque, in phospholipids it was 8.8% versus 1.8%, and in triglycerides it was 4.7% versus 0.7% (p<0.001 for each lipid class). The two major co-3 fatty acids (DHA and EPA) behaved differently. Compared with their respective plasma levels, relatively more DHA than EPA was deposited into the plaques. Whereas the increase of eo-3 fatty acids in plasma reached a plateau 3 weeks after initiation of fish oil feeding, a linear increase in plaque to-3 fatty acids continued with time. As a result of the changes in fatty acid composition, the lipid classes of both plasma and plaque had a higher unsaturation index in the fish oil-fed group. Our data demonstrate that dietary to-3 fatty acids are readily incorporated into advanced human atherosclerotic plaques. Changes in the fatty acids of plasma lipids are reflected in substantial changes in the plaque fatty acid content over a relatively short time. Because

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Comparison of Cod-Liver Oil and Aspirin-Dipyridamole for the Prevention of Intimal Hyperplasia in Autologous Vein Grafts

Cited by 54 publications

References 13 publications

Pharmacology of smooth muscle cell replication.

Pharmacology of smooth muscle cell replication.

n–3 Fatty acids and cardiovascular disease: evidence explained and mechanisms explored

Dietary eicosapentaenoic acid and docosahexaenoic acid from fish oil. Their incorporation into advanced human atherosclerotic plaques.

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