Knut Pettersson

Anti-atherogenic effect of coenzyme Q10 in apolipoprotein E gene knockout mice.

Oxidation of low-density lipoprotein (LDL) lipid is implicated in atherogenesis and certain antioxidants inhibit atherosclerosis. Ubiquinol-10 (CoQ10H2) inhibits LDL lipid peroxidation in vitro although it is not known whether such activity occurs in vivo, and, if so, whether this is anti-atherogenic. We therefore tested the effect of ubiquinone-10 (CoQ10) supplemented at 1% (w/w) on aortic lipoprotein lipid peroxidation and atherosclerosis in apolipoprotein E-deficient (apoE-/-) mice fed a high-fat diet. Hydroperoxides of cholesteryl esters and triacylglycerols (together referred to as LOOH) and their corresponding alcohols were used as the marker for lipoprotein lipid oxidation. Atherosclerosis was assessed by morphometry at the aortic root, proximal and distal arch, and the descending thoracic and abdominal aorta. Compared to controls, CoQ10-treatment increased plasma coenzyme Q, ascorbate, and the CoQ10H2:CoQ10 + CoQ10H2 ratio, decreased plasma alpha-tocopherol (alpha-TOH), and had no effect on cholesterol and cholesterylester alcohols (CE-OH). Plasma from CoQ10-supplemented mice was more resistant to ex vivo lipid peroxidation. CoQ10 treatment increased aortic coenzyme Q and alpha-TOH and decreased the absolute concentration of LOOH, whereas tissue cholesterol, cholesteryl esters, CE-OH, and LOOH expressed per bisallylic hydrogen-containing lipids were not significantly different. CoQ10-treatment significantly decreased lesion size in the aortic root and the ascending and the descending aorta. Together these data show that CoQ10 decreases the absolute concentration of aortic LOOH and atherosclerosis in apoE-/- mice.

Nervous control of the branchial vascular resistance of the Atlantic cod,Gadus morhua

SummaryThe effects on branchial vascular resistance of electrical stimulation of the nervous supply to the gills of the Atlantic cod were studied in constant pressure perfused gill preparations.Stimulation of the right sympathetic chain immediately anterior to the coeliac ganglion produces either a β-adrenoceptor mediated decrease in branchial vascular resistance of the gill arches on the right side, or an α-adrenoceptor mediated increase which is reversed by phentolamine to a β-adrenoceptor mediated decrease in branchial vascular resistance.Stimulation of the entire ‘vago-sympathetic’ nerve trunk to the third isolated gill arch produces an increase in branchial vascular resistance, which in some preparations can be reversed by atropine to a β-adrenoceptor mediated decrease. A second type of constrictory innervation of vagal origin (non-adrenergic, non-cholinergic) may be concluded from the lack of blocking capacity of cholinergic and adrenergic antagonists.It is concluded that the branchial vascular bed of the cod is controlled by both sympathetic (dilatory and sometimes also constrictory) and parasympathetic (constrictory) fibres. The site of action of the nerve supply on the various effectors of the complex vasculature of the gills is not known. An autonomic innervation with its direct, rapid and restricted effects may reinforce the more general effects of circulating vaso-active substances.

Sympathetic nervous control of blood flow in the gills of the Atlantic cod,Gadus morhua

SummaryThe effects of sympathetic nerve stimulation, adrenaline and isoprenaline on the inflow pressure and efferent arterial and venous flow rates were studied in a cod gill preparation perfused at constant flow rate.The dominant effect of adrenaline was a reduced inflow pressure, accompanied by an increase in arterial flow and a decrease in venous flow. Isoprenaline also decreased the inflow pressure, but the changes in both outflow rates were small or absent.Sympathetic nerve stimulation gave arterial and venous flow changes comparable to the adrenaline effects, but the inflow pressure increased during nerve stimulation. Propranolol has little effect on the nerve responses, but phentolamine abolished or reversed the increase in inflow pressure, and also decreased or abolished the changes in outflow rates.The possible sites of action of the sympathetic fibres, and the distribution of adrenoceptors in the effector tissue is discussed. It is concluded that the main effect of sympathetic nerve stimulation is α-adrenoceptor mediated, involving constriction of the arterio-venous pathway. Theβ-adrenoceptor mediated control of total branchial vascular resistance may largely depend on circulating catecholamines.

Drug induced changes in cardio-vascular parameters in the Atlantic cod,Gadus morhua

SummaryVentral (VAP) and dorsal (DAP) aortic blood pressure, heart rate (HR) and cardiac output (n

In vivo administration of the C16:0 fatty acid isoform of sulfatide increases pancreatic sulfatide and enhances glucose-stimulated insulin secretion in Zucker fatty (fa/fa) rats

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Protective effects of probucol in two animal models of atherosclerosis.

n) were recorded simultaneously in unanaesthetized Atlantic cod, and the effects of vasoactive drugs on the cardio-vascular parameters studied. Mean resting values for the parameters were VAP=4,39 kPa, DAP=2,49 kPa, HR=41 beats/min, andn

Adrenergic and cholinergic effects on the heart, the lung and the spleen of the African lungfish, Protopterus aethiopicus

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