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Biomedical subjects

J P Chin

Publications and source records attributed to J P Chin.

10 recordsLinked to original sources
PubMed1995

How do fish oils affect vascular function?

1. This is a review on the mechanisms by which fish oils affect vascular function and how such changes contribute to their documented cardioprotective effects. 2. Evidence that fish oils depress vascular responses to contractile agents will be examined. It is concluded that this effect of fish oils is mediated predominantly by alterations in prostanoid profile. 3. Effects of fish oils on arterial relaxation are discussed with particular emphasis on endothelium dependent relaxation. It is suggested that the functional impairment of endothelium dependent relaxation documented in a number of cardiovascular disease states can be reversed by dietary fish oils. 4. In addition, possible effects of fish oils on growth factors, inositol trisphosphate and lipid metabolism, the sympathetic nervous system, rheological and membrane properties and inducible nitric oxide are reviewed.

Acetylcholine↗
PubMed1994

Measurement of human sympathetic nervous responses to stressors by microneurography.

Human sympathetic nervous responses have been extensively studied using various stressors; however, there have been few comparisons of the patterns of sympathetic nervous activation which may be produced by different stressors. The purpose of this study was to explore whether different stressors produce differing degrees of sympathetic activation in muscle vasoconstrictor nerve fibres.

Adult↗
PubMed1994

HBPRCA Astra Award. Therapeutic restoration of endothelial function in hypercholesterolaemic subjects: effect of fish oils.

1. Endothelial dysfunction, evidenced as an impaired response to acetylcholine, is well documented in hypercholesterolaemic subjects. We examined the ability of dietary supplementation with fish oils to restore endothelial function in forearm resistance vessels in these patients and compared this with restoration by lipid-lowering therapy. 2. Responses of forearm blood flow to acetylcholine (4.6, 9.25, 18.5 and 37 micrograms/min) and sodium nitroprusside (200, 400, 800 and 1600 ng/min) were obtained using forearm venous occlusion plethysmography in nine hypercholesterolaemic and seven age-matched control subjects. The dose-response curve to acetylcholine was significantly blunted in hypercholesterolaemic subjects when compared with controls (P < 0.001). Responses to sodium nitroprusside were not different between the two groups (P = 0.37). 3. Lipid-lowering therapy decreased total plasma cholesterol levels by 33% and significantly augmented the responses to acetylcholine (P = 0.001) but not to sodium nitroprusside in the hypercholesterolaemic subjects. 4. Dietary supplementation with fish oils had no effect on either total or low density lipoprotein-cholesterol but significantly augmented the responses to acetylcholine (P = 0.011) in hypercholesterolaemic subjects. Responses to sodium nitroprusside were not altered (P = 0.94). 5. This study shows that endothelium-dependent relaxation is impaired in subjects with high cholesterol levels and that this impairment can be reversed by lowering low density lipoproteins (LDL) cholesterol levels. In addition, we demonstrate that restoration of endothelial function can occur without changes in LDL levels, by dietary supplementation with fish oils.

Acetylcholine↗
PubMed1994

Effects of dietary marine oil supplementation on reactivity of human buttock subcutaneous arteries and forearm veins in vitro.

1. The vascular reactivity of resistance arteries isolated from gluteal skin biopsies and veins isolated from forearms of subjects fed marine oils were examined. 2. Twenty seven healthy adult males were randomly allocated to one of two different treatment groups. The first group received maxEPA (eicosapentaenoic acid 0.178 g g-1; docosahexaenoic acid 0.116 g g-1) capsules 10 g per day for 28 days while the second group received an equivalent amount of mixed oil placebo capsules. Biopsies were performed on day 29 (13 for gluteal sections; 14 for forearm vein biopsies). Subcutaneous arteries and veins were mounted in myographs and standard organ baths, respectively. 3. The internal diameter of the subcutaneous arteries at a calculated transmural pressure of 100 mmHg averaged 183.7 +/- 10.3 microns in the maxEPA group and 182.6 +/- 19.8 microns in the placebo controls. Arteries from subjects on maxEPA demonstrated increased sensitivity to angiotensin II (maxEPA vs placebo: -log EC50 (M) -8.36 +/- 0.18 vs -7.91 +/- 0.14) but not to noradrenaline or 5-hydroxytryptamine. Concentration-response curves to acetylcholine, substance P and sodium nitroprusside obtained for noradrenaline precontracted vessels were unaltered with marine oil treatment as was the concentration-response curve to calcium in K(+)-depolarized vessels. 4. Vein internal diameter at a calculated transmural pressure of 20 mmHg averaged 3.06 +/- 0.23 mm in the maxEPA group and 2.96 +/- 0.89 in the placebo group. Responses to noradrenaline, 5-hydroxytryptamine, angiotensin II and endothelin-1 were obtained in the absence and presence of indomethacin (1 microM) in veins from both maxEPA and placebo-treated subjects. Neither dietary supplementation with marine oils nor indomethacin had any effect on the responses obtained to these agonists.5. The major finding of the present study was that in general, maxEPA supplementation did not affect responses to various vasoactive substances on isolated subcutaneous arteries or forearm veins. An exception was the observation of an enhanced response to angiotensin II in subcutaneous resistance arteries studied in vitro. This effect was selective for angiotensin II and was not apparent in veins isolated from the forearm.

Adolescent↗
PubMed1993

Marine oils dose-dependently inhibit vasoconstriction of forearm resistance vessels in humans.

The effects of dietary supplementation with marine oils on vascular reactivity in human forearm resistance arteries were studied. Healthy male adults (six to nine subjects per group) were given either maxEPA capsules (content: eicosapentaenoic acid, 0.178 g/g; docosahexaenoic acid, 0.116 g/g) at doses of 20, 10, or 5 g/day or placebo capsules at 20 g/day for 28 days. Capsule compliance was confirmed by measurement of platelet membrane incorporation of n-3 fatty acids. Blood pressure was not affected by either maxEPA or placebo. The influence of treatment interventions on forearm vasoconstrictive responses to local infusions of angiotensin II and norepinephrine was examined using venous occlusion plethysmography before and after treatment. Responses to both agonists were significantly suppressed by 20 g/day maxEPA (slopes before and after maxEPA, respectively: angiotensin II, 3.34 and 0.89; norepinephrine, 0.91 and 0.41). When analyzed as difference in area under the dose-response curves, the suppressive effects of maxEPA were clearly dose dependent (angiotensin II: 20 g area reduced by 72%, 10 g by 67%, 5 g by 33%). Similarly, responses to norepinephrine were dose-dependently suppressed by maxEPA (20 g area reduced by 61%, 10 g by 63%, and 5 g by 33%). Placebo had no effect on the responses to either constrictor. The responses to both agonists returned to preoil levels after 2 months' discontinuation of 20 g/day maxEPA. We conclude that the suppressive effects of marine oils on vascular reactivity may, in part, contribute to their cardioprotective influence in humans.

Adolescent↗
PubMed1993

Indomethacin inhibits the effects of dietary supplementation with marine oils on vasoconstriction of human forearm resistance vessels in vivo.

OBJECTIVE: Dietary supplementation with marine oils attenuates the responses to noradrenaline and angiotensin II in human forearm resistance arteries. The mechanisms underlying these effects were the subject of the present study. METHODS: Twenty-two normal male adults were allocated to one of three groups. The first group (n = 11) received 10 g/day marine oil capsules (maxEPA) for 28 days. The second group (n = 7) received maxEPA plus 25 mg indomethacin three times a day on days 28 and 29. The third group (n = 4) received 10 g/day mixed-oil placebo capsules for 28 days, plus indomethacin on days 28 and 29 as in group 2. Forearm venous occlusion plethysmography was performed before and immediately after each treatment period. RESULTS: Responses to acetylcholine, sodium nitroprusside or reactive hyperaemia (area under the time-response curve: pre-maxEPA 14,850 +/- 3502, post-maxEPA 17,118 +/- 4576 units) were unaffected by maxEPA. The suppressive effect of maxEPA on responses to noradrenaline and angiotensin II (from group 1) was no longer apparent in the group receiving indomethacin in addition to maxEPA. Indomethacin, in subjects on placebo capsules, had no effect on the responses to either agonist. CONCLUSION: We conclude that the suppressive effects of maxEPA result from alterations to in vivo prostanoid profiles.

Adolescent↗
PubMed1992

Classification of the beta-adrenoceptor subtype in the rat portal vein: effect of altered thyroid hormone levels.

The potencies of the beta 1-adrenoceptor agonist, noradrenaline, and the beta 2-adrenoceptor agonist, fenoterol, at beta-adrenoceptors in portal vein were examined using preparations isolated from control, methimazole-treated or l-thyroxine-treated rats. Tissues were preincubated with phenoxybenzamine (1 mumol/l) to block alpha-adrenoceptors and neuronal and extraneuronal uptake. Fenoterol was approximately 400 times more potent than noradrenaline (-log IC50 7.85 vs. 5.26) in inhibiting the spontaneous contractions of the portal vein. The beta 2-adrenoceptor antagonist, ICI 118,551, was approximately 3000 fold more potent than the beta 1-adrenoceptor antagonist, atenolol, in blocking the effects of fenoterol (pA2 9.32 and 5.88 respectively) and 400 times more potent in antagonising noradrenaline (pA2 8.96 vs. 6.23). Treatment of rats with methimazole led to decreased myogenic tone, and treatment with thyroxine to increased tone. beta-Adrenoceptor binding densities and the relative potencies of the agonists and antagonists used were unaffected by methimazole treatment. Thyroxine administration was also without effect on the relative potencies of these compounds. Our data indicate that although the portal vein is a target tissue for thyroxine, as indicated by its influence on myogenic tone, the beta-adrenoceptor population in this preparation, confirmed to be of the beta 2-subtype, is unaffected.

Adrenergic beta-Antagonists↗
PubMed1990

Effect of long-term administration of testosterone oenanthate on sympathetic neurotransmission to rat isolated seminal vesicles.

1. The effects of prolonged administration of testosterone oenanthate (TE) on sympathetic neurotransmission to the rat isolated seminal vesicle were examined. 2. TE was administered at either 1.2 or 2.4 mg/kg subcutaneously (s.c.) thrice weekly for 8 weeks. A separate group of rats was administered the vehicle, sesame oil, 0.5 mL/kg, s.c. at the same regime and used as controls. TE administration increased plasma testosterone and dihydrotestosterone levels and seminal vesicle weights. TE 2.4 mg/kg suppressed fertility in male rats. 3. The mean -log EC50 values of adrenalin and noradrenaline in seminal vesicles from the control group were 5.30 (95% confidence limits: 5.14, 5.58; d.f. = 14) and 4.92 (95% confidence limits: 4.56, 5.49; d.f. = 14) respectively. Neither of these estimates were modified by TE administration. 4. The mean noradrenaline content (microgram/tissue) in seminal vesicles from control rats was 0.88 +/- 0.09 microgram/tissue. This did not change with TE treatment. Tissue noradrenaline concentration (microgram/g tissue), on the other hand, decreased by more than 50% in preparations from rats treated with TE. This was paralleled by a decrease in the density of catecholamine fluorescence. 5. Mean responses to field stimulation (20 pulses, 60 V dial setting, 2 ms, 1-70 Hz) appeared to decrease in preparations from TE treated groups; this decrease was, however, not statistically significant (P greater than 0.05; d.f. = 15). 6. It is concluded that prolonged administration of testosterone oenanthate to rats, at doses sufficient to suppress fertility, decreases the density of sympathetic innervation to the seminal vesicle by increasing smooth muscle mass. Treatment does not, however, modify the responses of this preparation to exogenously added catecholamines.

Animals↗