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Biomedical subjects

S J Hutchison

Publications and source records attributed to S J Hutchison.

At least 19 recordsLinked to original sources
PubMed1997

Testosterone worsens endothelial dysfunction associated with hypercholesterolemia and environmental tobacco smoke exposure in male rabbit aorta.

OBJECTIVES: To assess the effects of interaction of sex hormones, hypercholesterolemia (HC) and environmental tobacco smoke (ETS) exposure on endothelium-dependent relaxation, we examined vascular reactivity in vitro in an animal model of atherogenesis. BACKGROUND: Animal and human studies indicate the presence of interactions between classic coronary artery disease risk factors and endothelium-dependent relaxation. Sex hormones have also been shown to influence release of endothelium-derived relaxing factor. METHODS: New Zealand White rabbits were randomized to receive either an HC diet (n = 8) or ETS exposure plus HC diet (n = 8). Eight rabbits receiving a normal diet, without exposure to ETS, served as the control group. The HC diet consisted of 3% soybean oil and 0.3% cholesterol by weight over 13 weeks. The source of ETS was sidestream smoke of 4 cigarettes/15 min, 6 h/day, 5 days/week over 10 weeks in a smoking chamber. Rabbits were killed, and fresh aortic rings were harvested and maintained in oxygenated Krebs solution in an organ bath at 37 degrees C. Rings were precontracted with norepinephrine and exposed to acetylcholine in increasing doses, and isometric tension was recorded. Rings were also exposed to physiologic concentrations (1 nmol/liter) of either 17-beta-estradiol, testosterone or progesterone before pre-contraction with norepinephrine and relaxation with acetylcholine. Endothelium-independent relaxation was studied using nitroglycerin. The surface area of the ring covered by lipids was measured by Sudan IV staining. RESULTS: HC and ETS significantly reduced endothelium-dependent relaxation (p = 0.01 and p < 0.0005, respectively) and caused atherogenesis (p < 0.0005 and p = 0.047, respectively) but did not affect endothelium-independent relaxation. Incubation with estradiol and estradiol plus progesterone did not influence endothelium-dependent relaxation. Testosterone reduced endothelium-dependent relaxation (p = 0.049) and augmented the endothelial dysfunction associated with ETS exposure and HC (p = 0.03). CONCLUSIONS: Both HC and ETS are atherogenic and impair endothelial function but do not affect endothelium-independent relaxation. Physiologic levels of estradiol and estradiol plus progesterone do not affect endothelium-dependent relaxation. Physiologic levels of testosterone impair relaxation and augment the endothelial dysfunction associated with ETS exposure and HC.

Animals↗
PubMed1997

Everest nails.

Explore the source record for details and available documents.

Adult↗
PubMed1997

Determination of coronary flow measurements by transesophageal echocardiography: dependence of flow velocity reserve on the location of stenosis.

Doppler velocimetry with the use of transesophageal echocardiography can record flow in the proximal left anterior descending artery (LAD). To assess whether this limited sampling ability influences the recording of velocity and the calculation of coronary flow reserve (CFR), 32 patients with LAD stenosis (4 ostial stenoses, 18 proximal stenoses, 10 mid-LAD stenoses) and 33 patients with arteriographically normal LADs were studied. Basal flow and dipyridamole-induced hyperemic flow rates were recorded. The mean basal flow velocity in ostial stenoses was greater than in other groups, and the mean basal flow velocity in proximal stenoses was less than that in mid-LAD stenoses and in the normal group. Maximal hyperemic velocity did not differ between the groups. CFR in all stenoses groups was less than that in the normal group. Ostial CFR was less than in all other groups, and proximal CFR was less than that in either the mid-LAD or the normal LAD groups. With this technique, coronary flow velocimetry and estimation of CFR is affected by the location of stenosis.

Aged↗
PubMed1997

Chronic dietary L-arginine prevents endothelial dysfunction secondary to environmental tobacco smoke in normocholesterolemic rabbits.

Our goal was to determine whether environmental tobacco smoke causes endothelial dysfunction in the absence of hypercholesterolemia and whether such an effect can be prevented by supplementation with L-arginine. Environmental tobacco smoke exposure is associated with an increase in coronary artery disease events and mortality. We have previously demonstrated that environmental tobacco smoke causes endothelial dysfunction and atherosclerosis in rabbits with diet-induced hypercholesterolemia and atherosclerosis and that chronic dietary L-arginine supplementation prevents this. The effects of L-arginine supplementation (2.25% solution ad libitum) and environmental tobacco smoke (smoking chambers for 10 weeks) were examined with a 2 x 2 design in 32 rabbits fed a normal diet. Acetylcholine, calcium ionophore A23187, and nitroglycerin-induced vasorelaxation were assessed in aortic rings precontracted with phenylephrine. Endothelial L-arginine levels were measured by chromatography. Chronic L-arginine supplementation increased serum (P < .001) and endothelial (P = .003) L-arginine levels. Environmental tobacco smoke reduced endothelium-dependent acetylcholine-induced relaxation, and L-arginine blocked this adverse effect (P = .04). Environmental tobacco smoke tended to increase phenylephrine-induced contraction (P = .06). Neither environmental tobacco smoke nor L-arginine influenced A23187-induced relaxation nor endothelium-independent nitroglycerin-induced relaxation. Endothelial dysfunction secondary to environmental tobacco smoke may occur in the absence of diet-induced hypercholesterolemia and atherosclerosis. Chronic dietary supplementation with a nitric oxide donor such as L-arginine offsets the endothelial dysfunction associated with environmental tobacco smoke in normocholesterolemic rabbits, possibly through substrate loading of the nitric oxide pathway.

Animals↗
PubMed1996

Testosterone induces dilation of canine coronary conductance and resistance arteries in vivo.

BACKGROUND: Although estrogens have been shown to be vasoactive hormones, the vascular effects of testosterone are not well defined. Like estrogen, testosterone causes relaxation of isolated rabbit coronary arterial segments. We examined the vasodilator effects of testosterone in vivo in the coronary circulation and the potential mechanisms of its actions. METHODS AND RESULTS: Using simultaneous intravascular two-dimensional and Doppler ultrasound, we examined the effect of intracoronary testosterone in coronary conductance and resistance arteries in 10 anesthetized dogs (5 male, 5 female). We also assessed the contribution of NO, prostaglandins, ATP-sensitive K+ channels, and classic estrogen receptors to testosterone-induced vasodilation. Testosterone induced a significant increase in cross-sectional area, average coronary peak flow velocity, and calculated volumetric coronary blood flow at the 0.1 and 1 mumol/L concentrations. This effect was independent of sex. Pretreatment with N omega-nitro-L-arginine methyl ester to block NO synthesis decreased testosterone-induced increase in cross-sectional area, average coronary peak flow velocity, and coronary blood flow. Pretreatment with glybenclamide to assess the role of ATP-sensitive K+ channels did not influence testosterone-induced dilation in epicardial arteries but did attenuate its effect in the microcirculation. Pretreatment with indomethacin or the classic estrogen-receptor antagonist ICI 182,780 did not alter testosterone-induced changes. CONCLUSIONS: Short-term administration of testosterone induces a sex-independent vasodilation in coronary conductance and resistance arteries in vivo. Acute testosterone-induced coronary vasodilation of epicardial and resistance vessels is mediated in part by endothelium-derived NO. ATP-sensitive K+ channels appear to play a role in the vasodilatory effect of testosterone in resistance arteries.

Animals↗
PubMed1996

Coronary vasodilation induced by angiotensin-converting enzyme inhibition in vivo: differential contribution of nitric oxide and bradykinin in conductance and resistance arteries.

BACKGROUND: We studied in coronary conductance and resistance arteries the coronary vasodilator effects of the angiotensin-converting enzyme inhibitor ramiprilat and the contribution of nitric oxide, bradykinin, and prostaglandins to this vasodilation. METHODS AND RESEARCH: In seven anesthetized dogs, a Doppler guidewire was placed in the circumflex coronary artery to measure coronary flow velocity, and an ultrasound imaging catheter was introduced over the Doppler wire to measure coronary cross-sectional area. Drugs were infused directly into the left main coronary artery to minimize systemic effects. Ramiprilat increased both epicardial cross-sectional area and coronary blood flow velocity, resulting in an increase in absolute coronary blood flow. Pretreatment with N omega-nitro-L-arginine methyl ester (100 micromol/L intracoronary) to block nitric oxide synthase attenuated ramiprilat-induced increase in epicardial coronary cross-sectional area (P<.05) but not in coronary flow velocity or coronary blood flow. In contrast, pretreatment with the selective bradykinin antagonist HOE 140 (10 micromol/L) attenuated ramiprilat-induced increase in flow velocity (P<.025) and coronary blood flow (P<.05) but not epicardial coronary cross-sectional area. Pretreatment with indomethacin (5 mg/kg body wt IV) did not alter ramiprilat-induced increase in epicardial cross-sectional area, nor did it significantly influence coronary blood flow. CONCLUSIONS: Other than decreasing angiotensin II production, acute ramiprilat-induced vasodilation in canine coronary conductance arteries is mediated in part by nitric oxide. Ramiprilat-induced vasodilation in resistance arteries is in part mediated by the action of bradykinin.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1995

Morphological characteristics of the regurgitant rheumatic mitral valve.

Reparative surgery for valvular insufficiency is attempted frequently. The success of surgery depends partly on the underlying etiology. To establish the morphological characteristics of rheumatic mitral valve disease (insufficiency) (n = 12), mitral insufficiency due to infective endocarditis (n = 12), mitral insufficiency postinfarction (n = 6), rheumatic (predominant) mitral insufficiency postinfarction (n = 6), rheumatic (predominant) mitral stenosis (n = 12) and normal patients (n = 12) were examined retrospectively. In the groups of patients with mitral insufficiency< the mobility of the posterior leaflet tip (change in angle from the annular plane) was significantly less than normal 48 +/- 9 degrees only in the rheumatic group (12 +/- 7 degrees, P < 0.01). The posterior mitral leaflet tip had greater than normal mobility in the other mitral insufficiency groups: infective endocarditis 53 +/- 15 degrees (P = 0.35 versus normals), postinfarction 63 +/- 11 degrees (P = 0.02 versus normals), myxomatous 63 +/- 19 degrees (P = 0.03 versus normals). The mobility of the posterior mitral leaflet tip was also significantly less than normal in the rheumatic mitral stenosis group: 16 +/- 7 degrees, P < 0.01 versus normals. In the two rheumatic groups, diastolic doming of the anterior mitral leaflet was seen solely in mitral stenosis. In the predominant regurgitant group, the tip of the anterior mitral leaflet was much more mobile than in the stenosis group. Doming of the anterior mitral leaflet was absent from the predominant regurgitant group (2.1 +/- 0.9 cm, P < 0.001). The stenotic mitral valves domed 0.75 +/- 0.15 cm.(ABSTRACT TRUNCATED AT 250 WORDS)

Echocardiography, Doppler, Color↗
PubMed1994

Endocarditis.

The continuing medical literature attests to the fact that infective endocarditis is a serious and complex disease, which in many populations continues to occur at an incidence of approximately 20 per 100,000, and carries a 5% to 40% mortality, depending on numerous pathogen and patient factors. Clinical investigation continues along several lines, including analysis of the clinical utility of diagnostic imaging, especially the contribution of transthoracic and transesophageal echocardiography (and, conversely, the risk of endocarditis from transesophageal imaging). Epidemiological and cohort descriptive studies give insight into the underlying causes of the disease, and risk factors for poor outcome, from which guidelines for management can be surmised.

Cross Infection↗
PubMed1991

Hyperinsulinaemia and microvascular angina ("syndrome X")

Glucose and insulin responses to a glucose load in 11 patients with angina attributed to microvascular coronary dysfunction were compared with those in 11 healthy subjects matched for age, sex, and body mass. Stimulated hyperinsulinaemia was demonstrated in the microvascular angina group. The findings suggest a role for increased concentrations of insulin in coronary microvascular dysfunction.

Adult↗
PubMed1991

Syndrome X and hyperventilation.

The cardiorespiratory responses to exercise and forced hyperventilation were measured in 17 unselected patients with syndrome X (angina, positive exercise test, normal coronary arteriogram, no other cardiovascular disease) and compared with those in 15 healthy subjects. Forced hyperventilation produced hypocapnia and metabolic alkalosis but no chest pain or electrocardiographic change. Patients with syndrome X showed reduced maximum oxygen consumption with an increased respiratory exchange ratio at peak exercise, confirming that exercise was limited by skeletal muscle perfusion--and thus that the increase in cardiac output with exercise is limited in syndrome X as in heart failure. Arterial carbon dioxide tension (PCO2) homoeostasis during exercise was normal but the ventilatory cost of carbon dioxide excretion was increased in syndrome X (as in heart failure). End tidal PCO2 measurements correlated only poorly with arterial PCO2 in individual patients with syndrome X, providing a possible explanation for previous reports, based on end tidal PCO2 of inappropriate hyperventilation. Patients with syndrome X did not show inappropriate hyperventilation but they did show hyperventilation that was appropriate to maintain normal arterial PCO2 in the face of reduced cardiac reserve.

Adult↗
PubMed1990

Coexistent coronary artery disease and oesophageal spasm: the importance of establishing the source of chest pain.

A 55 year old woman presenting with chest pain was found to have significant triple vessel coronary artery disease. Non-invasive investigations showed that she had a good exercise tolerance without inducible ischaemia. The history was more suggestive of an oesophageal source of pain, an impression supported by manometry. This case illustrates some of the problems encountered during the investigation of chest pain and the need to interpret angiographic findings in the context of the patient's functional state.

Chest Pain↗