ISSN:0009-7322    

出版商:OVID    

年代:1993

数据来源: OVID

ISSN:0009-7322    

出版商:OVID    

年代:1993

数据来源: OVID

ISSN:0009-7322    

出版商:OVID    

年代:1993

数据来源: OVID

ISSN:0009-7322    

出版商:OVID    

年代:1993

数据来源: OVID

摘要:

The nitrovasodilators are a diverse group of pharmacological agents that produce vascular relaxation by releasing nitric oxide. The mechanisms by which these compounds release nitric oxide vary, depending on their chemical structure. Compounds with lower oxidation states of nitrogen such as nitroprusside, nitrosamines, and nitrosothiols release nitric oxide nonenzymatically. In the case of nitroprusside, this involves a one-electron reduction that may occur upon exposure to a variety of reducing agents and tissues such as vascular smooth muscle membranes. In the case of the organic nitrates, which have higher oxidation states of nitrogen, the release of nitric oxide in vascular tissue occurs predominantly by a poorly understood enzymatic process. This interesting property of nitroglycerin is important because it “targets” its effect to vascular tissues that are capable of this enzymatic process. In the case of the coronary circulation, nitroglycerin predominantly dilates the larger coronary arteries while having a minimal effect on coronary resistance vessels <100 μm in diameter. This prevents the development of coronary steal, which is often encountered with agents that produce intense vasodilation of the coronary resistance vessels. In this review, the mechanisms by which the nitrovasodilators (particularly nitroglycerin) release nitric oxide will be considered, and recent studies of nitroglycerin bioconversion in various-sized coronary vessels will be discussed in detail.

ISSN:0009-7322    

出版商:OVID    

年代:1993

数据来源: OVID

摘要:

BackgroundPatients with essential hypertension have abnormal endothelium-dependent vasodilation. Because the endothelium exerts its action on the vascular smooth muscle through the release of several substances, it is important to identify which of these factors is involved in the abnormal response of hypertensive arteries.Methods and ResultsTo investigate the role of endothelium-derived nitric oxide in this abnormality, we studied the vascular effect of the arginine analogue NG-monomethyl-L-arginine, an inhibitor of the endothelial synthesis of nitric oxide, under baseline conditions and during infusion of acetylcholine, an endothelium-dependent vasodilator, and sodium nitroprusside, a direct smooth muscle dilator. The study included 11 hypertensive patients (seven men; age, 46.5+9 years) and 10 normal control subjects (seven men; age, 45.7±7 years). Drugs were infused into the brachial artery, and the response of the forearm vasculature was measured by strain-gauge plethysmography. Basal blood flow was similar in normal control subjects and hypertensive patients (2.97±0.7 versus 2.86±+1.1 mL min-1100 mL-1', respectively). NG-monomethyl-L-arginine produced a significantly greater decrease in blood flow in control subjects than in patients (1.08±0.6 versus 0.32+0.4 mL1, min-1. 100 mL'; p<0.004). The vasodilator response to acetylcholine was reduced in patients compared with control subjects (maximum flow, 8.2±4 versus 16.4±8 mL1min'1100 mW1; p<0.001). NG-monomethyl.L-arginine blunted the vasodilator response to acetylcholine in control subjects (maximum flow decreased from 16.4±8 to 7.01±3 mL min'1100 mL1; p<0.004); however, the arginine analogue did not significantly alter the response to acetylcholine in hypertensive patients (maximum flow, 8.2+4 versus 8.01±5 mL. min1100 mL'1). NG-monomethyl-Larginine did not modify the vasodilator response to sodium nitroprusside in either control subjects or patients.ConclusionsThese findings indicate that patients with essential hypertension have a defect in the endothelium-derived nitric oxide system that may at least partly account for both the increased vascular resistance under basal conditions and the impaired response to endothelium-dependent vasodilators.

ISSN:0009-7322    

出版商:OVID    

年代:1993

数据来源: OVID

摘要:

BackgroundPatients with essential hypertension have a deficit in the endothelium-derived nitric oxide system that results in impaired endothelium-dependent vascular relaxation. The objective of this study was to determine whether this abnormality is caused by a deficiency of substrate for nitric oxide synthesis.Methods and ResultsThe vascular responses to acetylcholine (an endothelium-dependent vasodilator infused at 7.5, 15, and 30 μg/min) and sodium nitroprusside (a direct smooth muscle dilator infused at 0.8, 1.6, and 3.2 μg/min) were studied during combined administration of dextrose 5% or L-arginine (substrate for nitric oxide synthesis infused at 40 μmol/min) in 12 normal control subjects (seven men and five women; age, 49.3+7 years) and 14 hypertensive patients (nine men and five women; age, 48.4±7 years). In addition, the effect of Darginine (stereoisomer of arginine that is not a precursor of nitric oxide) on the vascular responses to acetylcholine was studied in eight normal control subjects and seven hypertensive patients. Drugs were infused into the brachial artery, and the response of the forearm vasculature was measured by strain gauge plethysmography. The vasodilator response to acetylcholine was significantly blunted in hypertensive patients compared with normal control subjects (maximum flow, 8.9±5 versus 15.7±6 mL min-1, 100 mL1, respectively; p <0.007); however, no difference was observed in the response to sodium nitroprusside (11.4±6 and 11.7+mL. min-1. 100 mL-1, respectively). L-Arginine did not significantly change basal blood flow or vascular resistance in either group. In normal control subjects, the infusion of L-arginine significantly augmented the vasodilator response to acetylcholine (maximum flow, 15.7±6 versus 21.4±8 mL. min-1100 mL-1before and after L-arginine, respectively;p<0.001). In contrast, in hypertensive patients, the infusion of L-arginine did not alter the response to acetylcholine (maximum flow, 8.9±5 and 8.4+4 mL min-1.100 mL-1before and after L-arginine, respectively). The administration of L-arginine did not modify the response to sodium nitroprusside in either group. Similarly, the infusion of D-arginine did not alter the response to acetylcholine in either group.ConclusionsIn normal humans, availability of substrate for production of nitric oxide is a rate-limiting step for endothelium-dependent vascular relaxation. In contrast, increased availability of nitric oxide precursor does not modify endothelium-mediated vasodilation in hypertensive patients. These findings provide further evidence of a defect in the endothelium-derived nitric oxide system in hypertension and indicate that this abnormality is not related to decreased availability of substrate for nitric oxide production.

ISSN:0009-7322    

出版商:OVID    

年代:1993

数据来源: OVID

摘要:

BackgroundVarious prospective studies have found that lean hypertensive patients have greater cardiovascular morbidity and mortality than obese hypertensive subjects. It was therefore hypothesized that hypertension is more benign when associated with obesity. In the present study, we evaluated effects of obesity on early target organ damage in patients with essential hypertension.Methods and ResultsIn a total of 207 subjects, systemic and renal hemodynamics as well as left ventricular structure and function were assessed by measuring cardiac output (indocyanine green dye dilution), renal blood flow (clearance of 'l~I paraimmunohippuric acid), and mean arterial pressure (invasively) and by two-dimensionally guided M-mode echocardiographic findings. Systemic and renal vascular resistance, compliance of the large arteries evaluated by the stroke volume/pulse pressure index, and left ventricular mass served as parameters for early target organ damage. All individuals were categorized into four groups: lean and obese normotensive as well as lean and obese hypertensive subjects. In obese hypertensive patients, total peripheral resistance was significantly lower and stroke volume/pulse pressure index was higher than in the lean hypertensive group, almost reaching values of normotensive control subjects. No effect of obesity on the renal circulation was noted, whereas in hypertension, renal vascular resistance was elevated. The degree of left ventricular hypertrophy was more pronounced in the hypertensive groups than in their normotensive counterparts and progressively increased with obesity. Nevertheless, in obese hypertensive patients, left ventricular function, as measured by fractional fiber shortening and velocity of circumferential fiber shortening, was maintained despite the fact that the heart had been exposed to the double burden of an increased preload (obesity) and afterload (hypertension).ConclusionsObesity had a disparate effect on target organs in hypertension. At rest, obesity seemed to mitigate cardiovascular changes in the systemic vascular bed caused by hypertension. However, no such mitigation was observed in the renal vasculature, and left ventricular hypertrophy was even exacerbated by the presence of obesity. Our findings in part negate the concept that obesity is able to exert a protective effect on early target organ damage in hypertensive patients and, in particular, on the heart.

ISSN:0009-7322    

出版商:OVID    

年代:1993

数据来源: OVID

摘要:

BackgroundCoronary angioplasty is frequently performed in the United States, with more than 300,000 procedures in 1990. Despite the high rate of use of the procedure, there have been few studies addressing practice patterns.Methods and ResultsFrom a private insurance claims data base of 5.4 million individuals, a total of 2,101 patients who underwent coronary angioplasty during 1988-1989 were identified. Using their 4,578 hospital admission records and 87,578 outpatient claim records, with an average follow-up of 332±+182 days, we compared patients' outcomes and charges according to whether they had an exercise stress test before the procedure, by sex, by region of the country, and by whether the angioplasty was performed in an institution with a training program. Only 29% of the study cohort had exercise testing before angioplasty; patients in the West (p=0.001), those undergoing multivessel angioplasty (p =0.00001), and those whose procedures were performed at sites with training programs (p=0.04) were more likely to have a screening test, whereas women (p=0.008) and those with a recent myocardial infarction (p=0.00001) were less likely to have a screening test. The average length of stay for patients without myocardial infarction as a primary diagnosis was 5.6 days, with a total hospital charge of $15,027. In follow-up, 15.1% had coronary artery bypass surgery and 15% had at least one additional angioplasty procedure; the average follow-up charges were $4,879. Charges varied according to sex, region of the country, and academic status of the angioplasty institution. Certain outcomes showed variation by region of the country and academic status of the angioplasty institution.ConclusionsThe relative lack of an objective definition of myocardial ischemia and the marked variability of use of procedures according to geographic region suggest the need for further implementation of established guidelines.

ISSN:0009-7322    

出版商:OVID    

年代:1993

数据来源: OVID

摘要:

BackgroundPrevention of abrupt vessel closure after percutaneous transluminal coronary angioplasty (PTCA) represents one of the current indications for intracoronary stent implantation. After the procedure, the stented segment undergoes luminal changes that may lead to late restenosis. This study was undertaken to assess the time course of luminal changes during the first year after emergency placement f coronary stents.Methods and ResultsCoronary stenting was indicated in patients with present or threatened vessel closure secondary to large dissections after PTCA. From June 1989 to May 1991, 82 patients who received Palmaz-Schatz stents and did not have early vessel occlusion after stenting were enrolled into a serial angiographic follow-up study. Coronary normal reference diameter and minimal luminal diameter were measured with an automated edge detection technique. Patients who underwent repeat PTCA for restenosis were excluded from further serial angiography. The restudy rate at 3, 6, and 12 months was 96% 81% and 90% of the eligible patients, respectively. The incidence of restenosis (defined as a diameter stenosis .50%) was 22.0% at 3 months, 31.9% at 6 months, and 33.2% at 12 months. Minimal luminal diameter was increased from 0.66±0.32 mm before to 2.85±0.43 mm immediately after stenting. It was 0.46±0.31 mm smaller than the diameter of the maximally inflated balloon during the procedure. The reduction in minimal luminal diameter was 0.80±0.69 mm (p =0.0001) for the first 3 months, 0.29 ± 0.52mm (p=0.0001) between 3 and 6 months, and 0.13±0.32 mm (p=0.01) for the last 6 months. The percentage of patients who presented a significant change in minimal luminal diameter (defined as >0.60 mm) declined from 50.6% during the first 3 months and 18.9% between 3 and 6 months to 6.5% for the period between 6 and 12 months.ConclusionsThe incidence and the time course of restenosis after emergency coronary stenting are similar to that reported for conventional PTCA. Coronary lumen dimensions demonstrated a peak change at 3 months and remained mostly stable after the first 6 months.

ISSN:0009-7322    

出版商:OVID    

年代:1993

数据来源: OVID