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Biomedical subjects

K Chatterjee

Publications and source records attributed to K Chatterjee.

At least 55 records · Page 3Linked 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

Sex hormones and vascular reactivity.

It is increasingly recognized that sex steroids have, among many other effects, the ability to cause vasodilation. The vasodilatory effects of estradiol have been the best documented and described. At low concentrations, estradiol has the ability to improve impaired endothelium dependent (nitric oxide mediated) relaxation in estrogen deficient subjects. At high concentrations, estradiol causes vasodilation principally by endothelium independent mechanisms, in a gender independent fashion, which appear to involve a number of pathways such as ATP-dependent K+ channels. Testosterone also has ability, at higher doses, to cause vasodilation of the coronary circulation, in a gender independent fashion. The mechanisms of sex steroid-induced vasodilation are reviewed in this article.

Animals↗
PubMed1997

Effects of second-hand smoke and gender on infarct size of young rats exposed in utero and in the neonatal to adolescent period.

OBJECTIVES: We sought to assess the effects of second-hand smoke (SHS) and gender on infarct size in young rats exposed in utero or in the neonatal to adolescent period, or both. BACKGROUND: We previously demonstrated that exposure to SHS increases infarct size in a rat model of ischemia and reperfusion, with a dose-response relation. These results are consistent with epidemiologic studies demonstrating that SHS increases risk of death from heart disease. METHODS: Thirty-one pregnant female rats were randomly divided into two groups: those exposed to SHS and a control group (non-SHS). After 3 weeks, each rat had given birth to 10 to 12 rats. One hundred one neonatal rats were divided into four groups according to exposure to SHS in utero (SHSu) and randomized to SHS exposure in the neonatal to adolescent period (SHSna). After 12 weeks, all rats were subjected to 17 min of left coronary artery occlusion and 2 h of reperfusion. RESULTS: Birth mortality was higher in the SHSu group than in the non-SHSu group (11.9% vs. 2.8%, p < 0.001). Body weight of neonatal rats at 3 and 4 weeks in the two SHSu groups was lower than that of rats in the two non-SHSu groups (p < 0.001). Exposure to SHSna increased endothelin-1 levels in plasma (p = 0.001). In all 70 young rats who survived the neonatal period, infarct size (Infarct mass/Risk area x 100%) was greater in the SHSna groups than in the non-SHSna groups (p = 0.005) and in the male groups than in the female groups (p < 0.001). CONCLUSIONS: Exposure to SHS in the neonatal to adolescent period and male gender increased myocardial infarct size in a young rat model of ischemia and reperfusion. These results are consistent with epidemiologic studies demonstrating that SHS increases the health risk to neonates and adolescents.

Angiotensin II↗
PubMed1997

Markers for transfusion-transmissible infections in north Indian voluntary and replacement blood donors: prevalence and trends 1989-1996.

BACKGROUND AND OBJECTIVES: Twenty five to 30% of multiple-transfusion recipients in India show evidence of infection with both HBV and non-A non-B hepatitis or HCV. To be licensed, blood banks must screen each donor unit for HBsAg, antibodies to HIV-1 and -2, and VDRL. MATERIALS AND METHODS: Between 1989 and 1996, 132,093 voluntary and replacement donors at this centre were screened for the above markers, using commercially available kits. Some 19,531 donors were screened for HCV antibodies in 1995 and 1996 with an in-house EIA, using a synthetic peptide from core, NS3 and NS4 region proteins of all major HCV strains. RESULTS: Data were tabulated annually. The proportion of voluntary donors increased from 15 to 32% during the eight years. HBsAg rates remained below 2.5%, antibodies to HIV increased from 0.04% to 0.55%, and VDRL reactivity increased from 0.23 to 0.52% between 1989 and 1995. Prevalence of all three infections showed a small but significant drop in 1996, and all three were significantly less frequent in voluntary donors. HCV antibodies were detected in 1.49% of donors tested. Donors with multiple infections were uncommon. CONCLUSIONS: A change to voluntary blood transfusion service and addition of anti-HBc, anti-HCV, and possibly HIV antigen to the mandatory list for screening donor blood would reduce posttransfusion infections. Indigenous production of these assays would mitigate the financial burden, as has been the experience with the in-house HCV assay.

Biomarkers↗
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↗
PubMed1997

Successful immunomodulation with intravenous gamma globulin and cyclophosphamide in an alloimmunized heart transplant recipient.

A highly human leukocyte antigen-sensitized heart transplant candidate underwent immunomodulation with intravenous gamma globulin and cyclophosphamide. His panel reactive antibody screen fell from 64% to 14%. He underwent successful orthotopic heart transplantation with a histoincompatible, T-cell cross-match-negative heart without the development of hyperacute rejection. The combination of intravenous gamma globulin and cyclophosphamide may be a simple and effective means to overcome the human leukocyte antigen-barrier in sensitized heart transplant candidates.

Combined Modality Therapy↗
PubMed1997

Assessment of early left ventricular remodeling in orthotopic heart transplant recipients with cine magnetic resonance imaging: potential mechanisms.

We performed short axis cine magnetic resonance imaging studies in 11 patients 2 months after they underwent orthotopic heart transplantation (OHT), and in 10 control subjects, to measure left ventricular (LV) volumes, mass, and end-systolic wall stress to assess ventricular remodeling after OHT. Although there were no significant differences in ventricular volumes and ejection fractions between heart transplant recipients and control subjects, heart transplant recipients had significantly higher LV mass (198 +/- 61 vs 132 +/- 27 gm, p = 0.001). As a consequence of myocardial hypertrophy, end-systolic wall stress was significantly reduced in heart transplant recipients compared with control subjects (34 +/- 16 vs 57 +/- 10 kdyne/cm2, p = 0.001). Moreover, heart transplant recipients had significantly reduced end-systolic wall stress/volume ratio when compared with control subjects (0.89 +/- 0.3 vs 1.26 +/- 0.3 kdyne/cm2/ml, p < 0.01), indicating an already reduced LV contractility 2 months after heart transplantation. Univariate regression analysis revealed a significant correlation between LV mass and averaged cyclosporine levels, but no correlation between LV mass and blood pressure, cold ischemic time, acute rejection, age, body mass, blood pressure, plasma catecholamine levels, or plasma renin activity. Magnetic resonance imaging demonstrates early LV remodeling after OHT with reduced myocardial contractility. Cyclosporine may be contributing to these changes.

Adult↗
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

Comparison of adenosine to dipyridamole in degree of coronary hyperemic response in heart transplant recipients.

Transplant coronary vasculopathy is associated with endothelial dysfunction. Microvascular function, assessed as coronary flow reserve, has been reported to be normal. We used intracoronary ultrasound technology to simultaneously assess conductance and resistance vessel function in response to standard dosages of the vasodilators adenosine and dipyridamole. Coronary hemodynamic changes were assessed in 11 heart transplant recipients, at a mean duration of 784 +/- 516 days after transplantation, using a 3.2Fr or 4.3Fr, 30-MHz ultrasound imaging catheter over a 0.014-inch Doppler guidewire. Measures of coronary average peak flow velocity (APV) and coronary cross-sectional area (CSA) were used to calculate volumetric flow during intravenous infusions of adenosine (140 micrograms/kg/min over 4 minutes) and dipyridamole (140 micrograms/kg/min over 4 minutes). Flow reserve was assessed as a ratio of maximal pharmacologically induced flow to steady baseline flow before infusion. Increase in APV (261.9% vs 194.6%, p = 0.005), lumenal CSA (+11.8% vs +4.2%, p = 0.01), peak volumetric blood flow (515.8 vs 317.2 ml/min, p = 0.007), and coronary flow reserve (2.93 +/- 0.74 vs 1.99 +/- 0.53, p < 0.001) were higher with adenosine than dipyridamole. Both agents caused similar decreases in systemic blood pressure and little change in heart rate. Adenosine appears to be a more potent coronary vasodilator than dipyridamole in denervated human transplant subjects. Adenosine has a vasodilator effect at the epicardial and microvascular levels, resulting in an overall increase in volumetric flow. Flow reserve in response to both endothelium-independent agents is decreased in comparison with previously established values, but the attenuation is greater with dipyridamole.

Adenosine↗
PubMed1996

Effects of A1 adenosine receptor agonism using N6-cyclohexyl-2'-O-methyladenosine in patients with left ventricular dysfunction.

BACKGROUND: The role of adenosine as a neuromodulator in heart failure was studied with the use of a selective adenosine A1 receptor agonist, N6-cyclohexyl-2'-O-methyladenosine (SDZ-WAG 994). METHODS AND RESULTS: Fifty patients with heart failure symptoms and moderate left ventricular systolic dysfunction had a balloon flotation catheter inserted. Patients received placebo or a single oral dose of either 1, 2, or 5 mg SDZ-WAG 994. After baseline measurements were obtained, hemodynamic and electrophysiological recordings were repeated at 30-minute intervals for the next 4 hours, then every 6 hours for the next 24 hours. Blood samples for norepinephrine, epinephrine, aldosterone, atrial natriuretic peptide, and plasma renin activity were drawn at baseline and 2 hours after drug administration. A adenosine receptor agonism produced no important effects on systemic, right atrial, pulmonary artery, or pulmonary capillary wedge pressures; cardiac index; respiratory rate; or heart rate. The PR interval (a reflection of A1 receptor-mediated activity) increased significantly in a stepwise fashion. At the 5-mg dose of SDZ-WAG 994, significant increases in atrial natriuretic peptide (216 +/- 137 to 407 +/- 146 pg/mL) and norepinephrine (477 +/- 243 to 618 +/- 237 pg/mL) levels were noted. CONCLUSIONS: A1 adenosine receptor agonism with SDZ-WAG 994 resulted in no significant hemodynamic changes at rest in this subset of patients with left ventricular dysfunction. An increase in the PR interval and atrial natriuretic peptide level, consistent with adenosine A1 receptor-mediated activity, was observed. In addition, an increase in the norepinephrine level was observed, suggesting a role for adenosine as a peripheral nervous system neuromodulator.

Adenosine↗
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↗
PubMed1996

Dominant-negative mutant thyroid hormone receptors prevent transcription from Xenopus thyroid hormone receptor beta gene promoter in response to thyroid hormone in Xenopus tadpoles in vivo.

We describe a dominant-negative approach in vivo to assess the strong, early upregulation of thyroid hormone receptor beta (TR beta) gene in response to thyroid hormone, characteristic of the onset of natural and thyroid hormone-induced amphibian metamorphosis, 3,3',5-Triiodo-thyronine (T3) treatment of organ cultures of premetamorphic Xenopus tadpole tails coinjected in vivo with the wild-type Xenopus TR beta (wt-xTR beta) and three different thyroid responsive element chloramphenicol acetyltransferase (TRE-CAT) reporter constructs, including a direct repeat +4 (DR +4) element in the -200/+87 fragment of the xTR beta promoter, resulted in a 4- to 8-fold enhancement of CAT activity. Two human C-terminal TR beta 1 mutants (delta-hTR beta 1 and Ts-hTR beta 1), an artificial Xenopus C-terminal deletion mutant (mt-xTR beta), and the oncogenic viral homology v-erbA, none of which binds T3, inhibited this T3 response of the endogenous wt-xTR in Xenopus XTC-2 cells cotransfected with the -1600/+87 xTR beta promoter-CAT construct, the potency of the dominant-negative effect of these mutant TRs being a function of the strength of their heterodimerization with Xenopus retinoid X receptor gamma. Coinjection of the dominant-negative Xenopus and human mutant TR beta s into Xenopus tadpole tails totally abolished the T3 responsiveness of the wt-xTR beta with different TREs, including the natural DR +4 TRE of the xTR beta promoter.

Amino Acid Sequence↗
PubMed1996

L-arginine decreases infarct size in rats exposed to environmental tobacco smoke.

This study examined the effects of L-arginine on myocardial infarct size, hemodynamics, and vascular reactivity in environmental tobacco smoke (ETS)-exposed and non-ETS-exposed rats. We previously demonstrated that exposure to ETS increased myocardial infarct size in a rat model of ischemia and reperfusion. If reduced reperfusion was caused by endothelial cell damage and increased vascular tone, L-arginine (ARG) would increase nitric oxide and better protect the heart. Sixty Sprague-Dawley rats were randomly divided into four groups: ETS or non-ETS (control) with and without ARG (2.25% ARG in drinking water). The ETS groups were exposed to passive smoking (4 Marlboro cigarettes per 15 minutes, 6 hours a day) for 6 weeks. After 6 weeks, all rats were subjected to 35 minutes of left coronary artery occlusion and 120 minutes of reperfusion, with hemodynamic monitoring. Aortic rings were harvested to evaluate vascular reactivity. Average air nicotine, carbon monoxide, and total particulate concentrations were 1304 +/- 215 microgram/m3, 78 +/- 2.0 ppm, and 31 +/- .7 mg/m3 (mean +/- SEM) for the ETS-exposed rats. Infarct size (infarct mass/risk area x 100%) increased with ETS exposure but decreased significantly in the ETS-with-ARG group compared with the ETS-without-ARG group (42% +/- 6% vs 64% +/- 6%, mean +/- SEM; p = 0.043). The benefit of ARG was dependent on ETS exposure (ETS x ARG interaction, p = 0.043). There were no significant differences between groups in heart rate, systolic pressure, and rate-pressure product. ARG significantly decreased myocardial infarct size after ischemia and reperfusion in ETS-exposed rats. Neither the adverse effects of ETS on infarct size nor the blockage of this effect by ARG appears to be the result of ETS-induced alterations in hemodynamics.

Animals↗
PubMed1995

Testosterone relaxes rabbit coronary arteries and aorta.

BACKGROUND: Until menopause, women appear to be protected from coronary heart disease. Evidence suggests that estrogen may play a role in the protection of the cardiovascular system by exerting a beneficial effect on risk factors such as cholesterol metabolism and by a direct effect on the coronary arteries. To date there has been no evidence linking testosterone with the occurrence of coronary heart disease. Testosterone may affect the cardiovascular system directly, thus partially explaining the difference in the incidence of coronary artery disease in men and premenopausal women. The purpose of this study was to assess the direct effect of testosterone and a number of testosterone analogues on rabbit coronary arteries and aorta in vitro. METHODS AND RESULTS: Rings of coronary artery and aorta of adult male or nonpregnant female New Zealand White rabbits were suspended in organ baths containing Krebs solution; isometric tension then was measured. The response to testosterone was investigated in prostaglandin F2 alpha (PGF 2 alpha)- and KCl-contracted rings. The effects of endothelium and nitric oxide synthase, prostaglandin synthetase, and guanylate cyclase inhibition on testosterone-induced relaxation were investigated. The effects of ATP-sensitive potassium channels and potassium conductance were also assessed. Relaxing responses in the presence of aromatase inhibition and testosterone receptor blockade were performed. The relaxing responses to the testosterone analogues etiocholan-3 beta-ol-17-one, epiandrosterone, 17 beta-hydroxy-5 alpha-androst-1-en-3-one, androst-16-en-3-ol, and testosterone enanthanate were measured. Testosterone relaxed rabbit coronary arteries and aorta. There was no significant difference between the relaxation effect of testosterone with or without endothelium. Similar results were obtained from male and nonpregnant female rabbits. The relaxing response of testosterone in the coronary artery was significantly greater than in the aorta. The relaxing response of testosterone in the coronary artery was significantly reduced by the potassium channel inhibitor barium chloride but not by the ATP-sensitive potassium channel inhibitor glibenclamide. The relaxing response to testosterone was greater in PGF 2 alpha-contracted rings compared with KCl-contracted rings. Inhibitors of nitric oxide synthase, prostaglandin synthetase, and guanylate cyclase did not affect relaxation induced by testosterone. Inhibition of aromatase and testosterone receptors did not affect relaxation. Testosterone did not shift the rabbit coronary arterial calcium concentration-dependent contraction curves, whereas verapamil did. There were, however, significant differences in the relaxing response to testosterone compared with testosterone analogues. Testosterone was the most potent relaxing agent, suggesting that there may be a structure-function relation in the relaxing response. CONCLUSIONS: Testosterone induces endothelium-independent relaxation in isolated rabbit coronary artery and aorta, which is neither mediated by prostaglandin I2 or cyclic GMP. Potassium conductance and potassium channels but not ATP-sensitive potassium channels may be involved partially in the mechanism of testosterone-induced relaxation. The in vitro relaxation is independent of sex and of a classic receptor. The coronary artery is significantly more sensitive to relaxation by testosterone than the aorta. Testosterone is a more potent relaxing agent of rabbit coronary artery than other testosterone analogues.

Animals↗
PubMed1995

Contribution of endothelium-derived nitric oxide to coronary arterial distensibility: an in vivo two-dimensional intravascular ultrasound study.

Reduced epicardial coronary arterial distensibility associated with early atherosclerosis may be mediated in part by reduced nitric oxide (NO) release. To directly assess the contribution of endogenous NO to coronary arterial distensibility, we examined the effect of intracoronary N omega nitro-L-arginine methyl ester (L-NAME), an inhibitor of NO synthase, and L-arginine, its natural substrate, on the circumflex artery in seven anesthetized dogs. We also used intracoronary acetylcholine to examine the effect of pharmacologically induced NO release on coronary distensibility. Electrocardiographically gated measurements of epicardial coronary lumen area were made by a blinded observer from images obtained with a 4.3F, 30 MHz intravascular ultrasound catheter. Aortic root pressure was continuously monitored, and neither systemic arterial pressure nor pulse pressure changed significantly with intracoronary drug administration. Change in lumen area (delta LA) from end systole to end diastole was measured, and an arterial distensibility index was calculated. Delta LA increased with acetylcholine from 8.2% +/- 0.5% at baseline to 16.3% +/- 2.8% (10(-6) mol/L; p < 0.001), with increases in both end-systolic and end-diastolic lumen area and decreased delta LA to 3.1% +/- 1.3% (p < 0.01). Lumen area and delta LA were both restored to baseline by L-arginine (10(-4)). The calculated distensibility index of the epicardial coronary artery was enhanced by acetylcholine, reduced below baseline by L-NAME, and restored to baseline by L-arginine.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1995

Abnormal pulmonary artery pressure profile after cardiac transplantation: an exercise Doppler echocardiographic study.

This study was designed to test the hypothesis that pulmonary artery pressure at rest and during exercise differs between patients with a transplanted heart and normal subjects and to determine the mechanisms responsible for the difference. Twenty-one patients who had undergone heart transplantation 1.5 to 27 months earlier without current evidence of acute cardiac rejection and 25 normal subjects were studied by exercise Doppler echocardiography. Systolic pulmonary artery pressure was higher at baseline in heart transplant patients than in normal subjects, at 31.6 +/- 9 mm Hg (mean +/- SD) versus 22.5 +/- 4, respectively (p = 0.0001). The increase in systolic pulmonary artery pressure with exercise was 1.4 times higher in heart transplant patients and correlated with pretransplantation pulmonary vascular resistances (r = 0.55; p = 0.01). In contrast, cardiac index at baseline or during exercise did not differ between the two groups. Diastolic parameters and ejection fraction at baseline or during exercise did not correlate with systolic pulmonary artery pressure. In conclusion, Doppler exercise echocardiography offers an alternative, safe method hemodynamic study of the transplanted heart. Although an abnormal increase in left ventricular filling pressure with exercise has been well documented, further studies are needed to investigate and characterize potential abnormalities in pulmonary vascular tone in the transplanted heart.

Adult↗