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Biomedical subjects

S U Sys

Publications and source records attributed to S U Sys.

At least 55 records · Page 3Linked to original sources
PubMed1995

Positive inotropic effect of nitric oxide in myocardium.

Cardiac endothelium modulates underlying cardiac muscle performance probably by releasing certain regulatory factors. Nitric oxide (NO), which accounts for the biological activity of the vascular endothelium-derived relaxing factor and relaxes vascular smooth muscle by elevating intracellular cyclic GMP (cGMP), may be involved in this cardiac modulation. Many recent studies have examined inotropic effects of NO utilizing NO donors and NO-synthase inhibitors, both in vitro and in vivo, with apparently contradictory results. We examined the myocardial effects of NO-releasing nitrovasodilators (sodium nitroprusside (SNP), SIN-1 and S-nitrosoacetyl penicillamine (SNAP)), a cGMP analogue, 8-bromo-cGMP, and the cGMP phosphodiesterase inhibitor zaprinast, in isolated cat papillary muscle. A novel concentration-dependent positive inotropic effect of SNP and SIN-1 in muscles with damaged endocardial endothelium (EE) was observed which contrasted to their negative inotropic effect in muscles with intact EE. Both NO-induced positive and negative inotropic effects were attenuated by methylene blue, suggesting a role for cGMP. Concentration response curves with addition of SNAP and 8-bromo-cGMP resulted in a biphasic inotropic response. While administration of low concentrations of SNAP and 8-bromo cGMP induced a positive inotropic effect, higher concentrations induced a negative inotropic effect. Administration of zaprinast caused a monophasic concentration-dependent positive inotropic effect. We conclude that basal release of NO and consequent modest (physiological?) elevation in cGMP may preserve myocardial function, while large (pathological?) increases would depress myocardial function.

Animals↗
PubMed1995

Quantitative coronary angiography in predicting functional significance of stenoses in an unselected patient cohort.

OBJECTIVES: This study investigated the value of quantitative coronary angiography for predicting coronary flow reserve, as calculated from the transstenotic pressure gradient in a large, unselected patient cohort. BACKGROUND: In patients with extensive coronary artery disease, quantitative coronary angiographic findings fail to correlate with functional variables of coronary stenoses. New developments in pressure-monitoring wire technology permitted validation in humans of the concept of myocardial fractional flow reserve as assessed from coronary pressure measurements. METHODS: One hundred ten patients with normal left ventricular function were studied in the setting of coronary angioplasty. Quantitative coronary angiography was performed on-line using the ACA system. Myocardial and coronary fractional flow reserve were calculated from aortic and distal coronary pressures during maximal coronary hyperemia. RESULTS: When data before and after angioplasty were pooled, a curvilinear relation was found between myocardial fractional flow reserve and both diameter stenosis (r = 0.79) and minimal lumen diameter (r = 0.82), and a linear relation was found between myocardial fractional flow reserve and angiographic stenosis flow reserve (r = 0.78). Correlations between quantitative angiographic and pressure-derived indexes, although significant, were characterized by a large dispersion of the values of myocardial fractional flow reserve for a similar angiographic degree of stenosis. Nevertheless, the sensitivity and specificity of a minimal lumen diameter < 1.5 mm to predict myocardial fractional flow reserve < 0.72 were 96% and 89%, respectively. The corresponding values for a diameter stenosis > 50% were 93% and 85%, respectively. CONCLUSIONS: 1) In an unselected patient cohort, geometric indexes of stenosis severity derived from quantitative coronary angiography correlate significantly with physiologic variables, although these relations are imprecise in individual patients. 2) Nevertheless, the diagnostic accuracy of quantitative coronary angiography in predicting myocardial fractional flow reserve < 0.72 is high and allows its use for clinical decision making in the individual patient during diagnostic or interventional procedures.

Aged↗
PubMed1995

Endothelin-mediated positive inotropic effect induced by reactive oxygen species in isolated cardiac muscle.

Cardiac endothelium, both coronary and endocardial, produces a number of inotropic molecules. Changes in cardiac endothelial function by substances in the superfusing blood may thus participate in the control of muscle-pump performance of the heart. Reactive oxygen species (ROS) have been implicated in normal and pathological vascular physiology by influencing vascular endothelial function. Therefore, we examined the influence of ROS on endocardial endothelial modulation of myocardial performance. Right ventricular cat papillary muscles were briefly (15 s) exposed to electrolysis-generated ROS. Peak total isometric twitch tension and peak rate of tension development increased by 7.8 +/- 0.7% (P < .05) and 9.7 +/- 1.5% (P < .05), respectively (n = 12). Isometric twitch duration was slightly increased (time from stimulus to half isometric relaxation, +2.7 +/- 0.6%; P < .05). ROS scavengers such as ascorbic acid (n = 6), superoxide dismutase and catalase (n = 8), or catalase alone (n = 6), but not superoxide dismutase alone (n = 6), blocked the inotropic effect. Interestingly, the positive inotropic effect was completely blocked by selectively damaging endocardial endothelium (Triton X-100, 0.5%, 1-s immersion, n = 7) before ROS generation and by preincubating the muscles with the endothelin-A receptor antagonist BQ 123 (n = 11). Preincubation with NG-nitro-L-arginine methyl ester and indomethacin (n = 5) or with atenolol (n = 6) did not influence the inotropic effect.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Myocardial performance is modulated by interaction of cardiac endothelium derived nitric oxide and prostaglandins.

OBJECTIVE: The endocardial endothelium modulates the performance of the subjacent myocardium and plays an important role in regulating cardiac function. The aim of this study was to investigate the effects on cardiac function of the mutual interaction of nitric oxide (NO) and prostaglandins released from the endocardial endothelium. METHODS: The effects of NO and prostaglandin interaction were investigated in isolated cat papillary muscle (Krebs Ringer; 1.25 mM Ca2+; 35 degrees C), using substance P (1 mumol.litre-1) to release NO, L-nitroarginine (L-NOARG:30 mumol.litre-1) to inhibit NO synthase, arachidonic acid (10 mumol.litre-1) to stimulate endogenous prostaglandin (mainly prostacyclin) release, and indomethacin (1 mumol.litre-1), a cyclooxygenase inhibitor. RESULTS: Administration of substance P resulted in a negative inotropic effect. This response to substance P was abolished by arachidonic acid, while it was preserved in the presence of indomethacin. In the presence of L-NOARG, arachidonic acid induced a positive inotropic effect with prolongation of the twitch duration, while indomethacin reduced the twitch duration. CONCLUSIONS: Activation of prostaglandins abolishes the effect of NO, while prostaglandin-induced positive inotropic effect requires NO synthesis inhibition. Accordingly NO and prostaglandins interact to regulate myocardial performance.

Animals↗
PubMed1995

Morphoregulatory interactions of endocardial endothelium and extracellular material in the heart.

The endocardium forms the inner lining of the cavities of the heart. The luminal surface of the cardiac wall is subjected to considerable cyclical physico-chemical forces. These forces can have structural and physiological consequences both for the endocardial endothelium and for the subjacent interstitial tissue. In the latter tissue space, the extracellular matrix (ECM) plays a dominant role during cardiogenesis. For example, this role becomes evident from the influence of fibronectin in the directional migration of proendocardial cells and in the formation of a trabeculated heart. In particular, the complex processes occurring in the valves of the developing heart illustrate a spatiotemporally regulated expression of ECM components and adhesion molecules. In the adult heart, the endocardial interstitial tissue consists of a thin basal lamina, a reticular lamina and a fibroelastic layer which contains some fibroblasts, smooth muscle cells and a heterogeneous population of nerve fibers. Unlike in arteries, elastic fiber in the fibroelastic layer of ventricular endocardium do not constitute an elastic lamina. Differences in thickness of the endocardium between atria and ventricles, as well as the diffuse and focal endocardial fibrosis during ageing have been related to mechanical stress and local turbulence of flow. Although endocardial fibrosis is a common pathological finding in various cardiomyopathies, our knowledge on the structural organization and on the pathogenetic role of ECM is very limited, mainly by the lack of suitable experimental models.

Age Factors↗
PubMed1995

The role of increased nitric oxide in the vascular hyporeactivity to noradrenaline in long-term portal vein ligated rats.

To test the possible role of nitric oxide production in long-term portal vein ligation in the rat, where the hyperdynamic circulation was reported to be absent, in vivo experiments on isolated thoracic aortic rings from partial portal vein ligated or sham-operated rats were performed, 6 months postoperatively. The concentration-response curves to noradrenaline of both intact and endothelium-denuded rings from portal hypertensive rats were significantly shifted to the right as compared to those from sham-operated animals. In intact rings, addition of NG-nitro-L-arginine, a specific inhibitor of nitric oxide synthase, resulted in a significant shift of the curves to the left in sham-operated and portal vein ligated rats. In endothelium-denuded rings, addition of NG-nitro-L-arginine resulted in a significant shift of the curves to the left in portal vein ligated but not in sham-operated animals. After blockade of the nitric oxide biosynthesis with NG-nitro-L-arginine, the negative logarithm of the concentration of nonadrenaline causing half-maximal response did not significantly differ any more between portal vein ligated and sham-operated rats; in endothelium-denuded rings hyporeactivity to noradrenaline persisted in portal vein ligated rats. Only in the intact rings did NG-nitro-L-arginine significantly increase the maximal contractions. No differences were demonstrated in endothelium-dependent relaxations to acetylcholine between sham-operated and portal hypertensive animals. From these results, it can be concluded that in vitro aortic hyporeactivity to noradrenaline is still present in long-term portal vein ligated rats, and that it results at least partially from activation of the L-arginine: nitric oxide pathway in the aortic vascular wall.

Animals↗
PubMed1994

Positive inotropic effect of Streptococcus faecalis in isolated cardiac muscle.

Infective endocarditis is caused by bacterial colonization of the endocardium. Because endocardium modulates mechanical performance of subjacent myocardium, we studied acute effects of bacteria on isolated cardiac muscle and on the functional role of the endocardium. Bacteria, grown in broth at 37 degrees C, were added at increasing concentrations (10(2) to 10(6) bacteria/ml) to cat papillary muscles in Krebs-Ringer solution (1.25 mM Ca2+, 35 degrees C). The endocardial surface was damaged by exposing muscles to a stream of dry air for 30 s. Streptococcus (Enterococcus) faecalis induced significant increases in total peak isometric twitch tension (TT) and maximal velocity of unloaded shortening (Vmax) and significant decreases in time to TT (TtTT) and time to half isometric twitch tension decline (RT 1/2), both before and after removal of endocardial endothelium. This response could also be elicited with bacterial filtrate, after boiling the filtrate or after extracting the polysaccharides from it with KIO4. Increasing Ca2+ concentrations progressively reduced the response to the filtrate. Propranolol slightly, although not significantly, diminished the effects on TT and Vmax while abolishing the effects on TtTT and on RT 1/2. By contrast, Streptococcus bovis and Staphylococcus aureus did not affect TT or Vmax but induced a slight but significant decrease in TtTT at the highest concentration of bacteria. Accordingly, the filtrate of Strep. faecalis induces a positive inotropic effect. The active component is neither a protein nor a polysaccharide, and its effect may be partly beta-adrenoceptor mediated. Strep. bovis and Staph. aureus have negligible acute effects on contractility.

Adrenergic beta-Antagonists↗
PubMed1994

Coronary flow reserve calculated from pressure measurements in humans. Validation with positron emission tomography.

BACKGROUND: Experimental studies have shown that fractional flow reserve (defined as the ratio of maximal achievable flow in a stenotic area to normal maximal achievable flow) can be calculated from coronary pressure measurements only. The objectives of this study were to validate fractional flow reserve calculation in humans and to compare this information with that derived from quantitative coronary angiography. METHODS AND RESULTS: Twenty-two patients with an isolated, discrete proximal or mid left anterior descending coronary artery stenosis and normal left ventricular function were studied. Relative myocardial flow reserve, defined as the ratio of absolute myocardial perfusion during maximal vasodilation in the stenotic area to the absolute myocardial perfusion during maximal vasodilation (adenosine 140 micrograms.kg-1 x min-1 intravenously during 4 minutes) in the contralateral normally perfused area, was assessed by 15O-labeled water and positron emission tomography (PET). Myocardial and coronary fractional flow reserve were calculated from mean aortic, distal coronary, and right atrial pressures recorded during maximal vasodilation. Distal coronary pressures were measured by an ultrathin, pressure-monitoring guide wire with minimal influence on the trans-stenotic pressure gradient. Minimal obstruction area, percent area stenosis, and calculated stenosis flow reserve were assessed by quantitative coronary angiography. There was no difference in heart rate, mean aortic pressure, or rate-pressure product during maximal vasodilation during PET and during catheterization. Percent area stenosis ranged from 40% to 94% (mean, 77 +/- 13%), myocardial fractional flow reserve from 0.36 to 0.98 (mean, 0.61 +/- 0.17), and relative flow reserve from 0.27 to 1.23 (mean, 0.60 +/- 0.26). A close correlation was found between relative flow reserve obtained by PET and both myocardial fractional flow reserve (r = .87) and coronary fractional flow reserve obtained by pressure recordings (r = .86). The correlations between relative flow reserve obtained by PET and stenosis measurements derived from quantitative coronary angiography were markedly weaker (minimal obstruction area, r = .66; percent area stenosis, r = -.70; and stenosis flow reserve, r = .68). CONCLUSIONS: Fractional flow reserve derived from pressure measurements correlates more closely to relative flow reserve derived from PET than angiographic parameters. This validates in humans the use of fractional flow reserve as an index of the physiological consequences of a given coronary artery stenosis.

Coronary Angiography↗
PubMed1994

The relaxant action of betaxolol on isolated bovine retinal microarteries.

We investigated the possible effects on retinal blood flow of betaxolol, a beta blocker which is used as antiglaucomatous medication. Ring segments of retinal microarteries were isolated from bovine eyes and mounted in an organ bath for measurement of contractile force. The effects of betaxolol were studied during K(+)-, stretch-, and serotonin-induced contractions, to enable comparison to the effects of the standard beta blocker propranolol and the Ca2+ channel blocker verapamil. Betaxolol relaxed K(+)-induced contractions in a dose-dependent manner. The drug relaxed the phasic part of the K(+)-induced contractions more than the tonic part. Betaxolol had no effect on stretch-induced contractions. The tonic part of the serotonin-induced contractions showed a trend to decrease in response to betaxolol. These highly specific effects of betaxolol resembled the effects of propranolol. Since betaxolol has significantly less membrane stabilizing activity than has propranolol, this activity is not responsible for the relaxant action of beta blockers on retinal microarteries. The action of both beta blockers resembled the action of the Ca2+ channel blocker verapamil.

Animals↗
PubMed1993

Percutaneous transluminal coronary angioplasty catheters versus fluid-filled pressure monitoring guidewires for coronary pressure measurements and correlation with quantitative coronary angiography.

The functional significance of a coronary stenosis can be assessed by measuring the translesional pressure gradient. Thirty-four patients were studied in the setting of percutaneous transluminal coronary angioplasty (PTCA) to evaluate the clinical relevance of the pressure gradient measurements by means of a PTCA balloon catheter. Both before and after PTCA, the mean pressure gradient across the stenosis was measured by means of a newly developed, 0.015-inch pressure-monitoring guidewire, first with only the wire across the stenosis (delta Pw, considered as the actual gradient), and second with the deflated balloon catheter advanced over the wire in the stenosis (delta Pb). Pressure gradients were correlated with quantitative coronary angiography of the stenotic segment. Before PTCA, mean delta Pb was larger than delta Pw (62 +/- 14 vs 30 +/- 20 mm Hg; p < 0.01). After PTCA, delta Pb remained systematically higher than delta Pw (23 +/- 14 vs 3 +/- 5 mm Hg; p < 0.01), despite a significant reduction of percent area stenosis from 84 +/- 9 to 46 +/- 17%, and an increase in minimal obstruction area from 0.98 +/- 0.48 to 3.49 +/- 1.32 mm2. A significant correlation was found between delta Pw and percent area stenosis (r2 = 0.66), with a marked increase after percent area stenosis reached 80%. The correlation between delta Pb and percent area stenosis was weaker (r2 = 0.53), the scatter of the data was larger, and the inflection point of the curve was shifted toward less severe degrees of stenosis severity.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Transstenotic coronary pressure gradient measurement in humans: in vitro and in vivo evaluation of a new pressure monitoring angioplasty guide wire.

OBJECTIVES: The present study was designed to investigate 1) the feasibility and accuracy of coronary pressure measurements with a novel 0.015-in. (0.038 cm) fluid-filled guide wire, and 2) the effect of the guide wire itself on stenosis hemodynamics. BACKGROUND: To assess the functional results of coronary angioplasty, measurements of the transstenotic pressure gradient have been advocated. However, this gradient is no longer routinely measured because it is not reliable when determined with the angioplasty catheter. METHODS: A fluid-filled 0.015-in. guide wire to be connected to a conventional pressure transducer was developed. Five wires were tested for their frequency response characteristics and for their accuracy in measuring hydrostatic pressure. In an in vitro model of stenosis (reference diameter 4 mm), the pressure gradient was determined at incremental flow levels for varying stenosis severity with and without a 0.015-in. guide wire through the narrowing. In 37 patients, the transstenotic pressure gradient was measured before and after angioplasty and compared with obstruction area and percent area stenosis as determined by quantitative coronary angiography. RESULTS: The correlation between the actual pressure and the pressure recorded by the guide wire was excellent (r = 0.98) despite a slight underestimation (-3 +/- 5%). Phasic pressure recordings were precluded by a long time constant of 16 +/- 4 s. The presence of the guide wire produced a significant overestimation (> 20%) of the pressure decrease only in cases of tight stenosis (> 90% area reduction). Furthermore, a theoretic model based on the fluid dynamic equation predicted that this overestimation was inversely proportional to the reference diameter of the vessel, yet was only slightly influenced by the flow. The lesion was crossed in all but one patient (97%) and pressure gradient was recorded throughout the study in 34 (94%) of 36 patients. The mean pressure gradient decreased from 30 +/- 19 before to 3 +/- 5 mm Hg after angioplasty (p < 0.01). A curvilinear relation was found between the pressure gradient and both percent area stenosis (r2 = 0.67) and obstruction area (r2 = 0.72). A sharp increase in pressure gradient was noted once the stenosis exceeded 75% area reduction. CONCLUSIONS: Mean transstenotic pressure gradients can be easily and reliably recorded with a 0.015-in. fluid-filled guide wire. This ability should facilitate the functional assessment of coronary stenoses of intermediate severity and of immediate postangioplasty results.

Adult↗
PubMed1993

Diastolic failure: pathophysiology and therapeutic implications.

Primary diastolic dysfunction or failure is a distinct pathophysiologic entity. It results from increased resistance to ventricular filling, which leads to an inappropriate upward shift of the diastolic pressure-volume relation, particularly during exercise (exercise intolerance). The causes of diastolic failure are inappropriate tachycardia, decreased diastolic compliance and impaired systolic relaxation. Impaired (incomplete or slowed) systolic relaxation must be conceptually distinguished from compensatory prolonged systolic contraction (delayed or retarded relaxation). Optimal therapy will depend on the type of disease, the phase during the course of a given disease and the coexistence and relative contribution of various (de)compensatory processes. Treatment may consist of bradycardic, remodeling and lusitropic drugs.

Diastole↗
PubMed1993

Diastolic dysfunction in post-cardiac surgical management.

Although an appropriate definition of primary diastolic failure is still not at hand, primary diastolic failure is a distinct pathophysiologic syndrome. It is due to an increased resistance to ventricular filling and results in an inappropriate upward shift of the diastolic P-V relationship, especially during exercise. This leads to exercise intolerance with symptoms of congestion. The causes are known, ie, impaired systolic relaxation, decreased diastolic compliance, and inappropriate tachycardia. Pathophysiologically impaired (incomplete or slowed) systolic relaxation must be distinguished from physiologic, compensatory prolonged contraction (delayed or retarded relaxation). Treatment of diastolic failure is feasible, but necessitates a clear understanding of the etiology, pathogenesis, and pathophysiology of the underlying cardiac disease. Optimal therapy will depend on the type of disease, on the phase during the pathophysiologic evolution of a given disease, and on the coexistence and relative contribution of various compensatory or decompensatory mechanisms. This often requires a comprehensive analysis of hemodynamics, for example, with echo-doppler, completed, whenever necessary, by catheterization.

Cardiac Output, Low↗
PubMed1993

In vitro study of the contractility of the wall of the preovulatory follicle in the Japanese quail.

In the present study, we examined in vitro the potassium-induced contractions of isolated parts of the wall of the quail preovulatory follicle through use of an electromagnetic force-length transducer system. We studied longitudinal and transverse strips of the whole wall, of the theca, and of the outer layer (tunica albuginea and surface epithelium). It was observed that force development and shortening of strips of the whole wall and those of the theca are similar. Statistical analysis of maximal isometric force, peak shortening length, and percentage of reduction of follicular volume showed that the orientation of strips is without importance. Results from different orientations were pooled, and the different layers were compared statistically. The general result of this analysis was that the contractile activity of the outer layer was significantly lower than the performance of either the whole wall or the theca. We concluded that contraction of the follicular wall is mainly dependent on the contractile activity of the theca externa. This contractile system is comparable to that of mammals. We suggest that the main function of the theca externa during ovulation is to maintain a constant intrafollicular pressure.

Animals↗
PubMed1992

Failure of myocardial inactivation: a clinical assessment in the hypertrophied heart.

BACKGROUND: Abnormal intracellular calcium handling is observed in hypertrophied cardiac muscle and in end-stage heart failure muscle. This abnormal calcium handling results in prolongation of the calcium transient and in a biphasic calcium transient with prominent late component. In the present studies, the mechanical correlates of abnormal calcium handling were investigated in the hypertrophied human left ventricle by analysis of: 1) isovolumic left-ventricular relaxation kinetics after drastic left-ventricular unloading in patients with severe aortic stenosis after sequential balloon aortic valvuloplasty-arterial vasodilation; and 2) morphology of the diastolic left-ventricular pressure signal in patients with aortic stenosis and hypertrophic cardiomyopathy. METHODS AND RESULTS: Drastic left-ventricular unloading in patients with severe aortic stenosis by sequential aortic valvuloplasty-arterial vasodilation resulted in a slow and dyssynchronous left-ventricular relaxation pattern, as evident from a prolongation of the time constant of left-ventricular pressure decay from 46.6 +/- 12.5 to 73.2 +/- 23.3 ms (p < 0.01), and from the development of a convex downward negative dP/dt upstroke pattern. Abnormal diastolic left-ventricular pressure wave forms consisting of continuous left-ventricular pressure decay throughout diastole and/or a secondary pressure rise in mid-diastole were observed in patients with aortic stenosis and with hypertrophic cardiomyopathy. Postextrasystolic potentiation caused further slowing of this abnormal diastolic left-ventricular pressure decay, as evident from the decrease in phase of the first harmonic of a Fourier transform applied to the diastolic left-ventricular pressure wave. When an abnormal diastolic left-ventricular pressure wave form was observed at rest or after postextrasystolic potentiation, a simultaneously recorded left-ventricular monophasic action potential signal revealed the occurrence of delayed afterdepolarizations. CONCLUSIONS: The mechanical correlates of abnormal calcium handling or of inactivation failure in the hypertrophied human left ventricle consist of slow and dyssynchronous left-ventricular isovolumic relaxation after left-ventricular unloading and of diastolic left-ventricular aftercontractions, which hinder left-ventricular filling and which are accompanied by delayed afterdepolarizations.

Action Potentials↗
PubMed1991

Orifice variability of the stenotic aortic valve: evaluation before and after balloon aortic valvuloplasty.

The effects of balloon aortic valvuloplasty on orifice variability of the stenotic sclerocalcific aortic valve were evaluated by hemodynamic measurements of aortic valve function in 14 patients before balloon aortic valvuloplasty, during nitroprusside infusion before valvuloplasty, 48 h after valvuloplasty and during nitroprusside infusion 48 h after valvuloplasty. Aortic valve function was assessed by aortic valve area calculations with use of the Gorlin and Cannon formulas. Nitroprusside infusion before balloon aortic valvuloplasty caused no change in mean aortic valve gradient but a significant increase in mean aortic transvalvular flow from 186 +/- 46 to 202 +/- 61 ml/s (p less than 0.05), in Gorlin aortic valve area from 0.49 +/- 0.17 to 0.53 +/- 0.21 cm2 (p less than 0.05) and in Cannon aortic valve area from 0.45 +/- 0.18 to 0.49 +/- 0.22 cm2 (p less than 0.05). Nitroprusside infusion 48 h after valvuloplasty induced no change in mean aortic valve gradient but a significant increase in mean aortic transvalvular flow from 214 +/- 61 to 254 +/- 78 ml/s (p less than 0.005), in Gorlin aortic valve area from 0.71 +/- 0.25 to 0.83 +/- 0.32 cm2 (p less than 0.01) and in Cannon aortic valve area from 0.78 +/- 0.33 to 0.88 +/- 0.40 cm2 (p less than 0.05). Forty-eight hours after valvuloplasty, nitroprusside infusion induced a larger increase (40 +/- 40 ml/s) in mean transvalvular flow than before valvuloplasty (16 +/- 27 ml/s; p less than 0.05) and a larger increase (0.12 +/- 0.14 cm2) in Gorlin aortic valve area than before valvuloplasty (0.05 +/- 0.07 cm2; p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗