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Biomedical subjects

B Silke

Publications and source records attributed to B Silke.

At least 73 records · Page 4Linked to original sources
PubMed1993

Haemodynamic comparison of amlodipine and atenolol in essential hypertension using the quantascope.

1 We have utilised a non-imaging echo-Doppler cardiac output device, using the principle of attenuated compensation volume flow (ACVF), to assess the cardiovascular effects of amlodipine and atenolol over 3 months in 24 patients with essential hypertension. 2 Both amlodipine and atenolol, at 4 and 12 weeks, similarly reduced mean arterial pressure (12 weeks amlodipine -12.6 mmHg, atenolol -14.9 mmHg; P < 0.01 for each vs baseline). 3 The heart rate fell on atenolol, both at 4 weeks (amlodipine -3 vs atenolol -12 beats min(-1); P < 0.05) and 12 weeks (-1 vs -11 beats min(-1); P < 0.05), without change on amlodipine. 4 Stroke volume initially rose on atenolol without change on amlodipine (4 weeks amlodipine -1.3 ml vs atenolol +10.1 ml; P = 0.05) but between drug effects were not different at 12 weeks. 5 The systemic vascular resistance was reduced on amlodipine (12 weeks: amlodipine -176 dyn s cm(-5): P < 0.05) without change on atenolol (atenolol -48 dyn s cm(-5): NS). 6 The cardiac stroke work was lowered on amlodipine both at 4 weeks (P < 0.01) and 12 weeks (P < 0.05) and statistically different from the unaltered atenolol values at both time points. 7 Skin nutrient flow or fingertip temperature was not altered by either treatment. 8 These results are consistent with contrasting mechanisms of action--vasodilator for amlodipine and decreased cardiac pumping for atenolol. The greater reduction in cardiac stroke work on amlodipine compared with atenolol warrants further investigation during longer-term studies.

Amlodipine↗
PubMed1993

Cardiotonic actions of selective phosphodiesterase inhibitors in rat isolated ventricular cardiomyocytes.

1. The contractile effects of the novel cardiotonic agent HN-10200 (2-[3-methoxy-5-methylsulphinyl-2-thienyl]-1H-imidazo-[4,5-c]-p yri dine hydrochloride), were examined and comparisons made with the responses obtained to a structurally similar compound, sulmazole, and to a number of other compounds which are known to inhibit phosphodiesterase (PDE) isoenzymes with differing selectivities; namely, enoximone (PDE III inhibitor), Ro 20-1724 (PDE IV inhibitor) and 3-isobutyl-1-methylxanthine (non-selective PDE inhibitor). 2. Contractile function, as measured by mechanical shortening, and biochemical systems involving cyclic AMP were investigated in ventricular cardiomyocytes isolated from adult Sprague-Dawley rats (200-250 g). 3. HN-10200 exerted a concentration-dependent (10(-8) M-10(-4) M) positive contractile effect, which was independent of alpha- or beta-adrenoceptor, or histamine receptor stimulation. 4. The efficacies of the contractile responses to the PDE inhibitors were of the order: HN-10200 > IBMX > sulmazole > enoximone and maximum stimulations, which were obtained at concentrations of 10(-4) M, were 54 +/- 4%, 41 +/- 7%, 38 +/- 7% and 26 +/- 5% (mean +/- s.e.) greater than basal levels, respectively (n = 6); the basal value of contractile amplitude (dL), in the absence of PDE inhibitors was 7.39 +/- 0.18% (mean +/- s.e.). Ro 20-1724 did not have any effect on contractile activity. 5. Due to low basal levels of cyclic nucleotides in isolated cells, accumulation of cyclic AMP due to the presence of the PDE inhibitors was detected only when the levels of cyclic nucleotide were enhanced with forskolin (10 microM). 6. The PDE inhibitors increased levels of cyclic AMP only at concentrations> 10-4 M. HN-10200 and sulmazole had similar concentration-dependent profiles for the accumulation of cyclic AMP; their potencies were lower than that of IBMX (concentrations of forskolin required to increase cyclic AMP by 4 pmol mg-1 protein, in the presence of maximum concentrations of the PDE inhibitors, were 13 +/- 311M, 14 +/- 3 JAM and 3 +/- 0.6 JAM [mean +/- s.e.], respectively).7. These results indicate that a similar mechanism, probably through a weak inhibition of the cyclic AMP-specific PDE isoenzymes, is responsible for the increase in levels of cyclic AMP by HN-10200 and sulmazole. However, cyclic AMP is only partially responsible for the positive contractile effect of HN-10200 and, similarly, sulmazole and IBMX. The lack of apparent increase in levels of cyclic AMP by enoximone, highlights its degree of selectivity for the PDE III isoenzyme, such that the PDE IV isoform is still present in sufficient quantity to degrade cyclic AMP within the cell. On the other hand,the potent action of Ro 20-1724 on accumulation of cyclic AMP, in addition to the lack of effect on contractile function, is in agreement with the selectivity of this compound for the PDE IV isoenzyme and compartmentalization of cyclic AMP in rat isolated ventricular cardiomyocytes.

4-(3-Butoxy-4-methoxybenzyl)-2-imidazolidinone↗
PubMed1992

A double-blind, parallel-group comparison of flosequinan and enalapril in the treatment of chronic heart failure.

The effects of flosequinan and enalapril on exercise capacity (bicycle exercise duration), quality-of-life symptomatology (visual analogue scales) and New York Heart Association (NYHA) grading, were compared in 61 patients with chronic heart failure (NYHA, grade III). Bicycle exercise duration improved similarly with flosequinan (+27%) and enalapril (+18%); in patients completing the study, flosequinan produced a significantly greater increase in exercise time at week 12, compared with enalapril (P = 0.02). Improvements in visual analogue scores relating to general health, energy and vitality, ability to perform physical activities and breathing performance, were equivalent for both drugs. Changes in NYHA classification showed that 27 (55%) of 49 patients completing the study had improved by at least one NYHA grade (15 (68%) patients on flosequinan; 12 (44%) on enalapril). The overall safety and tolerability of the two treatments was similar; 18 patients reported adverse effects while on flosequinan, compared with 19 patients on enalapril. Neither treatment was associated with any clinically important changes in haematological or biochemical variables, although some treatment-related effects were observed. This study confirms that flosequinan achieved similar efficacy to enalapril in the symptomatic relief of chronic heart failure. The effect of flosequinan on survival in chronic heart failure has not been tested; pending such studies, our data suggest that it may prove a useful alternative therapy in patients where ACE inhibitors are contraindicated or poorly tolerated.

Adult↗
PubMed1992

Modulation of inotropic therapy by venodilation in acute heart failure: a randomised comparison of four inotropic agents, alone and combined with isosorbide dinitrate.

The effects of four inotropic agents with differing ancillary properties [a cardiac glycoside (digoxin), a combined alpha- and beta-adrenergic agonist (dobutamine), a beta-adrenergic agonist (prenalterol), and a phosphodiesterase inhibitor (amrinone)] alone and with subsequent addition of isosorbide dinitrate were compared in 48 consecutive acute myocardial infarction patients with radiographic and haemodynamic (pulmonary artery occluded pressure greater than 18 mm Hg) left ventricular failure. All agents with the exception of dobutamine reduced the elevated left heart filling pressure; only digoxin and dobutamine augmented the cardiac stroke volume index. All drugs except digoxin reduced the SVRI; an arteriolar constrictor response was evident 60 min after digoxin and a tachycardia resulted after combined alpha- and beta- and beta-adrenergic stimulations (dobutamine and prenalterol, respectively). The addition of isosorbide dinitrate reversed the inotrope-induced elevations of systemic arterial pressure and resulted in additional reductions in left heart filling pressure. These data suggest that, in the absence of substantial venodilator properties in an inotropic compound, reduction in elevated left heart filling pressure is not achieved with inotropic therapy alone in acute left ventricular failure and combining a venodilator may be haemodynamically advantageous.

Adult↗
PubMed1992

Comparison of antihypertensive and lipid actions of terazosin and atenolol in essential hypertension.

Terazosin is a selective alpha 1-adrenoceptor antagonist; its actions on the serum lipoprotein profile were compared with those of the cardioselective beta-adrenoceptor antagonist atenolol in 40 patients with mild to moderate hypertension. Atenolol and terazosin were titrated over six weeks until blood pressure control (diastolic blood pressure less than 90 mmHg or greater than 10 mmHg fall in blood pressure) or a maximum dose of atenolol 100 mg or terazosin 10 mg had been achieved. Patients not controlled were then prescribed additional diuretic therapy (cyclopenthiazide 0.5 mg and potassium 1200 mg). At each visit blood pressure and adverse events were recorded; plasma lipids were measured at baseline, six and 12 weeks. During titration there was a linear decrease in systolic (-29 mmHg on atenolol and -24 mmHg on terazosin) and diastolic blood pressure (-17 and -12 mmHg) in both groups without subsequent change over the next six weeks; atenolol reduced heart rate (-11 bpm) without change on terazosin. During the initial six weeks the total cholesterol fell in both groups; however, there were significant between-treatment differences in triglyceride responses with a fall on terazosin and a rise on atenolol. Comparing atenolol and terazosin over the total 12 week study (irrespective of thiazide treatment) increased triglyceride levels and reduced cholesterol ratios and HDL were demonstrated on atenolol, contrasting with reduced triglyceride levels and elevated HDL and cholesterol ratios of terazosin.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Antagonists↗
PubMed1992

Vasodilator therapy for acute heart failure: haemodynamic comparison of hydralazine/isosorbide, alpha-adrenoceptor blockade, and angiotensin-converting enzyme inhibition.

Haemodynamic comparison of three vasodilation regimens [intravenous (i.v.) hydralazine and isosorbide dinitrate (ISDN) combined, i.v. doxazosin, and i.v. enalaprilat] was undertaken in 36 patients with acute left ventricular (LV) failure due to recent myocardial infarction. Each regimen achieved similar reductions in pulmonary artery occluded pressure (PAOP, preload) and systemic arterial pressures (afterload), with increased cardiac and stroke volume (SV) indexes (p less than 0.01). Only the hydralazine and isosorbide combination induced resting tachycardia. Balanced vasodilatation after selective alpha-adrenoceptor blockade (doxazosin) and angiotensin-converting enzyme (ACE) inhibition (enalaprilat) without increase in heart rate (HR) suggests that these therapies may have definite haemodynamic advantages over the hydralazine/ISDN combination.

Adrenergic alpha-Antagonists↗
PubMed1991

Hemodynamic interactions of a new beta blocker, celiprolol, with nifedipine in angina pectoris.

The hemodynamic consequences of blockade at both beta-adrenoceptors and slow calcium channels is of therapeutic importance for patients with angina pectoris. The hemodynamic interaction of a new cardioselective beta blocker, celiprolol, and nifedipine was examined in an acute hemodynamic study using three prospectively matched groups with angiographically confirmed coronary artery disease (n = 10/group). Patients were randomly allocated to intravenous celiprolol (8 mg), sublingual nifedipine (20 mg), or their combination. Rest and exercise (supine bicycle) hemodynamics were determined before and following each therapy. At rest, celiprolol did not alter pumping function; nifedipine reduced diastolic blood pressure and systemic vascular resistance index (SVRI), with a small increase in heart rate. Combination therapy reduced systemic arterial pressure and SVRI; heart rate and cardiac stroke volume index increased. During exercise celiprolol tended to reduce heart rate and cardiac index; nifedipine reduced exercise SVR and cardiac stroke work indices. Combination therapy reduced all components of blood pressure; cardiac stroke work and SVR indices fell. These hemodynamic data suggest that beta blockade with celiprolol may result in a slight depression of cardiac pumping during exercise; however, such effects are offset by the vasodilating actions of nifedipine (reflex sympathetic action offsetting cardiodepression). Thus the acute hemodynamic effects of this combination were seemingly safe in these patients; the longer term effects during maintained therapy should be further assessed.

Adrenergic beta-Antagonists↗
PubMed1991

Dobutamine stress testing in chronic heart failure--dose-response effects assessed by echo-Doppler.

In patients with cardiac failure, data on haemodynamic function at rest may indicate impaired cardiac function but do not assess the capacity of the heart to respond to stress which may be useful in determining prognosis. Inotropic challenge with dobutamine has been shown to be at least as effective as exercise testing in assessing cardiac pumping capability. One of the limitations of dobutamine stress testing has been the need for invasive haemodynamic measurements. A new non-imaging echo-Doppler cardiac output device, incorporating the principle of attenuated compensation volume flow (ACVF), has been shown to be accurate, reproducible and useful in pharmacodynamic studies. In this study we examined the dose-response effects of dobutamine in 8 patients with chronic heart failure. Dobutamine was infused at 2, 5, 10 and 15 micrograms/kg/min with the dose being increased at 5 minute intervals and haemodynamics being determined (using the echo-Doppler) in the final 2 minutes of infusion. Our results were comparable to previous studies. There were dose-related increases in heart rate (P less than 0.05), cardiac output (P less than 0.05), and cardiac power output (work done by the heart per unit time) (P less than 0.05). Systolic blood pressure increased (P less than 0.001) and there were modest increases in mean arterial blood pressure without change in diastolic blood pressure. Time averaged mean velocity increased significantly with a trend to increase in flow acceleration. Three patients developed arrythmias during the early recovery period. The echo Doppler attenuated compensated volume flow method of determining haemodynamics proved useful but in view of the high incidence of dysrhythmia we feel that dobutamine testing in severe heart failure should be employed cautiously.

Aged↗
PubMed1990

An exercise hemodynamic comparison of verapamil, diltiazem, and amlodipine in coronary artery disease.

A prospective, randomized study compared the effects of equivalent intravenous doses of three slow calcium-channel blockers (verapamil, diltiazem, and amlodipine) on rest and exercise haemodynamics in 30 ischemic heart disease patients. Following a stable control period during which rest and exercise (supine bicycle) hemodynamics were assessed, equivalent hypotensive doses of each compound were administered over 20 minutes and rest/exercise parameters were assessed 10 minutes later. At rest all agents similarly reduced systemic blood pressure; the fall in systemic vascular resistance and the increase in cardiac indices was ranked: amlodipine greater than diltiazem greater than verapamil. The heart rate increase for amlodopine differed from verapamil and diltiazem (+19.4% vs. +1.5% vs. -7%; p less than 0.01). On exercise, similarly greater falls in the systemic vascular resistance index followed amlodipine, compared with verapamil and diltiazem (p less than 0.05). Only amlodipine significantly reduced the exercise pulmonary artery occlusion pressure (PAOP). Exercise cardiac stroke volume improved after diltiazem and amlodipine. In terms of cardiac performance, both amlodipine and diltiazem produced an improvement, whereas verapamil depressed cardiac pumping activity. Thus, hemodynamic differences between slow-calcium-channel blocking drugs may be demonstrated in humans. These differences would be compatible with a predominant peripheral vascular site of action for amlodipine, in contrast with mixed cardiac and peripheral sites for diltiazem and verapamil.

Amlodipine↗
PubMed1990

How does posture influence the haemodynamic assessment of a cardiovascular drug? Experience with nicardipine.

The extent to which posture altered the haemodynamic response to slow calcium channel blocker nicardipine was evaluated in 22 male patients with angiographically confirmed coronary artery disease. Patients were randomly allocated to supine or upright posture and an otherwise identical protocol performed in each group. At rest, following a control saline period, four doses of the drug (log cumulative dosage: 1.25, 2.5, 5.0, and 10.0 mg) were administered by i.v. infusion over a total period of 40 min; haemodynamic indices were recorded during the 3-5 min following each 5 min infusion. The exercise effects of the drug, in each posture, were determined by comparison of a control predrug exercise with observations at the same workload following the maximal cumulative dose. Nicardipine reduced resting mean blood pressure (MBP) and systemic vascular resistance index (SVRI) in both postures, the decrease being more pronounced when upright (MBP, -12%, -18%; p less than 0.01: SVRI, -30%, -46%; p less than 0.01). The increases in cardiac index (CI) and stroke volume index (SVI) were higher when upright (29 and 54% vs. 10 and 27%; p less than 0.01). Pulmonary artery occluded pressure (PAOP) increased by 29% when upright, without change when supine. On exercise, the effects for HR, MBP, CI, SI, and SVRI responses were independent of posture; however, a qualitative difference was apparent for PAOP (-17% vs. +14%; p less than 0.05). Thus, although the actions of nicardipine were qualitatively similar, quantitative differences related to posture were confirmed. These differences appeared to relate to posture-related baseline haemodynamic differences between the groups but with similar postnicardipine absolute values.

Adult↗
PubMed1990

Haemodynamic and radionuclide effects of amlodipine in coronary artery disease.

1. The haemodynamic and radionuclide effects of a new long-acting slow-calcium channel blocking agent, amlodipine, were evaluated in 32 patients with coronary artery disease. 2. Haemodynamic measurements in 24 patients were made at rest and 10 to 15 min after 20 mg i.v. amlodipine. Amlodipine significantly reduced systemic arterial blood pressure and vascular resistance index with an increased heart rate and augmented cardiac index. Cardiac stroke volume index rose and stroke work fell without change in pulmonary artery occluded pressure (PAOP). 3. The exercise effects were determined by comparison of measurements during 4 min of supine bicycle exercise at a fixed workload before and after drug treatment. During dynamic exercise, amlodipine reduced systemic arterial pressure and vascular resistance index. Exercise cardiac index, stroke volume index and heart rate were higher. The left ventricular filling pressure was significantly reduced. 4. Radionuclide parameters were studied in 16 patients at rest and on exercise; ejection fraction was unaltered following amlodipine. 5. Pre-therapy haemodynamic values correlated with response following amlodipine for resting mean blood pressure, systemic vascular resistance and exercise PAOP. 6. Thus, the immediate impact of amlodipine in stable coronary artery disease was to reduce left ventricular afterload and thereby improve cardiac pumping performance.

Adult↗
PubMed1990

Pharmacodynamic monitoring during acute intervention in ischaemic heart disease using a new echo-Doppler device.

1. We have utilised a new non-imaging echo-Doppler cardiac output device, using the principle of attenuated compensated volume flow (ACVF), to assess the cardiovascular effects of atenolol and buccal nitroglycerin (NTG) in a placebo-controlled study of 30 patients with coronary disease. 2. Atenolol (4 mg i.v.) reduced heart rate, cardiac output and time-averaged mean aortic velocity (P less than 0.01) and increased systemic vascular resistance (P less than 0.01). 3. Buccal NTG (5 mg) reduced systemic mean arterial pressure (P less than 0.01), cardiac stroke volume (P less than 0.05) and stroke length (P less than 0.01). 4. Thus although both drugs reduced time-averaged aortic velocity (an index of cardiac performance), the concomitant reduction in cardiac stroke length and tachycardia suggested sub-optimal cardiac filling for buccal NTG, whereas for atenolol (with the associated increased systemic vascular resistance but unchanged stroke length) attenuation of sympathetic stimulation at cardiac beta-adrenoceptors. 5. The ACVF method of cardiovascular monitoring should prove useful in human pharmacodynamic studies.

Adult↗
PubMed1990

Haemodynamic dose-response effects of UK-52,046 in ischaemic disease with or without impaired left ventricular function.

1. The haemodynamic effects of a new cardioselective postsynaptic alpha 1-adrenoceptor antagonist UK-52,046, were evaluated in 25 patients with stable coronary disease, with or without impaired left ventricular function. At rest the haemodynamic effects to two dose-response regimens were determined. In an initial eight patients 0.125, 0.125 and 0.25 micrograms kg-1 were administered peripherally at 15 min intervals; the haemodynamic measurements were determined between 10 to 15 min after each dose. In a further 17 patients, the dose regimen was doubled yielding a cumulative dose-regimen of 0.25, 0.5 and 1.0 micrograms kg-1. The exercise effects were determined by comparison of measurements during 4 min of supine sub-maximal bicycle exercise at a fixed workload before and after drug treatment. 2. At rest, the lower dose regimen of UK-52,046 significantly reduced systemic mean arterial blood pressure (-5 mm Hg; P less than 0.05) and increased cardiac index (+0.2 l min-1 m-2, P less than 0.01). The higher dose regimen of UK-52,046 reduced systemic mean arterial blood pressure (-7 mm Hg; P less than 0.01), pulmonary artery occluded pressure (PAOP) (-2 mm Hg, P less than 0.01) and vascular resistance index (-314 dyn s cm-5 m2; P less than 0.05) with an increase in heart rate (+7%, P less than 0.05) and cardiac index (+0.2 l min-1 m-2, P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Antagonists↗
PubMed1990

The electrocardiogram as a tool for therapeutic monitoring: a critical analysis.

The authors review the scientific value of electrocardiographic studies and discuss the limitations that arise from variability in technology and in standards of recording and interpretation. A consistent recording procedure and objective assessment using standardized diagnostic criteria are required, particularly in multicenter studies. Tricyclic antidepressants depress cardiac conduction at therapeutic concentrations; therefore a comparison with the electrocardiographic profile of sertraline, a specific serotonin reuptake inhibitor with antidepressant activity, was made. In four studies, sertraline was compared with placebo, with amitriptyline or placebo, and with amitriptyline alone. There were decreases in RR interval and increases in PR, QRS, and QTC intervals with amitriptyline but no effect with sertraline. Thus, sertraline had no demonstrable effects on intraventricular conduction or electrocardiographic time intervals.

1-Naphthylamine↗
PubMed1990

Comparison of central and peripheral haemodynamic effects of dilevalol and atenolol in essential hypertension.

A new non-imaging echo-Doppler cardiac output device that works on the principle of attenuated compensation volume flow (ACVF), has been used to assess the cardiovascular effects of atenolol and dilevalol in 24 patients with essential hypertension. Compared with the baseline, one month of atenolol reduced systemic mean arterial blood pressure (12 mmHg; P less than 0.01), heart rate (-24 bpm; P less than 0.001), aortic velocity integral (-2.1 cm/sec; P less than 0.01) without a change in cardiac output or systemic vascular resistance. Dilevalol reduced systemic mean arterial pressure (-12 mmHg; P less than 0.01) and heart rate (-13 bpm; P less than 0.01), without a change in cardiac output or aortic velocity integral; systemic vascular resistance fell (-149 dyne/sec; P less than 0.01). Thermography and skin thermal clearance techniques were used to assess the effects of each compound on the peripheral circulation; both compounds reduced skin temperature and thermal clearance but the changes were more marked for atenolol than dilevalol. These results suggest that the mechanism of action of dilevalol is, in part, different from atenolol and would be compatible with a direct vasodilator action on the peripheral vasculature.

Analysis of Variance↗
PubMed1989

Hemodynamic assessment of nicardipine alone and with atenolol in coronary artery disease using a modified echo-Doppler device.

We have used a modified noninvasive echo-Doppler cardiac output device, based on the principle of attenuated compensation volume flow, to assess the cardiovascular effects of the slow-calcium antagonist nicardipine in coronary disease. The dose-response effects of 2.5, 5.0 and 10.0 mg intravenous nicardipine were determined in 8 patients with angina. Dose-related decreases were seen in systemic mean arterial pressure (p less than 0.01) after administration of nicardipine. Cardiac pumping indexes were improved, as evident from linear increases in cardiac stroke volume (p less than 0.001), stroke length (p less than 0.01) and time-averaged mean velocity (p less than 0.01). The echo-Doppler device was also used to assess beta-blocking/nicardipine combination therapy in patients with angina. When nicardipine was given after the cardioselective beta blocker atenolol the reduction in heart rate and cardiac output after atenolol was reversed compared with a group that received atenolol followed by placebo. Cardiac performance improved and the 35% reduction in systemic vascular resistance was associated with markedly increased cardiac index (p less than 0.01), augmentation of time-averaged mean velocity (p less than 0.01) and cardiac stroke length (p less than 0.05). These data are consistent with previous invasive studies of nicardipine, either alone or when combined with beta blockade in coronary disease. The data also suggest that nicardipine/beta-blocking combination is safe in patients with coronary heart disease and that the echo-Doppler method of cardiovascular monitoring will prove useful in human pharmacodynamic studies.

Adult↗
PubMed1989

Effects of nicorandil on left ventricular hemodynamics and volume at rest and during exercise-induced angina pectoris.

The hemodynamic effects of nicorandil (20 mg) were compared with placebo in a double-blind study of 20 patients with angiographically proved coronary artery disease at rest before and 7, 15, 30 and 60 minutes after oral dosing. The impact of the drug on left ventricular (LV) hemodynamics and volume during exercise-induced angina was determined by repeating exercise 60 minutes after drug administration, at the same work load that reliably induced angina during control predrug exercise. At rest, nicorandil reduced all components of systemic arterial pressure without change in cardiac or stroke volume indexes or heart rate. Pulmonary artery occluded pressure was reduced without change in LV ejection fraction or systemic vascular resistance index. Effects were evident at 7 minutes and peaked at 30 minutes with attenuation at 60 minutes. Compared with control supine bicycle exercise, the drug (at 60 minutes) reduced mean systemic arterial pressure and LV filling pressure without change in cardiac stroke volume indexes and heart rate. There was a smaller increase in LV ejection fraction. These data suggested greatest impact on LV function during exercise when substantial decreases in filling pressure occurred at maintained cardiac pumping indexes.

Adult↗