The American journal of physiology
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To investigate the role of autonomic reflexes in stroke-work optimization, we studied ventriculoarterial coupling in unanesthetized dogs with the autonomic system intact and blocked. Ventricular contractility was quantified by the slope of the end-systolic pressure-volume relation, ventricular elastance (Ees). Arterial system properties were quantified by the ratio of end-systolic pressure to stroke volume, arterial elastance (Ea). ⋯ After autonomic blockade, Ees tended to decrease during nitroprusside and increased during angiotensin II infusion in parallel with changes in Ea, so that the Ea-to-Ees ratio did not change from baseline as much as it did with the autonomic system intact. Again, the left ventricle maintained nearly 90% of its maximal stroke work. Thus, over a wide range of afterload, stroke work was kept near its theoretical maximum, independent of autonomic neural regulation.(ABSTRACT TRUNCATED AT 250 WORDS)
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We studied the effect of nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthase (NOS) inhibitor, on the increases in cerebral blood flow (CBF) elicited by stepwise elevations in arterial partial pressure of CO2 (PaCO2) from normocapnia up to 204 mmHg. Rats were anesthetized with halothane and ventilated. CBF was monitored over the parietal cortex using a laser-Doppler flowmeter. ⋯ Reduction of resting CBF (-50 +/- 4%; n = 6) by administration of chloralose (20-40 mg/kg i.v.) did not attenuate the CBF response to hypercapnia (P > 0.05). We also found that the attenuation by L-NAME of resting CBF (n = 5) and of the cerebrovasodilation elicited by hypercapnia (n = 6) has a relatively slow time course, the effects reaching a maximum 45-60 min after intravenous administration of the drug. We conclude that L-NAME does not attenuate the CBF response to CO2 uniformly at all levels of hypercapnia.(ABSTRACT TRUNCATED AT 250 WORDS)
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Clinical Trial Controlled Clinical Trial
On the fractal nature of heart rate variability in humans: effects of data length and beta-adrenergic blockade.
In the present study, we reinvestigated the question of whether human heart rate variability (HRV) is fractal in nature. Ten healthy volunteers participated in either of two studies conducted while beat-by-beat long-term HRV (8,500 heartbeats) was recorded for 2-3 h in the quiet, awake state in the supine position. In the first study, five subjects were tested four times each to evaluate the basic fractal nature of human HRV. ⋯ With propranolol, these basic properties of fractal HRV dynamics remained unchanged despite an increase in the mean RR interval (placebo, 912 +/- 111 ms; propranolol, 1,134 +/- 133 ms, P < 0.05) and a change in the harmonic spectral shape evaluated by LF/HF (placebo, 2.76 +/- 1.57; propranolol, 1.82 +/- 0.81, P < 0.05). For short-term data, less power was extracted as fractal because of the absence of the very low frequency component, yet the beta and LF/HF were unchanged from long-term data. These findings indicate that 1) the observed inversely proportional frequency (1/f) spectrum in human resting HRV is due to underlying random fractal dynamics and 2) the sympathetic nervous system seemed to play a minor role in modulating the fractal HRV dynamics.
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To determine whether direct ventricular interaction affects right ventricular (RV) relaxation, we compared the minimum rate of change of RV pressure (dP/dtmin) and the time constant, tau, of isovolumic RV pressure decline in open-chest, anesthetized pigs following a normal left ventricular (LV) contraction and an acutely unloaded LV contraction. Rapid removal of blood via the LV apex into a prosthetic ventricle during a single systole decreased the LV pressure-time integral 68.3% and peak systolic pressure 49.9% without changing RV end-diastolic conditions. Micromanometers measured ventricular chamber pressures during single RV isovolumic beats, which were produced by transient pulmonary artery occlusion in both the control and the LV-unloaded states. ⋯ Simultaneously, RV dP/dtmin decreased from -400.5 +/- 136.6 to -288.3 +/- 46.8 mmHg/s, P = 0.14 (pericardium intact), and -342.4 +/- 104.2 to -241.2 +/- 118.9 mmHg/s, P < 0.01 (pericardium opened). These data indicate that LV systolic unloading decreases the rate of RV relaxation. We conclude that RV relaxation is influenced by direct anatomic ventricular interaction.
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Myocardial O2 uptake (MVO2) and related variables were compared in right and left ventricles (RV and LV, respectively) during isovolemic hemodilution (HD) alone and combined with isoproterenol (Iso) infusion in 13 isoflurane-anesthetized open-chest dogs. Measurements of myocardial blood flow (MBF) obtained with radioactive microspheres were used to calculate MVO2. Lactate extraction (Lacext) was determined. ⋯ Higher MVO2 was satisfied by combination of increased MBF and O2 extraction in RV and by increased MBF alone in LV. Lacext remained consistent with adequate myocardial O2 delivery throughout study. Conclusions were that 1) both RV and LV tolerated extreme HD (Hct = 10%) because blood flow reserves were sufficient to fully compensate for reduced arterial O2 content; 2) significant cardiac reserve was evident during HD, which could be recruited Iso; and 3) because increase in MVO2 in RV caused by Iso in presence of HD was partially satisfied by increased O2 extraction, the absence of augmented O2 extraction during HD alone was not due to impaired release of O2 from diluted red blood cells.(ABSTRACT TRUNCATED AT 250 WORDS)