Determination of arterial compliance in vivo has long interested physiologists. Most current methods for estimating this parameter assume that compliance is constant, i.e., that arterial pressure-volume (P-V) relations are linear, and they also assume that diastolic aortic pressure decay is an exponential function of time. Both of these assumptions, however, are questionable. This study proposes improved methods of estimating compliance based on a Windkessel model of the arterial system but which utilize the area under the pressure tracing rather than the waveform itself. Formulations accounting for both linear and three hypothetical nonlinear arterial P-V relations (exponential, logarithmic, and parabolic) are presented. Data from patients with congestive heart failure and hypertension are used for illustration. Compliances assuming linear P-V relations are reasonably close to those assuming nonlinear P-V relations only at mean aortic pressure. At end-diastolic pressure the linear assumption underestimates and at peak systolic it overestimates the compliances obtained assuming nonlinear P-V relations. The simpler linear assumption still allows a first approximation to compliance, but we show that existing methods for obtaining compliance under this assumption have severe theoretical as well as practical shortcomings. Our proposed method avoids these shortcomings primarily because deviations from an exact exponential form of the pressure wave have less influence on these compliance estimates than currently used methods.

Differences in aortic impedance between normotensives and hypertensives are not well characterized. We examined impedance in 8 normotensive and 11 hypertensive (mean 96.7 vs. 122.2 mmHg) age-matched, Chinese patients undergoing cardiac catheterization at rest, during nitroprusside, and handgrip exercise before and after beta blockade (propranolol). Hypertensives had higher resistance (2,295 vs. 1713 dyn-s/cm5), characteristic impedance (145.7 vs. 93.9 dyn-s/cm5), total external power (1,579 vs. 1174 mW), peripheral reflections (ratio of backward to forward wave components of 0.54 vs. 0.44), and first zero crossing of impedance phase angle (4.15 vs. 2.97 Hz). These abnormalities were eliminated with vasodilatation. Differences between groups were not further exacerbated when pressure was increased during handgrip exercise. Beta blockade further increased resistance and reflections. Thus, hemodynamic abnormalities of essential hypertension (increased resistance, reflections, and pulse wave velocity, and decreased compliance) are compatible with an increased vasomotor tone that is further unmasked during generalized beta blockade.

(Circulation 1989;79:854-862)

A B S T R A C T The late photoproducts that result from the isomerization of rhodopsin have been identified in the isolated all-rod retina of the skate by means of rapid spectrophotometry. The sequence in which these intermediates form and decay could be described by a scheme that incorporates two pathways for the degradation of metarhodopsin II (MII) to retinol: one via metarhodopsin III (MIII) and the other (which bypasses MIII) through retinal. Computer simulation of the model yielded rate constants and spectral absorbance coefficients for the late photoproducts which fit experimental data obtained at temperatures ranging from 7°C to 27°C. Comparing the kinetics of the thermal reactions with the changes in rod threshold that occur during dark adaptation indicated that the decay of MII and the fall in receptor thresholds exhibit similarities with regard to their temperature dependence. However, the addition of 2 mM hydroxylamine to a perfusate bathing the retina gready accelerated the photochemical reactions, but had no significant effect on the rate of recovery of rod sensitivity. It appears, therefore, that the late bleaching intermediates do not control the sensitivities of skate rods during dark adaptation. I N T R O D U C T I O NSpectrophotometry o f the isolated vertebrate retina has shown that after a photically induced isomeric change in its c h r o m o p h o r e , the rhodopsin molecule degrades thermally t h r o u g h several short-lived intermediates to metarhodopsin II (MII). T h e latter decays, in turn, at a much slower rate to other photoproducts before the c h r o m o p h o r e is hydrolyzed from the protein moiety (opsinj and reduced to the relatively colorless retinol (vitamin A); at this stage, rhodopsin is said to have "bleached."T h e reactions that follow the formation of MII take place too long after photic exposure to be involved in the initial transduction process. However, D o n n e r and Reuter (1967, 1968) have suggested that one or m o r e o f the late photoproducts is responsible for regulating the sensitivity of the rod mechanism during the initial phase of the dark-adaptation process; i.e. the relatively rapid changes in threshold that occur independently of rhodopsin regeneration (Dowling, 1963). T h e nearly linear relation between the fall in log threshold and the exponential decay o f intermediates with ~-max ~-" 380 nm (i.e. MII and retinal) led them to the conclusion that these substances have a p r o f o u n d desensitizing effect on the

SUMMARY We studied the effect of nitroprusside on the hydraulic vascular load of the right and left ventricle in seven patients with severe left ventricular failure. At doses of 0.25-0.75 ,ug/kg/min, stroke volume increased progressively from 40.1 to 48.6 ml and left ventricular end-diastolic pressure decreased from 24.5 to 11.2 mm Hg. Accompanying this improvement in left ventricular performance were doserelated decreases in mean ventricular pressures, pulmonic and systemic resistances and the lower-frequency components of input impedance moduli. Characteristic impedance and both total and oscillatory external power were decreased in the pulmonic, but not the aortic, vasculature. We sought to determine the mechanism and magnitude of right ventricular unloading and the dose-response relationship of right relative to left ventricular hydraulic unloading with nitroprusside in patients with severe left ventricular failure. A primary concern was whether this agent, in doses just sufficient to produce a measurable alteration in systemic resistance and left ventricular performance, had a primary effect on right ventricular load through a direct effect on pulmonary vascular resistance and impedance. Methods PatientsWe studied patients with severe, chronic left ventricular failure from various causes. Clinically overt left ventricular congestive heart failure was manifested by pulmonary vascular congestion on chest x-ray, ventricular gallop sounds and recent history of both dyspnea and shortness of breath at rest. Patients who were scheduled to undergo diagnostic cardiac catheterization were asked to participate in the study. Any patient with suspected valvular or congenital heart disease was excluded. From this population, 20 patients were entered into the study after they gave informed consent.