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The input impedance of the main pulmonary artery in 26 pigs aged from 1 h to 2 weeks has been calculated from measurements of pressure and flow. From these data we have derived estimates of the hydraulic power output of the right heart. The impedance spectra were similar in form to those in many other studies and were consistent with the presence of a single reflection site within the lung. The frequency of the (single) minimum decreased steadily with increasing age as did the corresponding zero crossing point on the phase curve. From estimates of propagation velocity the position of this "reflection site" was found to coincide with the position of the lung periphery in each age group. An overall fall in characteristic impedance with increasing age was found to be due to the increasing diameter of the pulmonary artery rather than to changes in its elasticity. The total power output/body weight of the right heart fell from 10.4 to 4.8 mW X kg-1 from birth to 4 weeks of age. During this period the ratio of pulsatile to steady power fell from 0.5 to 0.31. We conclude that this fall is related to a reduction in the effective reflection of pressure and flow waves within the lung due to increasing attenuation and possibly to a reduction in the magnitude of the lumped reflection coefficient itself.

The contributions of the relative radius, relative wall thickness, incremental strain, incremental elastic modulus, and medial scleroprotein content to the static elastic properties of the rat aortic wall have been examined in three groups of rats. Controls, rats made hypertensive at four weeks of age, and rats whose blood pressure was lowered after 6 weeks hypertension, were studied. The results show evidence of adaptive changes in the aorta of hypertensive animals, and that irreversible alterations in the mechanical properties of the wall may be induced by a brief period of hypertension. A direct relationship between aortic medial scleroprotein content and the elastic properties of the wall is demonstrated.

The variation of radius with pressure was measured in vitro in the carotid artery of ten rabbits. Experiments were performed without prior conditioning of the vessel, over an inflation-deflation cycle at pressures in the range 0 to 24 kPa during treatment with, and in the absence of noradrenaline (referred to as active and passive conditions). The effect of a step change in pressure (2.7 kPa) on the radius of the vessel was investigated on a further three specimens. Under passive conditions, the variation of the static and the real part of the dynamic incremental elastic modulus with pressure and stress was similar during both inflation and deflation. Under active conditions a large degree of pressure-radius hysteresis was observed. At physiological pressures smooth muscle activity was associated with a decrease in elastic modulus when compared to passive values at the same pressure or stress. At a stress above 2 x 10(5) N.m-2 yield of the constricted vessels was observed and on further inflation and subsequent deflation the pressure radius curve was identical to that obtained under passive conditions. We suggest that conditioning a vessel, by means of repeated inflation to a high pressure and deflation to zero pressure, before measuring its elastic properties may give misleading results when applied to the vessels of living animals.

The propagation of a transient pressure impulse in a viscoelastic medium was investigated by experiments using water-filled latex rubber tubing and the aorta of anaesthetised dogs. A 5 ms pressure impulse was produced by the impact of a solenoid driven hammer. The propagation characteristics of the impulse (attenuation and propagation velocity) along the vessel were determined by means of a catheter-tip pressure manometer placed at various distances distal to the impulse generator. The presence of stenoses of varying degrees of severity resulted in reflection of the impulse and the appearance of reflected pulses whose magnitude depended on the stenotic severity. The experiments suggest that for the technique to be used in the detection of local reflecting sites such as might result from vascular occlusive disease, the lesions should occlude at least 70% of the lumen and should be no more than 0.20 m distal to the impulse generator.

The static elastic properties and structure of the intra-pulmonary arteries have been studied in pigs from fetal life to 4 months old, by radiographic and histological methods. During this period the average radius of the vessels examined varied from approximately equal to 0.9 mm at birth to 3.3 mm at the age of 4 months. The form of the pressure radius curves was similar to that observed in the systemic circulation and was characteristic of the gradual recruitment of collagen fibres with increasing pressure. In vessels near the hilum, wall thickness decreased from approximately equal to 180 microns to 100 microns during the first 2 weeks and thereafter increased to approximately equal to 250 microns. Throughout the lung and in all age groups there was a linear relationship between the logarithm of pressure strain elastic modulus (used as a measure of functional stiffness) and pressure. In contrast to the systemic arteries there was little change in functional stiffness towards the periphery, although the incremental elastic modulus (structural stiffness) did increase at sites further removed from the heart. During the first two weeks of life there was little change in functional stiffness (Ep approximately equal to 1.1 X 10(4) Nm2) although by 4 months Ep had increased by a factor of three. During this period despite fluctuations with age, an overall increase in structural stiffness was also observed (EINC approximately equal to 1 X 10(5) at 4 to 6 h to 2 X 10(5) Nm-2 at 4 months). The observations suggest that the changes in elasticity observed in early life are a consequence of the adaptation of the circulation to the lower pulmonary arterial pressure of extra-uterine life.

The static mechanical properties of the aorta have been examined in rats, aged between 4 weeks and 2 years. Internal radius, relative wall thickness, circumferential incremental strain, and circumferential incremental elastic modulus have been measured at pressures between 1.33 and 33.3 kPa (10 and 250 mm Hg). The results show that the value of the incremental elastic modulus does not change after 12 weeks. Changes observed in younger animals are related to alterations in relative wall thickness. The findings correlate with previously observed chemical and morphological changes. Studies of muscle function indicate that the smooth muscle of the media does not contribute significantly to the static elastic properties of the vessel wall.

The static elastic properties of the aorta ad systolic blood pressure in the caudal artery have been measured in 55 spontaneously hypertensive rats of the AS strain. Animals were divided into five groups and treated from the age of 4 to 12 weeks as follows: (1) 0.25 mm silver clip positioned around the right renal artery; (2) renal artery clipped as group (1) followed by daily injection of beta-aminopropionitrile fumarate (beta-APN); (3) daly injection of beta-APN without clipping; (4) daily injection of 0.09% saline; (5) untreated. Mean systolic blood pressures at 12 weeks of age were Group (1) 21.8; Group (2) 16.2; Group (3) 17.0; Group (4) 18.0; Group (5) 17.5 (units kPa). Thus, administration of beta-APN prevents the development of renal hypertension in clipped animals while producing no significant alteration in animals with intact renal arteries. At pressures within the physiological range the functional distensibility of all the treated animals was greater than that of the controls (pressure strain elastic modulus significantly lower). Similar changes were observed in the variation of structural distensibility (incremental elastic modulus) with pressure. At any level of total strain greater than 0.7 the incremental elastic modulus of both groups of animals treated with beta-APN was significantly less than control values. These observations are consistent with reports in the literature that administration of beta-APN causes a reduction in either the amount of cross-linked or normal scleroprotein in the aorta.

The static elastic properties and medial scleroprotein content of the aorta have been examined in spontaneously hypertensive rats (AS strain) aged 6 and 20 weeks (group SH). The results are compared with data from two previous studies on normal (group N) and induced hypertensive animals (group H). Spontaneous hypertension is associated with a relative increase in elastin and decrease in collagen when compared with the normal aorta. These changes are similar to, although smaller in magnitude than, those associated with induced hypertension. Elasticity measurements show that the functional stiffness (incremental strain) of the aorta in group SH is greater than normal. However, this difference diminishes with age, suggesting an adaptive response which tends to maintain the functional stiffness near to normal levels.

The arterial pressure wave, Pm, is composed of a forward travelling wave, Pf, and a backward travelling wave, Pb, resulting from partial reflection of PI at the peripheral beds. The magnitude of Pb depends on the degree of vasoconstriction. Total occlusion of the vessel distal to the pressure measurement site results in a wave which is equal to 2Pf. Subtraction of the derived Pf wave from Pm gives Pb, provided there is no re-reflection of Pb by proximal discontinuities. To test the validity of this total occlusion method for the determination of the components of Pm, measurements were carried out in an anaesthetised dog and the results compared with the method of Westerhof et al., (1972). The measurements were made at three arterial sites: 1. in the aorta just proximal to the junction of the renal artery; 2. at the termination of the aorta; and 3. in the femoral artery. The magnitude of Pb was varied by the infusion of vasoactive drugs. There was good agreement between the two methods at site 1 but at the other two sites the agreement was less good. It is shown that this is the result of re-reflection of the backward travelling waves produced by the occlusion at the aortic termination and the renal artery junction.