No abstract

Experiments on 12 anesthetized dogs were performed to study the effects of changes in blood volume on the pulsatile hemodynamics of the arterial system as seen from its input. Pressure and flow were measured in the ascending aorta under control conditions, after volume expansion with dextran 70 (+30% of estimated blood volume), and after hemorrhage (-15% of estimated blood volume). The input inpedance of the arterial system was calculated for each condition. It was found that after volume expansion the characteristic impedance of the proximal aorta, Zc, was decreased by 26.6 +/- 5.1% (SE) (P less than 0.01). After hemorrhage Zc was increased by 30.4 +/- 3.4% (P less than 0.01). Since it is well known that Zc is a very weak function of the mean arterial pressure, it is concluded that the changes in Zc seen with volume expansion or hemorrhage are caused mainly by changes in aortic smooth muscle activity. This conclusion is also supported by direct measurements of aortic pressure diameter relationships in earlier work from our lab.

Experiments were performed on eight anesthetized dogs to study the response of the characteristic impedance (Zc) of the main pulmonary artery to changes in circulating blood volume. Pressure and flow were measured in the proximal main pulmonary artery under control conditions, after hemorrhage (-15% of the estimated blood volume), again under control conditions, and finally after volume expansion (+30% of the estimated blood volume). Two different methods were used to determine Zc from these recordings. With the frequency-domain method values for Zc were obtained by averaging the input impedance moduli between 2 and 15 Hz. With the time-domain method Zc was derived as the slope of the early ejection pressure-flow relationship. The values for Zc obtained with the two methods were not statistically different. In the time-domain method the average increase in Zc with hemorrhage was 30.7 +/- 7.4 (SE) %, and the average decrease with volume expansion was -21.1 +/- 5.0 (SE) %. Because the time-domain method allowed the values of Zc during control conditions and after hemorrhage to be obtained in the same pressure range, it was concluded that the observed changes were caused by a change in the activity of the smooth muscle in the pulmonary arterial wall. Similarly, it was concluded that the decrease in Zc after volume expansion was active in nature.

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Strips of canine saphenous vein, inferior vena cava, and femoral artery were studied isometrically in vitro to compare quantitatively the α₁- and postsynaptic α₂-adrenoceptor contributions to the contractile force generated by l-norepinephrine (NE). Effects mediated by each receptor type were measured independently by quantitative blockade of virtually all α₁ -receptors with prazosin, or α₂-receptors with rauwolscine. Appropriate concentrations of the antagonists were calculated from dissociation constants previously determined by binding or competition with [³H]prazosin or [³H]rauwolscine in tissue homogenates. The contribution of α₁-adrenoceptors was larger than that of α₂-receptors in all vessels. The α₂-type was responsible for 38% of the maximum unblocked response to NE in saphenous vein, 32% in vena cava, and 28% in femoral artery. The occupation-response relationship for α₁-receptors was almost linear, without the marked upward convexity reported in some other vessels. α₂-Occupation-response curves were convex towards the occupation axis, with a relatively small response at low levels of occupation.