No abstract

Regional heterogeneity of lung blood flow can be measured by analyzing the relative dispersion (RD) of mass (weight)-flow data. Numerous studies have shown that pulmonary blood flow is fractal in nature, a phenomenon that can be characterized by the fractal dimension and the RD for the smallest realizable volume element (piece size). Although information exists for the applicability of fractal analysis to pulmonary blood flow in whole animal models, little is known in isolated organs. Therefore, the present study was done to determine the effect of blood flow rate on the distribution of pulmonary blood flow in the isolated blood-perfused canine lung lobe by using fractal analysis. Four different radiolabeled microspheres (141Ce, 95Nb, 85Sr, and 51Cr), each 15 microns in diameter, were injected into the pulmonary lobar artery of isolated canine lung lobes (n = 5) perfused at four different flow rates (flow 1 = 0.42 +/- 0.02 l/min; flow 2 = 1.12 +/- 0.07 l/min; flow 3 = 2.25 +/- 0.17 l/min; flow 4 = 2.59 +/- 0.17 l/min), and the pulmonary blood flow distribution was measured. The results of the present study indicate that under isogravimetric blood flow conditions, all regions of horizontally perfused isolated lung lobes received blood flow that was preferentially distributed to the most distal caudal regions of the lobe. Regional pulmonary blood flow in the isolated perfused canine lobe was heterogeneous and fractal in nature, as measured by the RD. As flow rates increased, fractal dimension values (averaging 1.22 +/- 0.08) remained constant, whereas RD decreased, reflecting more homogeneous blood flow distribution. At any given blood flow rate, high-flow areas of the lobe received a proportionally larger amount of regional flow, suggesting that the degree of pulmonary vascular recruitment may also be spatially related.

The aim of this study was to determine the relationship of pulmonary vascular resistance (PVR) hysteresis and lung volume, with special attention to the effects of ventilation around closing volume (CV). Isolated, blood-perfused canine left lower lung lobes (LLL) were incrementally inflated and deflated. Airway and pulmonary artery pressures (PAP) were recorded after each stepwise volume change. Constant blood flow was provided (600 ml/min) and the pulmonary vein pressure (PVP) was held constant at 5 cm H2O. PAP changes, therefore, were a direct index of PVR changes. Group 1 lobes underwent a full inflation from complete collapse to total lobe capacity (TLC) followed by a full deflation. Group 2 lobes underwent two deflation/inflation cycles, after an initial full inflation. These cycles, both beginning at TLC, had deflation end above and below CV, respectively. Significant PVR hysteresis was noted when the first inflation and deflation were compared. The maximum difference in PAP on deflation was 3.3 cm H2O or 11%. The mean decrease was 2.7 cm H2O for 18 lobes (p < 0.0001). The PAPs on all subsequent inflations or deflations that began above CV remained 9% lower than the initial inflation (n = 9, p < 0.0001), but were not different from each other. However, the final inflation which began from below CV resulted in a 30% return of PVR hysteresis (mean increase in PAP of 0.8 cm H2O, n = 7, p < 0.004). We conclude that there is hysteresis in the PVR response during ventilation, with decreased PVR during deflation relative to the initial inflation, that this hysteresis is absent when lung volume is maintained greater than CV, and that hysteresis returns when inflation occurs after deflation below CV.

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Coronary vascular resistance during whole-body hypocapnia was studied in anesthetized dogs in which coronary blood flow (CBF) was monitored from a catheter-tip flow meter. Intravascular placement of this flow meter did not require opening the chest and avoided possible coronary denervation. Rapid flow meter response permitted determination of coronary vascular resistance during late diastole when vascular compression during systole does not affect the calculation. With rate and depth of ventilation held constant, hypocapnia was induced by a rapid change of the ventilating gas from 95% 0,-5% CO, to 100% 0,. Within 30 sec of the change to 100% 0, and prior to any change in mean arterial blood pressure (AP), late diastolic coronary vascular resistance (LDR) decreased from 2.04 * 0.26 to 1.44 t 0.20 mm Hg/ml/min. LDR remained below control throughout the hypocapnic period while AP decreased from 122 2 7 to 1 1 1 t 7 mm Hg and CBF was unchanged. P-Adrenergic blockade with propranolol eliminated the decrease in LDR seen during hypocapnia prior to block, AP was unchanged, and CBF decreased from 36 * 8 to 27 t 7 ml/min. The decrease in LDR during hypocapnia was reversed following combined aand P-adrenergic blockade with propranolol plus dibenamine and LDR increased from 0.90 t 0.14 to 2.27 t 0.85 rnm Hg/mVmin. After combined block, CBF decreased from 78 k 8 to 53 * 8 mumin by 3 min of hypocapnia and AP increased from 84 t 19 to 108 t 16 mm Hg by 264 0037-9727/80/ 100264-07$0 1 .OO/O