Maternal blood pressure and fetal ultrasonography in normal baboon pregnancies

Pregnancy in baboons is characterized by lower systolic, diastolic, and mean blood pressures than in the nonpregnant state. As pregnancy progresses, diastolic and mean pressures tend to increase whereas systolic pressure remains low. Sonographic measurements of fetal growth follow a sigmoid pattern, but their increase in relation to length of gestation approximates a straight line between 6 and 21 weeks of gestation (23 to 84% of term).     

Performance characteristics of conditioned blood pressure elevations in the baboon

Operant conditioning of diastolic blood pressure elevation was accomplished in six baboons (Papio sp.) by a procedure using food delivery when diastolic pressure was maintained above a prespecified level, and shock delivery when diastolic pressure remained below that level. Data from steady-state performance indicated a rise in diastolic pressure by a median 22 mm Hg when the daily session was begun. Elevated levels of diastolic blood pressure and low shock frequencies were maintained throughout the 12-hour session. The frequency and duration of shifts in diastolic pressure to below criterion level were found to be variable during the first 1–2 hours but were stable throughout the remainder of the session. Heart rate had a phasic temporal pattern over the 12-hour session, characterized for most subjects by a rate increase at session onset followed by a rate decrease. Analysis of individual performance records showed that the blood pressure increases could occur without concomitant elevations in heart rate.This research was supported by grant No. 2R01HL17958-05 from the National Heart, Lung, and Blood Institute. The authors wish to thank J. V. Brady and I. Iversen for helpful editorial suggestions.     

Airway mechanics, gas exchange, and blood flow in a nonlinear model of the normal human lung

Amodel integrating airway/lung mechanics, pulmonary blood flow, and gasexchange for a normal human subject executing the forced vital capacity(FVC) maneuver is presented. It requires as input the intrapleuralpressure measured during the maneuver. Selected model-generated outputvariables are compared against measured data (flow at the mouth, changein lung volume, and expired O₂ and CO₂concentrations at the mouth). A nonlinear parameter-estimation algorithm is employed to vary selected sensitive model parameters toobtain reasonable least squares fits to the data. This study indicatesthat 1) all three components of the respiratory model arenecessary to characterize the FVC maneuver; 2) changes in pulmonary blood flow rate are associated with changes in alveolar andintrapleural pressures and affect gas exchange and the time course ofexpired gas concentrations; and 3) a collapsible midairway segment must be included to match airflow during a forced expiration. Model simulations suggest that the resistances to airflow offered bythe collapsible segment and the small airways are significant throughout forced expiration; their combined effect is needed toadequately match the inspiratory and expiratory flow-volume loops.Despite the limitations of this lumped single-compartment model, aremarkable agreement with airflow and expired gas concentration measurements is obtained for normal subjects. Furthermore, the modelprovides insight into the important dynamic interactions betweenventilation and perfusion during the FVC maneuver.

     

Hemodynamic, gas exchange, and hormonal consequences of LBPP during PEEP ventilation

Hemodynamic, gas exchange, and hormonal response induced by application of a 25- to 40-mmHg lower body positive pressure (LBPP), during positive end-expiratory pressure (PEEP; 14 +/- 2.5 cmH2O) were studied in nine patients with acute respiratory failure. Compared with PEEP alone, LBPP increased cardiac index (CI) from 3.57 to 4.76 l X min-1 X m-2 (P less than 0.001) in relation to changes in right atrial pressure (RAP) (11 to 16 mmHg; P less than 0.01). Cardiopulmonary blood volume (CPBV) measured in five patients increased during LBPP from 546 +/- 126 to 664 +/- 150 ml (P less than 0.01), with a positive linear relationship between changes in RAP and CPBV (r = 0.88; P less than 0.001). Venous admixture (Qva/QT) decreased with PEEP from 24 to 16% (P less than 0.001) but did not change with LBPP despite the large increase in CI, leading to a marked O2 availability increase (P less than 0.001). Although PEEP induced a significant rise in plasma norepinephrine level (NE) (from 838 +/- 97 to 1008 +/- 139 pg/ml; P less than 0.05), NE was significantly decreased by LBPP to control level (from 1,008 +/- 139 to 794 +/- 124 pg/ml; P less than 0.003). Plasma epinephrine levels were not influenced by PEEP or LBPP. Changes of plasma renin activity (PRA) paralleled those of NE. No change in plasma arginine vasopressin (AVP) was recorded. We concluded that LBPP increases venous return and CPBV and counteracts hemodynamic effects of PEEP ventilation, without significant change in Qva/QT. Mechanical ventilation with PEEP stimulates sympathetic activity and PRA apparently by a reflex neuronal mechanism, at least partially inhibited by the loading of cardiopulmonary low-pressure reflex and high-pressure baroreflex. Finally, AVP does not appear to be involved in the acute cardiovascular adaptation to PEEP.     

Modelling inert gas exchange in tissue and mixed-venous blood return to the lungs

Inert gas exchange in tissue has been almost exclusively modelled by using an ordinary differential equation. The mathematical model that is used to derive this ordinary differential equation assumes that the partial pressure of an inert gas (which is proportional to the content of that gas) is a function only of time. This mathematical model does not allow for spatial variations in inert gas partial pressure. This model is also dependent only on the ratio of blood flow to tissue volume, and so does not take account of the shape of the body compartment or of the density of the capillaries that supply blood to this tissue. The partial pressure of a given inert gas in mixed-venous blood flowing back to the lungs is calculated from this ordinary differential equation. In this study, we write down the partial differential equations that allow for spatial as well as temporal variations in inert gas partial pressure in tissue. We then solve these partial differential equations and compare them to the solution of the ordinary differential equations described above. It is found that the solution of the ordinary differential equation is very different from the solution of the partial differential equation, and so the ordinary differential equation should not be used if an accurate calculation of inert gas transport to tissue is required. Further, the solution of the PDE is dependent on the shape of the body compartment and on the density of the capillaries that supply blood to this tissue. As a result, techniques that are based on the ordinary differential equation to calculate the mixed-venous blood partial pressure may be in error.