J. Eugene Millen

Pulmonary Mechanics during Pregnancy

Previously reported changes in static lung volumes during pregnancy have been confirmed. Measurements of lung compliance (C(L)) and total pulmonary resistance (R(L)) were made in 10 women in the last trimester of pregnancy and 2 months postpartum, employing an esophageal balloon and recording spirometer. C(L) was unaffected by pregnancy, but R(L) was 50% below normal during pregnancy. Measurements of airway conductance (C(A)) were made, employing the constant pressure body plethysmograph on 14 nonpregnant and 13 pregnant women. Specific airway conductance was increased during pregnancy. Serial measurements of C(A) indicated a progressive increase beginning at about 6 months of gestation and a return to normal by 2 months postpartum. The mechanism of the increased C(A) during pregnancy is not known. It may be related to changes in bronchial smooth muscle tone and conceivably explains the tolerance of certain patients with lung resections to pregnancy.

Arterial constrictor response in a diving mammal

Angiograms were obtained in the harbor seal, Phoca vitulina, in air and during diving. During diving there is arterial constriction of the vascular beds of muscle, skin, kidney, liver, spleen, and presumably of all vascular beds except those perfusing the brain and heart. There is sudden constriction and narrowing of muscular arteries close to their origin from the aorta. Constriction of small arterial branches is so intense that blood flow is essentially lost in all involved organs.

Circulatory Adaptation to Diving in the Freshwater Turtle

The heart of the freshwater turtle has a functional ventricular septal defect. In ambient air there is some shunting of blood from the left to the right ventricle through the defect. During prolonged diving or N2 inhalation, the shunt is reversed and blood from the tissues bypasses the lung and enters the aorta directly. This adaptation appears to be based on the exclusive use of anaerobic glycolysis as an energy source during prolonged diving.

Intrathoracic pressure, pulmonary vascular pressures and gas exchange during pulmonary lavage

Intrathoracic pressure, blood pressures of intrathoracic vascular structures (central venous, mean pulmonary arterial, pulmonary- “capillary” (wedge) and left ventricular end-diastolic pressures) and Para were measured as a function of pulmonary lavage in a patient, three dogs and a calf. Instillation of liquid in a single lung leads to an increase in intrathoracic pressure generated by the hydrostatic pressure of the liquid column used fur instilling the liquid. The blood pressures of intrathoracically located vessels increase as a result of the increased intrathoracic pressure und as a result of an acute mediastinal shift away from the liquid-filled lung. There is loss of perfusion to liquid-filled alveoli because of increased alveolar pressure. As a result, Pao2 is increased, since pulmonary blood flow is shifted to non-liquid-filled (ventilated) alveoli. Drainage of the lung causes a reduction of Pao2 because of restoration of perfusion to nonventilated (collapsed) alveoli.

Ion and macromolecular transport in the alveolar macrophage

Abstract 1. 1. Some aspects of Na+, K+, Cl− and macromolecular transport have been studied in isolated rabbit alveolar macrophages. Steady-state intracellular concentrations in Ringers solution (pH 7.4) were as follows: Na+, 83 ± 7.1 (S.E.); K+, 75 ± 13.2 ; Cl, 59 ± 4.1 mequiv/kg cell water. Cl− is rapidly and completely lost from the cell in Cl−-free media suggesting rapid thermodynamic equilibrium between intracellular and extracellular phases. 2. 2. Na+ efflux has two rate constants (rapid phase 636 ± 302 (S.D.); slow phase 329 ± 125 mequiv/kg cell water per h). It appears that this cell has high permeability for Na+ and the high leak down the electrochemical gradient requires a high rate of active transport. Thermodynamic considerations suggest that the major energy source for active Na+ transport is derived from oxidative phosphorylation. 3. 3. Classical relatively high molecular weight extracellular markers are excluded from cell water. However, ferritin (mol. wt. 465000) influx is rapid with intracellular/extracellular concentrations greater than 1.0 within 3 min. Ferritin efflux is exceedingly slow so that there is essentially unidirectional transport. Simultaneous exposure of cells to both ferritin and dextran leads to no measurable increase in cellular dextran uptake suggesting high specificity for ferritin uptake.

Dissociation of bradycardia and arterial constriction during diving in the seal Phoca vitulina.

Bradycardia associated with diving in the harbor seal has been dissociated from the arterial constrictor response by intracardiac pacing. Development of arterial constriction does not depend upon the development of bradycardia. During pacing, arterial constriction continues in the absence of bradycardia. Increases in heart rate to values greater than 120 beats per minute during a dive produce a progressive decrease in mean aortic pressure, which suggests that one major function of bradycardia is to reduce cardiac output, thus matching left ventricular output to the restricted vascular bed and decreased venous return associated with diving.

Humoral agent from calf lung producing pulmonary arterial vasoconstriction.

Saline washings obtained in vivo from the lung of young calves produce pulmonary hypertension upon intrayascular (systemic or pulmonary) injection into either the dog or the calf. This pulmonary hypertension is produced by vasoconstriction of small, precapillary pulmonary vessels. The active agent, pulmonary arterial constrictor substance, differs chemically and physiologically from other substances which have been investigated with respect to vasomotor activity in the pulmonary circulation. Although the chemical nature of the active agent is not known it appears to have a relatively large molecular weight. Whether this agent plays a role in the physiological regulation of the pulmonary circulation is not known.

Histamine Receptor and Prostaglandin Synthetase Blockers in Ethchlorvynol-Induced Pulmonary Edema in Canines

The injection of ethchlorvynol intravenously in humans and animals causes an increased permeability form of pulmonary edema. The proximate cause for this increased alveolar capillary membrane permeability is unknown but humoral mediators such as histamine and prostaglandins could play a role. To determine whether these agents were a factor in the altered permeability, we employed the saline-filled dog lung model and measured the flux of albumin across the alveolar capillary membrane. Following the intravenous injection of ethchlorvynol, there was a marked increase in permeability which was not altered by treatment with H1 and H2 receptor blockers or a prostaglandin synthetase inhibitor. We conclude that histamine and prostaglandins play no role in the increased permeability associated with ethchlorvynol injection.