Regina Frayser

Studies of the Retinal Circulation in Man: Observations on Vessel Diameter, Arteriovenous Oxygen Difference, and Mean Circulation Time

By photographic techniques measurements have been made in the human retina of vessel size, arteriovenous oxygen difference across the retina, and mean retinal circulation time. By combination of these methods estimates can be made of relative changes in retinal blood flow rate and in the rate of oxygen delivery from the retinal vascular system. Observations are presented on the response of the normal and diseased retinal circulation to a variety of stimuli, particularly changes in blood oxygen and carbon dioxide tensions.

OBSERVATIONS ON THE EARLY ELEVATION OF SERUM POTASSIUM DURING RESPIRATORY ALKALOSIS

Respiratory alkalosis has been reported to cause both an increase and a decrease in serum potassium concentration, with the direction of the change depending upon the duration of alkalosis. Voluntary hyperventilation for 3 to 6 minutes has been found to cause an average increase of 0.5 mEq. per L. in the arterial serum potassium of normal subjects (1), but hyperventilation for 25 to 30 minutes causes a moderate fall in serum potassium (2-4). Over longer periods of time chronic passive hyperventilation was not found to produce a consistent change in arterial serum potassium in man (5), although it causes a drop in the serum potassium concentration of the dog (6, 7). The decrease in serum potassium concentration which eventually develops during respiratory alkalosis reflects the movement of potassium from an extracellular to an intracellular position as part of an ionic transfer which has the effect of buffering extracellular fluid (4, 6, 8). The initial increase in serum potassium during respiratory alkalosis does not have this effect and appears paradoxical. Because epinephrine can cause a transient rise in serum potassium, it has been suggested that the potassium rise during respiratory alkalosis may be mediated by secretion of epinephrine ( 1 ). It is the purpose of this report to describe some observations on the elevation of serum potassium during acute respiratory alkalosis, with particular attention to the early time-course of the changes, the source of the additional potassium, and the causative role of epinephrine.

Alterations in pulmonary diffusing capacity and pulmonary capillary blood volume with negative pressure breathing.

In 1915 Krogh first reported that the breathholding pulmonary diffusing capacity for carbon monoxide (DL) is increased during exercise (1). Although change in the volume of blood in the pulmonary capillary bed (Vc), as determined by change in DL, can be produced by several mechanisms, it is during exercise that the greatest changes are observed. Yet, in a previous investigation in which some of the physiologic changes of exercise were simulated, such as alterations in alveolar ventilation, alveolar volume, cardiac output, mixed venous Pco2, and mixed venous Po2, there was little change in breath-holding DL (2). Rosenberg and Forster (3), studying isolated cat lungs, concluded that the pressure across the walls of the pulmonary blood vessels is a primary factor in controlling the size of the pulmonary capillary bed as measured by DL. Observations by other investigators have agreed with this hypothesis (4). Breath-holding DL is increased by central venous engorgement with elevated pulmonary vascular pressure induced by pressure suit inflation (2, 5, 6). In addition, changes in gravitational orientation from the supine to erect position result in a small decrease in DL and Vc (7), which can be prevented by pressure suit inflation. Head-down tilt increases right atrial pressure and also increases DL and Vc (8). Atropine diminishes central venous pressure (9, 10) and pulmonary blood volume and decreases DL and Vc in

Tourniquet hyperpnea and its modification by agents which alter cerebral blood flow.

When CO2 is added to the inspired gas of a normal resting subject, the PCO2 of arterial blood rises quickly, but the ventilation rate increases gradually. The lag of ventilation behind change in arterial Pco2 has been ascribed to the time required for the tissues of the respiratory center to come into balance with the altered Pco2 of the perfusing blood (1-3). The response of ventilation to change in arterial Po2 is more prompt, presumably because the peripheral chemoreceptors are more richly perfused (2, 4-7). These relationships have been well established, but there is little information about factors which can affect the rate at which ventilation responds to a bloodborne stimulus. It is possible to produce an abrupt increase in arterial Pco2, as well as other arterial blood changes, by releasing tourniquets which have occluded blood flow through the legs for several minutes (8-11). A few seconds after the rise in arterial PCO2 begins, there is an abrupt increase in ventilation rate (Figure 1). It is found that the time of onset and the magnitude of this ventilation increase can be markedly altered by a variety of procedures which also have the common property of changing the rate of cerebral blood flow. It is, however, difficult to explain all of the observations satisfactorily in terms of our present understanding of the control of ventilation. It is the purpose of this report to present data on the production and modification of tourniquet hyperpnea with particular reference to apparent variations in the stimulus-response time of ventilation, and to speculate on the meaning of these data.

A COMPARATIVE STUDY OF INTRAPULMONARY GAS MIXING AND FUNCTIONAL RESIDUAL CAPACITY IN PULMONARY EMPHYSEMA, USING HELIUM AND NITROGEN AS THE TEST GASES

gas, a study was also made of the effect of substituting nitrogen for helium as the test gas in this procedure. The present report describes the results of these studies. In general, the results confirm the suspicion that the Darling method can significantly underestimate the functional residual capacity in advanced emphysema and indicate that the values obtained by the helium method are not dependent upon special properties of the test gas.

IN VIVO OBSERVATIONS ON THE PULMONARY CIRCULATION AND BLOOD OXYGEN SATURATION IN CATS FOLLOWING INTRAVENOUS INFUSION OF 15 PER CENT COTTON SEED OIL EMULSION.

* This work was supported (in part) by Research Grant H-4080 from the National Heart Institute, National Institutes of Health, U.S. Public Health Service and (in part) by U.S.A.F. contract 33(616)-8378 monitored by the Aerospace Medical Laboratory, Wright-Patterson Air Force Base, Ohio. In recent years attention has been focused on the relationship between high blood lipid levels and signs of tissue ischemia. Kuo and Joyner’ have found that .patients with coronary heart disease may have angina following a high fat meal. The angina and the associated electrocardiographic changes have been found to occur coincident with the peak of the plasma lipemic level 4 to 6 hours after ingestion of the high fat meal. Kuo, Whereat and Horwitz2 found a decreased arterial blood oxygen saturation in two patients with coronary disease and mild congestive failure. The arterial oxygen unsaturation occurred during the height of plasma lipemia and returned to normal levels following treatment and clearing of the lipemia. In another work Kuo