B. A. Waaler

Dynamics and dimensions of cardiac output changes in humans at the onset and at the end of moderate rhythmic exercise.

1. An improved Doppler ultrasound technique was used to measure stroke volume (SV) and cardiac output (CO) on a beat‐to‐beat basis in a group of supine humans before, during and after periods of standardized, rhythmic exercise, involving the quadriceps muscle groups on both sides. The development of CO on such bouts of exercise was compared to Doppler ultrasound records of the simultaneous femoral arterial flow (FF) response. 2. Records of CO at rest revealed spontaneous fluctuations around a mean level, with differences between the minimal and maximal values of the order of 1 l min‐1. The mean CO level at rest again varied considerably from one day to another and from test run to test run. 3. Upon start of exercise an immediate and rapid increase in heart rate (HR) and CO took place. The entire increase, the size of which varied appreciably from test run to test run, was completed within 10‐15 s. No or only minor changes were seen in the mean SV level during the exercise periods. 4. The time course of the increase in FF was indistinguishable from that of the increase in CO, which occurred without any detectable delay relative to the changes in FF. These closely parallel developments indicate a tight regulatory coupling between the two types of flow changes. 5. In the majority of tests the total and two‐sided increase in FF seen in the steady‐state situation in the last part of an exercise period was significantly larger than the recorded increase in CO. This discrepancy implies that some redistribution of flow from tissues other than the working muscles might take place, even at this moderate level of work. 6. Upon the end of exercise a striking but transient increase in CO occurred, resulting from an increase in SV concomitant with a maintained HR. In the course of five to eight post‐exercise cardiac cycles about 100 extra milliliters of blood were expelled from the heart. This cardiac outflow overshoot was found to occur during a post‐exercise fall in mean arterial blood pressure (MAP).

Effects of prostaglandin E1 and adrenaline on the pulmonary vascular resistance (PVR) in isolated rabbit lungs

Abstract Injections of from 1 to 50 μg of prostaglandin E 1 (PGE 1 ) almost invariably, caused vasodilatation in the pulmonary vascular bed of an isolated rabbit lung preparation. The same effect was usually obtained by injections of from 0.5 to 50 ωg of adrenaline. On a weight basis the two substances were about equally potent as pulmonary vasodilators, but large individual variations in responses were seen. Addition to the perfusate of adrenergic α- and β-inhibitors (phentolamine and propranolol, respectively), in doses high enough to abolish the responses to adrenaline, did hardly affect the responses to PGE 1 . The two substances do apparently have different sites of action in the rabbit pulmonary vascular bed.

Bradykinin and Pulmonary Vascular Permeability in Isolated Blood-Perfused Rabbit Lungs

Bradykinin causes a marked vasodilatation in most areas of the systemic circulation. In the pulmonary vascular bed of various species, however, bradykinin seems to cause vasoconstriction, as is shown by several investigators (Lecomte and Troquet, 1960; Gersmeyer and Spitzbarth, 1961; Klupp and Konzett, 1963; Hauge et al., 1964). Another important effect of bradykinin in systemic vascular areas is the increase in capillary permeability, which has been demonstrated by various techniques. Kjellmer and Odelram (1965) found that a marked and irreversible edema might develop in skeletal muscle on intravascular administration of bradykinin. We have been interested in the possible effect of intravascularly administered bradykinin on permeability of the small vessels in the lung, since vasoconstriction is the response of some larger pulmonary vessels to this substance. The problem related to such a permeability effect seemed to be of considerable practical, as well as theoretical, interest.