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The action of the ichthyotoxic secretion of the Red Sea flatfish Pardachirus marmoratus and its derived toxin, pardaxin, was examined in the dogfish shark (Squalus acanthias). Pardaxin was more toxic when administered to the bathing medium than when injected into a dorsal artery and it transiently diminished the spiracular rate and caused a severe struggling response in the adult shark only when administered to the head region of the shark. Pardaxin caused a transient leakage to urea and sodium between the shark and the seawater. In the isolated perfused rectal gland pardaxin irreversibly reduced the rate of chloride secretion and concentration gradient of urea between perfusate and rectal gland fluid. In addition, ultrastructural studies on the rectal gland showed that ionic lanthanum penetrated the tight junctions and foci of cell necrosis were observed. These studies indicate that in shark the gills are the most probable target of the toxicity of pardaxin.

In epithelia that secrete sodium chloride, high-conductance tight junctions between cells have been proposed as the primary pathway for transepithelial sodium flux. We examined the properties of tight junctions in the perfused rectal gland of the dogfish shark during basal secretion and following adenosine 3',5'-cyclic monophosphate stimulation of sodium chloride secretion. Freeze-fracture electron microscopy revealed extensive interdigitation of adjacent cells with an associated amplification in the length of tight junctions per area of luminal surface, averaging 102 +/- 4.7 m/cm2 in outer regions of 80 +/- 6.7 in inner regions of the gland. Marked heterogeneity of junctional structure was present with junctional elements varying from single strands to three duplex elements and junctional depth varying from 15 to 60 nm. In glands perfused with lanthanum chloride, ionic lanthanum filled the intercellular space up to but not through the tight junctions. Characteristics of tight junctions were not different during basal and maximally stimulated sodium chloride secretion. These studies define tight junctions in the rectal gland as an anatomical barrier capable of restricting the passage of relatively small molecules such as urea while providing a greatly amplified junctional area for the passive diffusion of sodium and water.

Three unusual cases are described which demonstrated hypomagnesemia and symptoms resembling magnesium deficiency syndrome. The hypomagnesemia was most likely secondary to urinary losses from diuresis following release of post-renal obstruction and renal homotransplantation. Heretofore, this association has not been described. Case 1 was unique because of the post-obstructive diuresis in the face of marked renal impairment. Case 2 is noteworthy because of the profound hypomagnesemia, 0.4 mEq/1, and because of the development of congestive heart failure. The rapid improvement noted in cardiac function with magnesium replacement suggests a relationship to magnesium deficiency.

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 N(2) 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.

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.

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.

A method is described for the measurement of total body exchangeable oxygen stores (TBO(2)). It is based on the dilution of the stable oxygen isotope, (18)O(2), by the body exchangeable oxygen stores under circumstances in which (18)O(2) steady-state equilibrium was evaluated simultaneously for both arterial and venous blood compartments. After evaluation of several simplifying assumptions, TBO(2) values in dog, normal man, and anemic patients were measured. The magnitude of the exchangeable nonlung oxygen stores was 11.0 +/- 3.1 ml/kg (SD) in 5 dogs, 11.9 +/- 2.1 ml/kg in 10 normal subjects, and 7.0 +/- 1.6 ml/kg in 8 patients with severe anemia (hematocrits of 25% or less).

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.