Adrenal Venous Flow Research Articles

The hemodynamics of adrenal veins with four-dimensional computed tomography using quantitative time-density curve: a study based on aldosteronism patients

Present study quantitatively analyzed adrenal venous flow using four-dimensional computed tomography (4D CT). We reviewed 4D CT images of 55 patients [mean age, 52 years ± 11 (standard deviation); 23 females] who underwent adrenal venous sampling between August 2017 and February 2021. Time–density curves were referred for the adrenal venous enhancement. The clinical factors affecting hemodynamics were assessed using uni- and multivariate linear regression analyses. The right and left adrenal veins (RAV and LAV, respectively) were visualized in all cases. Mean peak enhancement values in RAV and LAV were 247 ± 67 and 292 ± 70 Hounsfield units (P < 0.01), and were reached at 44.43 ± 6.86 and 45.39 ± 7.53 s (P < 0.01), respectively. The body mass index (BMI), plasma renin activity and potassium were significant factors influencing the peak enhancement of RAV blood flow [standardized regression coefficients, − 0.327 (P = 0.017), − 0.346 (P = 0.013), 0.426 (P = 0.016), respectively]. A linear relationship between sex and the time-to-peak was observed for RAV [standardized regression coefficient, 0.348 (P = 0.046)]. RAV had a lower contrast effect than LAV and reached its peak faster. BMI, plasma renin activity, and potassium were associated with flow density in RAV. Sex independently influenced the time-to-peak.

Converting Enzyme Inhibition Augments and Competitive Inhibition of Angiotensin II Partially Restores Reflex Adrenal Catecholamine Release in Anephric Dogs*

Adrenal epinephrine (E) release after hemorrhage in anesthetized dogs is blunted by acute nephrectomy and restored by angiotensin II infusion. In the present study, we report the effect of converting enzyme inhibition by SQ 20881, a decapeptide, and of competition inhibition of angiotensin II by saralasin (1-Sar-8-Ala-Ang-II) on reflexly stimulated adrenal release of E and norepinephrine (NE) in three groups of acutely anephric dogs. Aortic catheters and adrenal vein to femoral vein Silastic shunts were placed in dogs anesthetized with pentobarbital and mechanically ventilated. Adrenal secretion rates were calculated from adrenal vein to aorta catecholamine concentration differences divided by measured adrenal venous flow. Catecholamine concentrations were determined with trihydroxyindole technique. Blood samples were obtained before and 15, 30, and 60 min after rapid hemorrhage to a stable mean arterial pressure of 50 mm Hg. Saralasin infusion (10 microgram/kg/min) supported adrenal E release in anephric hemorrhaged dogs toward secretion rates comparable to those seen in intact dogs. Anephric SQ 20881 (approximately 0.5 microgram/kg) recipients had delayed (60 min) augmented adrenal E and NE release after hemorrhage. In resting animals not reflexly stimulated by hypovolemia, neither drug provoked adrenal E or NE release. These results suggest an agonist effect of saralasin on reflex adrenal E release and increased responsiveness of the stimulated adrenal medulla under the influence of converting enzyme inhibition.

Successful total adrenal autotransplantation into the spleen of dogs.

IN A RECENT communication from this laboratory 1 , a method of diversion of the adrenal venous effluent through the portal circulation of dogs by an adrenal venous-portal shunt was described. This method was based on the technique of Leeds et al 2 for transplantation of the adrenal gland. The method was not entirely satisfactory since it appeared that part of the adrenal venous flow entered the systemic circulation through collateral vessels rather than passing through the liver. In this report an improved method is described to completely divert the adrenal venous flow into the portal circulation. Although it has been abundantly demonstrated both experimentally and clinically that alteration by the liver of the biological activity of certain steroid hormones occurs, the blood pressure of dogs with Goldblatt hypertension was not appreciably altered when adrenal venous blood was diverted through the liver. 1 There were reservations, however, as to the completeness

Effects of the electrical stimulation of the central gray stratum of the midbrain on the blood and myocardial catecholamine.

Effects of the electrical stimulation of the central gray stratum of the midbrain on the blood and myocardial catecholamine were studied in 26 normal dogs anesthetized with intravenous injection of α-chloralose.(1) Blood pressure showed a biphasic pressor response consisting of a sharp rise with tachycardia during stimulation and a relatively slow elevation with bradycardia after stimulation.(2) The concentration of both arterial and adrenal venous catecholamine was determined simultaneously by the fluorimetric method. Adrenal venous catecholamines secretion increased most strikingly during stimulation. In the animal with the intact lumboadrenal veins both peripheral arterial norepinephrine and epinephrine levels elevated also immediately after stimulation. The arterial norepinephrine concentration when adrenal venous flow was separated from systemic circulation increased during stimulation, and the epinephrine level of the artery elevated immediately after stimulation.(3) The release of norepinephrine from the heart was confirmed by measuring the plasma norepinephrine level in bloods obtained simultaneously from the coronary sinus and femoral artery using coronary sinus catheterization under fluoroscopy.(4) The myocardial norepinephrine content increased significantly by stimulation, but the epinephrine level remained almost unchanged.A few possible explanation for these data was discussed.

Adrenocortical response during corrected and uncorrected hypercapnic acidosis.

Adrenal venous flow rate and cortisol synthesis have been measured in dogs subjected to hypercapnic acidosis before and after intravenous administration of 0.34 mm/kg of tris (hydroxymethyl) amino methane (THAM). A comparison was made of adrenal venous, peripheral venous, and arterial blood, pH, pCO2 and O2 saturation. During uncorrected hypercapnic acidosis the concentration of cortisol increased while adrenal venous flow rate decreased, but there was a significant increase in the minute output of cortisol. With the concomitant administration of 0.34 mM/kg THAM, adrenal venous flow rate doubled. However, since this enhanced flow rate was accompanied by a sharp reduction in cortisol secretion, the minute output of cortisol returned to control levels. The possibility of a direct effect of THAM on the adrenal vascular bed and synthetic processes is discussed. Throughout all the above experiments adrenal venous blood resembled arterial blood rather than peripheral blood in its pCO2, O2 saturation and pH.