Renal vascular system in right heart overload with varying circulatory compensation.
To determine the characteristics of renal vascular system adaptation to venous congestion, the right heart overload was induced in 32 puppies by surgical narrowing of the pulmonary trunk. The animals were followed up over the period as long as 2 years. Twenty-three puppies showed compensation of the functionally overloaded right heart ventricle. The signs of circulatory decompensation with exudative processes in the pericardium, thoracic and abdominal cavities were recorded in 9 animals. Ten dogs of the appropriate age were used as control. During experiments, all group animals underwent measurements of blood pressure in the skipping vein. After sacrifice the arteries, veins and renal glomerules were examined histologically, stereometrically and morphometrically. It has been established that in compensated stenosis of the pulmonary trunk, venous pressure rises 1.6-fold while in decompensated stenosis more than 2-fold. Compensated stenosis is associated with the adaptation hyper tone of the renal arteries and appearance of the bundles of oblique-longitudinal smooth muscle cells in the intima of some of the arteries. In venous hypertension this protects the renal glomerules from blood overload and prevents the development of gross sclerotic lesions in their capillary loops. In decompensated stenosis, such adaptation reactions are appreciably weaker and are marked by less pronounced pressor reaction of the arteries and lower development in them of the intimal musculature, which does not correlate with the level of hemodynamic disorders and pressure rise in the venous section of the greater circulation of the experimental animals. This leads to congestive hyperemia of the renal glomerules and subsequent development of noticeable sclerotic lesions in these structures.
Novikov
Iu V
IuV
Chair of Surgery and Topographic Anatomy, Chair of Urology, Yaroslavl State Medical Academy, Yaroslavl, Russia.
Shormanov
I S
IS
D000222:Adaptation, Physiological; D000818:Animals; D003097:Collateral Circulation / Q000502:physiology*; D003326:Coronary Circulation / Q000502:physiology; D004285:Dogs; D007668:Kidney / Q000098:blood supply* / Q000473:pathology; D011666:Pulmonary Valve Stenosis / Q000503:physiopathology; D012079:Renal Circulation / Q000502:physiology; D018497:Ventricular Dysfunction, Right / Q000503:physiopathology*