76 



HANDBOOK OF PHYSIOLOGY 



CIRCULATION I 



Plasma sodium and total solute concentration tended 

 to decline slightly. James and associates (62) gave 

 12% dextran (Commercial Solvents Corporation) 

 to 16 children with the nephrotic syndrome. The pa- 

 tients recei\ed 300 to 400 ml/ m- of body surface area 

 daily or on alternate days. All save one lost weight. 

 A decrease of serum sodium and potassium was seen. 

 There was a decrease of total serum osmolarity. 

 Water, sodium and chloride diuresis were produced. 

 Glomerular filtration rate increased significantly in 

 two of four instances. Renal plasma flow (CPAH) 

 increased markedly in all .seven instances where de- 

 termined. Michie and associates (77) gave si.x patients 

 1000 ml of 3 "^i modified fluid gelatin (Knox) daily 

 intravenously for 6 days. There were no important 

 variations in glomerular filtration rate or renal plasma 

 flow. The Tm PAH was increased in two and un- 

 changed in four. Michie & Ragni (76) gave human 

 subjects 1000 ml of 6% dextran intravenously daily 

 for 6 days. Renal function studies were made before 

 and 4 days after the last infusion. The maximal tubu- 

 lar excretion of para-aminohippurate was significantly 

 depressed in 2 of 5 patients with normal kidneys and 

 in 3 of 4 patients with pre-existing renal disease. 

 Fleming and associates (29) studied 13 patients who 

 received from 500 to 1500 ml of 6 per cent dextran 

 intravenously. There were no marked changes in 

 glomerular filtrationrate, tubular excretory mass, or in 

 para-aminohippurate clearance. Gowdey & Young 

 (38) infused 6 % dextran in normal saline intra- 

 venously at a rate of i ml per kg per min into dogs. 

 Progressive decreases of glomerular filtration rate and 

 renal blood flow were produced by the infusion. The 

 ratio of renal blood flow to cardiac output fell con- 

 sistently and was as low as 50% of control. The dex- 

 tran infusion invariably caused a diuresis, but when 

 cardiac failure occurred there was a marked decrease 

 in urine flow and occasionally anuria. The authors be- 

 lieved that hypoxia produced by dextran-induced 

 anemia caused renal vasoconstriction, thus producing 

 a redistribution of blood to other vascular beds. 



Hemodynamic Effects 



The hemodynamic effects produced by dextran 

 infusions in normovolemic and oligemic man and 

 animals have been of great interest. Witham and 

 associates (116) gave 500 ml of 6% dextran intra- 

 venously to five human subjects at a rate of 25 ml/ 

 min. Ten minutes after the infusion the subjects were 

 found to have an average increase in cardiac outjiut 



of 38"^; and comparable increase of stroke volume, 

 but little change in heart rate. The mean pulmonary 

 arterial pressure rose an average of 6 mm Hg. Pul- 

 monary wedge pressure ro.se in two subjects in whom it 

 was measured. Systemic venous pressure rose in two 

 subjects where it was measured. Hematocrits fell in 

 each instance. Two .subjects studied showed no change 

 in vital capacity. The venous pressure rose less than 

 the pulmonary arterial pressure. Fleming & Bloom 

 (30) made further studies of the hemodynamic effects 

 of dextran infusion in normal human subjects. Sixteen 

 patients received 1000 to 1500 ml of 6 '^v or 12% dex- 

 tran intravenously at a rate of 25 ml/niin. The cardiac 

 output increased in 13 of the 16; in 10 subjects the 

 increase averaged 44%; in the other 3 the increases 

 were small. There was no correlation between right 

 atrial or pulmonary arterial pressure rise and the in- 

 crease of cardiac output. The highest peripheral 

 venous pressure increase was associated with no 

 change in cardiac output. The pulmonary arterial 

 pressure increased in all 8 subjects where measured, 

 the mean increase being 11.5 mm Hg. The right 

 atrial pressure increased in all 10 subjects studied 

 and remained elevated in 8 of the 10 during the study 

 period of 22 to 120 min. The pulmonary wedge pres- 

 sure increased between 7 and 15 mm Hg in 5 pa- 

 tients studied. Pulmonary vascular resistance did not 

 change. The hematocrits fell, showing that plasma 

 volume expansion occurred. Systemic blood pressure 

 rose an average of i 7 mm Hg. The pressures were still 

 elevated at i hour. Systemic arterial pulse pressure in- 

 creased an average of 8.3 mm Hg. 



Werko (113) infused dextran into 20 normal sub- 

 jects and 25 patients with heart disease, 15 of whom 

 had mitral stenosis. Dextran was given as a 6 '/c solu- 

 tion at a rate of 25 ml/ min; normal subjects received 

 the infusion for 60 min; the subjects with heart dis- 

 ease were infused for 30 to 50 min. The infusion was 

 interrupted if the pulmonary arterial pressure rose 

 rapidly. Normal subjects shovsed at first progressive 

 increa.se in blood volume with increases of right atrial 

 mean pressure and pulmonary arterial mean pressure, 

 but with constant cardiac output. With greater ex- 

 pansion of blood volume, average cardiac outputs 

 and stroke outputs were increased 31 % and 20% re- 

 spectively. In 7 subjects, however, increa.ses of right 

 heart filling pressure of 4 to 12 mm Hg were associated 

 with cardiac output changes of less than 15%. There 

 was no consistent relationship between right heart 

 filling pressure and stroke volume, cardiac output, or 

 right ventricular stroke work. Similar changes were 

 seen in the patients witli heart disease, except tliat in 



