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HANDBOOK OF PHYSIOLOGY 



CIRCULATION II 



provide an important safeguard against abnormal 

 accumulations of capillary nitrate in the interstitial 

 fluid compartment. 



D. Functional Changes of Capillary Blood Pressure 



Hemorrhage and local application of epinephrine 

 produced vasoconstriction in the frog's mesentery 

 and reduced capillary blood pressure as shown in 

 the lowermost curves of figure 2.4 (198). In man the 

 marked vasoconstriction and cessation of blood flow 

 found in Raynaud's disease reduced capillary blood 

 pressure in the affected digits to between 5 and 8 

 mm Hg, i.e., to levels approaching local venous 

 pressure (204). During the hyperemia of recovery, 

 pressures in these same capillary loops rose rapidly 

 to between 32 and 45 mm Hg. In normal subjects, 

 however, local cooling and vasoconstriction reduced 

 capillary blood pressure only moderately and the 

 rise of pressure during the secondary hyperemia of 

 cold was likewise moderate (203). Also in man Eichna 

 & Wilkins (90) found that neurogenically induced 

 vasoconstriction reduced cutaneous capillary pressure 

 by 1 to 8 mm Hg in 52 of 89 observations with no 

 change or slight elevations of 1 or 2 mm Hg in the 

 remainder. Intravenous injection of 1 or 2 jug of 

 epinephrine reduced capillary pressure by 1.5 to 22 

 mm Hg in seven of ten experiments but in three 

 subjects elevations of 1 or 2 mm Hg were observed. 

 Svmpathectomy obliterated neurogenic effects, but 

 not those of epinephrine. In the vasoconstriction of 

 human hypertension capillary pressure was not 

 significantly elevated and minor increases found in 

 some subjects were independent of arterial pressure 

 (89); this was also true of the temporary rise of 

 arterial pressure produced by Paredrinol intra- 

 venously (87) with or without prior sympathectomy. 



Conversely, vasodilatation increased capillary 

 blood pressure, frequently to very high levels ap- 

 proaching arteriolar pressure (see fig. 2.4). Capillary 

 pressure also rose during local vasodilatation induced 

 in the frog by dilute urethan (198), by injuries which 

 produced hyperemia and capillary stasis (199), 

 by a simple triple response and after muscular con- 

 traction (205). In human skin the hyperemias of 

 local heating, intradermal histamine, inflammation, 

 and reactive hyperemia after cold (203) were ac- 

 companied by elevations of capillary pressure to 

 maxima between 49 and 60 mm Hg. In these ob- 

 servations room temperatures were low, 18 to 20 C. 

 At higher temperatures, 23 to 28 C, Eichna & 

 Bordley (89) found that intradermal histamine 



elevated capillary pressures much less conspicuously 

 and more in the venous than in the arteriolar limbs 

 in both normal and hypertensive subjects. It was 

 emphasized that arteriovenous anastomoses may 

 have been involved in these effects (203). 



From the higher capillary pressures found in 

 localized vasodilatation and hyperemia it might be 

 thought that excessive filtration and increased lymph 

 flow must occur with any vasodilatation. This is not 

 always the case, however. The most notable excep- 

 tion is the repeated finding that denervation of an 

 extremity produces hyperemia and evidence of 

 increased blood flow without change of lymph flow, 

 or at most a very slight increase, as reviewed by 

 Drinker & Field (76). This failure of widespread 

 vasodilatation to increase the flow of lymph was, in 

 fact, for many years cited as evidence against the 

 Starling hypothesis. Eichna & Bordley (89) found that 

 reactive hyperemia and also indirect or reflex vaso- 

 dilatation in man, produced by body warming, did 

 not increase cutaneous capillary pressure significantly. 

 The reason for this may lie in the lowering of pres- 

 sures in the digital arteries by 1 o to 40 mm Hg during 

 the generalized vasodilatation produced by body- 

 warming (73, 114, 115, 244), by exercising the 

 forearm muscles (73), or by reactive hyperemia 

 (365). The named arteries to an extremity are ap- 

 parently large enough to conduct blood at resting 

 flow rates with little pressure drop. The lesser in- 

 crements of flow required by localized vasodilatation 

 are associated with little drop in arterial pressure 

 and capillary pressure rises conspicuously. However, 

 when vasodilatation involves the resistance vessels 

 of a whole extremity, and blood flow through the 

 large arteries is increased severalfold, the pressure 

 drop from brachial artery to digital artery becomes 

 significant. Then, arterial pressure head being much 

 reduced locally, the rise of capillary pressure is 

 limited even with maximal arteriolar dilatation. 

 In addition, the capillaries lie between two resistances 

 and it is quite possible that arteriolar dilatation 

 will not raise capillary pressure if the venules and 

 veins are simultaneously dilated in similar or greater 

 proportion. 



E. Effects of J'erwus Pressures and of Venular 

 Constriction on Capillary Pressure 



Elevations of venous pressure produce, as might 

 be expected, a rapid increase of capillary pressure 

 to levels above the pressure in the veins. Direct 

 measurements have shown this to be true of localized 



