948 



HANDBOOK OF PHYSIOLOGY 



CIRCULATION II 



be advantageous to use a constant-flow technique. 

 This is particularly the case if the autoregulation is 

 operating to maintain flow in proportion to metabolic 

 need. Under these circumstances the change in 

 arteriovenous difference of pressure probably will re- 

 flect the action of the infused agent with a minimum 

 of complication. On the other hand, if constant pres- 

 sure perfusion is used the autoregulatory mechanism 

 may mask the effect of the vasoactive agent by provid- 

 ing a counterdilation or constriction in an attempt 

 to maintain flow constant (see p. 940). 



Interpretation of change of vasomotor tone in autoperfused 

 vascular beds. Intravenous infusion of a constrictor agent 

 which raises systemic arterial pressure may fail to 

 alter blood flow in a vascular bed showing autoregu- 

 lation. This lack of response may be interpreted 

 incorrectly as indicating that the agent has exerted a 

 vasoconstrictor effect. Such misinterpretation has been 

 made in the case of the cerebral vascular bed. In such 

 instances the vasoactive agent should be injected 

 directly into the arterial supply to the vascular bed. 

 If there should be no response to the intra-arterial 

 injection then the lack of response during the rise of 

 systemic arterial pressure with intravenous injection 

 of the agent would be due to local autoregulation. In 

 this case the vascular bed would be attempting to 

 maintain flow constant despite the rise of arterial 

 pressure (90b). 



Chemical Effects on Resistance Vessels 



Hypertonic solutions (above 5 '!c NaCl) decrease 

 the resistance to flow in systemic vascular beds (56) 



Control 



by an unknown mechanism, but increase that in the 

 lung. The latter seems to be due to intravascular red 

 cell agglutination (91). 



Potassium and magnesium ions cause active limb 

 arteriolar dilation, calcium induces constriction (54) 

 while sodium has little effect (86). Acetate, among 

 the anions, produces arteriolar dilation (82). 



Extrinsic Control of Resistance Vessels 



EFFECTS OF VASOACTIVE AGENTS ON TOTAL RESISTANCE 



in a vascular bed. Extrinsic control of resistance 

 vessels, i.e., of the peripheral resistance in the various 

 vascular beds is illustrated most typically by the 

 responses in a skeletal muscle vascular bed, since 

 reactions, characteristic of all beds, are present in this 

 bed. In a skeletal muscle bed, intra-arterial injections 

 of epinephrine and of levarterenol cause a marked 

 decrease in flow followed, often, by a secondary rise 

 above control level (fig. 16). Such response occurs 

 characteristically after all injections of levarterenol 

 and after injections of 1 fig or more of epinephrine. 

 Smaller amounts of epinephrine often induce either 

 no response or an increase in flow indicative of 

 vasodilation. Lumbar sympathetic chain stimulation 

 usually decreases flow (fig. 16), although occasionally 

 an initial increase followed by decrease or solely an 

 increase in flow occurs (30, 45, 1 17). 



After induction of adrenergic blockade (fig. 16), 

 levarterenol may have no effect or may cause a slight 

 increase in flow while both epinephrine and lumbar 

 sympathetic chain stimulation increase flow. Atropine 

 injected intra-arterially abolishes the increase in flow 



After Phenoxybenzamine 3rng/Kg 

 58 



fig. 16. Curves of arterial inHow in a skeletal muscle vascular bed in the dog in response to intra- 

 arterial injections of 10 /jg of epinephrine, 10 /ng of levarterenol (norepinephrine), and a 1 -min period 

 of stimulation of the lumbar sympathetic chain, during a control period {left half) and after an intra- 

 arterial injection of 0.3 mg/kg of phenoxybenzamine (right half). Flow measured in ml/min; arterial 

 pressure remained constant through the study. [Modified after Youmans et at. (1 17).] 



