Publication | Open Access
Experimental Renal Hypertension in Dogs FORELIMB HEMODYNAMICS
10
Citations
29
References
1971
Year
HypertensionSurgeryPump Blood FlowBlood PressureExperimental Renal HypertensionBlood FlowRenal FunctionVascular SurgeryRenal PharmacologyAnimal PhysiologyVeterinary PhysiologyAnesthesia PracticeMethacholine InjectionsPhysiologyVeterinary ScienceBlood Pressure ControlAnesthesiaMedicineNephrologyAnesthesiology
Blood flow arid segmental intravascular pressures were measured in the pump-perfused forelimb vascular beds of 25 dogs with chronic perinephritic hypertension and 26 normotensive control dogs (either unilaterally nephrectomized or sham-operated) under pentobarbital anesthesia. Measurements were made under resting conditions (pump-perfusion pressure set equal to aortic pressure) and during response to: (1) stepwise changes in pump blood flow over the range 21-330 ml/min; (2) intrabrachial arterial injection of supramaximal doses of methacholine chloride; and (3) limb denervation. Total limb vascular resistance and segmental pressure gradients were calculated. In hypertensive dogs, as compared to normotensive dogs, resting blood flow was equal ( P >0.3) and resting limb total vascular resistance was increased ( P <0.005). Small vessel pressure gradient was increased ( P <.005) and venous pressure gradient was decreased ( P <0.005). Limb vascular resistance following methacholine injections and residual resistance following neurectomy were lower ( P <0.05) in normotensive than in hypertensive dogs. The development of hypertension was accompanied by the upward displacement of limb flow-resistance curves without discernible change in shape of the curves. These data suggest that in chronic renal hypertension in dogs: (1) the limb vascular bed participates in the increased peripheral vascular resistance; (2) the increase in limb vascular resistance is confined to the small vessel segment with no evidence found for limb venoconstriction; (3) a portion of the elevated limb vascular resistance is not attributable to neural stimuli; and (4) structural changes in vessels may account for part of the increase in limb resistance.
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