Effects of vasodilators on the systemic capacitance vessels, a study with the measurement of the mean circulatory pressure in dogs.
There have been yet only a few studies on the action of vasodilators on the entire systemic capacitance vessels of the living body. In the present study, we studied the action of the vasodilators on the systemic capacitance vessels by measuring the mean circulatory pressure (MCP), introduced by Guyton, and that on the systemic resistance vessels from total peripheral resistance, in anesthetized open chest dogs. We also studied the venous return curves. Depending on vasodilators and the dosages used, resistance vessels could be dilated, but capacitance vessels could not be dilated. The reverse was never true. It was also found frequently that capacitance vessels could be dilated only when the tone of the capacitance vessels have been previously elevated by norepinephrine. Again, depending on vasodilators and their dosages, the venous return curves were changed in position and/or slope. We constructed a venous return curve by connecting 2 points on the venous return-right atrial pressure (VR-RAP) plane, one, VR-RAP plot, and the other, the point of VR = 0, RAP = MCP. Changes in the venous return curve caused by these vasodilators were classified into three types; (a) a clockwise rotation with a constant MCP, where one sees no change in MCP and decreased resistance to venous return (RVR), so that one may call this RVR-type, (b) a parallel shift of the venous return curve to the left, where one sees no change in RVR but a decreased MCP, so that one may call this MCP-type and (c) a shift to the left plus clockwise rotation, where one sees a decrease in MCP and decrease in RVR, so that this is a mixture of patterns (a) and (b). One may call this the mixed-type. The existence of the response of mixed-type is worth special attention, because, in this type, cardiac output (CO) was increased by the predominant decrease in RVR in spite of a decreased MCP, leading to an important condition that the CO does not necessarily decrease when systemic capacitance vessels were dilated by the vasodilators.
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects*; D001808:Blood Vessels / Q000187:drug effects*; D001810:Blood Volume / Q000187:drug effects; D002302:Cardiac Output / Q000187:drug effects; D004110:Diltiazem / Q000494:pharmacology; D004285:Dogs; D006339:Heart Rate / Q000187:drug effects; D007548:Isosorbide Dinitrate / Q000494:pharmacology; D008981:Molsidomine; D009536:Niacinamide / Q000031:analogs & derivatives / Q000494:pharmacology; D020108:Nicorandil; D009543:Nifedipine / Q000494:pharmacology; D005996:Nitroglycerin / Q000494:pharmacology; D011224:Prazosin / Q000494:pharmacology; D013558:Sydnones / Q000494:pharmacology; D014192:Trapidil / Q000494:pharmacology; D014655:Vascular Resistance / Q000187:drug effects*; D014665:Vasodilator Agents / Q000494:pharmacology*; D014690:Venous Pressure / Q000187:drug effects; D014700:Verapamil / Q000494:pharmacology
D013558:Sydnones; D014665:Vasodilator Agents; D009536:Niacinamide; D020108:Nicorandil; D014700:Verapamil; D008981:Molsidomine; D004110:Diltiazem; D014192:Trapidil; D005996:Nitroglycerin; D009543:Nifedipine; D007548:Isosorbide Dinitrate; D011224:Prazosin