Adrenergic and cholinergic regulation of splanchnic intravascular volume and cardiac output

Whether selective autonomic receptor stimulation influences cardiac output (CO) via changes in splanchnic intravascular volume (SIV) was assessed using radionuclide imaging. In anesthetized dogs, phenylephrine (.04-.08 mg min^-1 iv) for 20 min was associated with a 12 ± 2% (p < 0.001) increase in CO and a decrease in total SIV of 431 ± 95 ml (p < 0.001) due entirely to decreases in splenic and extrahepatosplenic volume of 26 ± 8% (p < 0.001) and 7 ± 2% (p < 0.001). In eviscerated animals, CO decreased 30 ± 2% (p < 0.001) with phenylephrine. With isoproterenol (.006 mg min^-1 iv) total SIV decreased 12 ± 1% (p < 0.001, 5.2 ± 1.6 ml kg^-1) due entirely to a decrease in splenic intravascular volume of 24 ± 3% (p < 0.001). The isoproterenol associated SIV decrement was dependent upon beta-2 and alpha adrenergic receptor stimulation but not beta-1 adrenergic stimulation. If beta-1 adrenergic stimulation was sufficiently minimized with metoprolol, splenectomy attenuated the isoproterenol associated CO increment. With acetylcholine (.005 mg kg^-1 min^-1 iv) total SIV decreased 4.9 ± 1.0% (p < 0.001, 65 ± 14 ml) due entirely to a decrease in splenic volume of 10.3 ± 2.0% (p < 0.001), and CO increased from 1916 ± 190 to 2290 ± 230 ml min^-1 (p < 0.001). Splenectomy or evisceration did not alter the acetylcholine associated CO response. Thus, alpha and beta adrenergic and cholinergic stimulation act to decrease total SIV. Only the SIV decrements associated with alpha or beta adrenergic stimulation, under conditions of minimal beta-1 adrenergic stimulation, act to enhance CO.