TY - JOUR
T1 - Effects of bolus infusion of normal saline and dopamine on blood volume and cardiac output
AU - Vane, Luiz A.
AU - Brauer, Lance P.
AU - Kilicturgay, Sadik
AU - Traber, Daniel L.
AU - Prough, Donald S.
AU - Kramer, George C.
PY - 1999
Y1 - 1999
N2 - Introduction: Critically ill patients are routinely treated with infusions of crystalloid and dopamine in order to increase vascular volume, filling pressures, myocardial function, and thus, cardiac output (CO). However, interactions between fluid therapy and dopamine remain poorly defined. We hypothesize that dopamine would reduce the volume expansion after a bolus crystalloid infusion. Methods: Six instrumented, splenectomized, conscious sheep were subjected to bolus infusion (24 ml/kg per 20-min) of normal saline (NS) in three paired experiments each. Groups were a no dopamine control, low (LD) and high dose (HD) dopamine of 5 and 15 ug/kg/min. Dopamine infusions were started 30-min before NS and maintained for 3-hrs after. Experiments were separated by at least 2 days. Blood volume (BV) was measured with indocyanine green dye and expansion was measured by dilution of blood hemoglobin. Results: Dopamine alone had no apparent effect on right atrial pressure (BAP) or BV during the 30-min infusion before the NS, but CO was increased by 0.5± 0.2 and 1.4 ± 0.3 L/min for LD and HD, respectively. At the end of the NS infusion, RAP was increased 4-6 mm Hg in all groups and BV was increased 10-13 ml/kg with highest values in the LD group. CO was increased 1.5±1.6, 2.7±0.7 and 3.7±1.3 L/min from the preinfusion levels of NS, LD and HD, respectively. One hour after the infusion, filling pressures and CO had returned to pre NS levels, and PV expansion was only 2-4 ml/kg with the highest value in the HD group. Conclusion: Dopamine infusion increased CO without altering filling pressure, and did NOT reduce the vascular retention of NS and may slightly enhance it. Our hypothesis is rejected.
AB - Introduction: Critically ill patients are routinely treated with infusions of crystalloid and dopamine in order to increase vascular volume, filling pressures, myocardial function, and thus, cardiac output (CO). However, interactions between fluid therapy and dopamine remain poorly defined. We hypothesize that dopamine would reduce the volume expansion after a bolus crystalloid infusion. Methods: Six instrumented, splenectomized, conscious sheep were subjected to bolus infusion (24 ml/kg per 20-min) of normal saline (NS) in three paired experiments each. Groups were a no dopamine control, low (LD) and high dose (HD) dopamine of 5 and 15 ug/kg/min. Dopamine infusions were started 30-min before NS and maintained for 3-hrs after. Experiments were separated by at least 2 days. Blood volume (BV) was measured with indocyanine green dye and expansion was measured by dilution of blood hemoglobin. Results: Dopamine alone had no apparent effect on right atrial pressure (BAP) or BV during the 30-min infusion before the NS, but CO was increased by 0.5± 0.2 and 1.4 ± 0.3 L/min for LD and HD, respectively. At the end of the NS infusion, RAP was increased 4-6 mm Hg in all groups and BV was increased 10-13 ml/kg with highest values in the LD group. CO was increased 1.5±1.6, 2.7±0.7 and 3.7±1.3 L/min from the preinfusion levels of NS, LD and HD, respectively. One hour after the infusion, filling pressures and CO had returned to pre NS levels, and PV expansion was only 2-4 ml/kg with the highest value in the HD group. Conclusion: Dopamine infusion increased CO without altering filling pressure, and did NOT reduce the vascular retention of NS and may slightly enhance it. Our hypothesis is rejected.
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U2 - 10.1097/00003246-199912001-00222
DO - 10.1097/00003246-199912001-00222
M3 - Article
AN - SCOPUS:33750643235
SN - 0090-3493
VL - 27
SP - A87
JO - Critical care medicine
JF - Critical care medicine
IS - 12 SUPPL.
ER -