title: Effects of simulated hypovolaemia on haemodynamics, left ventricular function, mesenteric blood flow and gastric Pco2.
abstract: BACKGROUND
  Compensated clinically silent hypovolaemia may lead to low cardiac output, hypoperfusion and ischaemia. We investigated the cardiovascular effects of simulated hypovolaemia to determine whether it caused mesenteric ischaemia detectable by gastric tonometry.
  
  
  METHODS
  Thirteen healthy volunteers, aged 21-36 years, were investigated. Lower body negative pressure (LBNP) was used to simulate normotensive hypovolaemia. Cardiovascular parameters were measured using echocardiography. Mesenteric blood flow was investigated using Doppler sonography of the superior mesenteric artery (SMA). Gastric Pco(2) (P(g)co(2)) was measured using gas tonometry. Data were collected at baseline, LBNP and during a recovery period.
  
  
  RESULTS
  Normotensive hypovolaemia was induced successfully in 11 volunteers. There were no significant differences in mean arterial pressure between the three data points (91 +/- 6, 93 +/- 10 and 95 +/- 9 mmHg, respectively). With the induction of LBNP, the heart rate increased from 64 +/- 16 to 73 +/- 16 beats/min (P < 0.001), the cardiac index decreased from 2.7 +/- 1.0 to 1.8 +/- 0.6 l/min/m(2) (P= 0.002) and the systemic vascular resistance increased from 1535 +/- 445 to 2270 +/- 550 dyn s/cm(5) (P < 0.001). The SMA mean flow velocity decreased from 53 +/- 18 to 37 +/- 20 cm/s (69 +/- 20%) (P= 0.007), and increased to 56 +/- 34 cm/s (106 +/- 38%) (P= 0.001) during reperfusion. The SMA resistance increased from 92 +/- 30 to 174 +/- 110 mmHg/l/min (P= 0.004). These changes were reversible after termination of LBNP. By contrast, there were no significant differences in P(g)co(2) between the three data points.
  
  
  CONCLUSIONS
  In these volunteers, the mesenteric vascular bed contributed importantly to the maintenance of arterial pressure during normotensive hypovolaemia. However, this compensated hypovolaemia did not compromise the mesenteric perfusion sufficiently to increase P(g)co(2) and to allow detection by tonometry.
authors.affiliation: Department of Anaesthesia, University Hospital Basel, Basel, Switzerland. lsteiner@uhbs.ch
authors.forename: L A
authors.initials: LA
authors.lastname: Steiner
authors.forename: S
authors.initials: S
authors.lastname: Staender
authors.forename: C C
authors.initials: CC
authors.lastname: Sieber
authors.forename: K
authors.initials: K
authors.lastname: Skarvan
mesh_terms: D000328:Adult; D000704:Analysis of Variance; D001810:Blood Volume / Q000502:physiology; D002245:Carbon Dioxide / Q000032:analysis / Q000378:metabolism*; D002302:Cardiac Output / Q000502:physiology; D004452:Echocardiography; D005753:Gastric Mucosa / Q000378:metabolism; D006339:Heart Rate / Q000502:physiology; D006801:Humans; D020896:Hypovolemia / Q000175:diagnosis / Q000209:etiology / Q000503:physiopathology*; D008150:Lower Body Negative Pressure; D008297:Male; D008365:Manometry / Q000379:methods; D017538:Mesenteric Artery, Superior / Q000502:physiology*; D015588:Observer Variation; D012039:Regional Blood Flow / Q000502:physiology; D018616:Ultrasonography, Doppler, Duplex; D014655:Vascular Resistance / Q000502:physiology; D016277:Ventricular Function, Left / Q000502:physiology*
chemical_list: D002245:Carbon Dioxide