title: Reduced transcapillary fluid absorption from skeletal muscle and skin during hypovolaemia in insulin-dependent diabetes mellitus.
abstract: OBJECTIVE
  Diabetes mellitus is associated with a high cardiovascular morbidity which has been linked to disturbances in microvascular function. This study was designed to examine the transcapillary fluid absorption during experimental hypovolaemia in type 1 diabetes.
  
  
  METHODS
  Twelve males with type 1 diabetes (age 25 +/- 3 years, duration 8 +/- 1 years) with no clinical microangiopathy and 12 healthy males (22 +/- 2 years).
  
  
  METHODS
  As a model for hypovolaemic circulatory stress, lower body negative pressure (LBNP: 15, 30 and 60 cmH2O) was used. Transcapillary fluid absorption from tissue to blood in the upper arm, as well as forearm blood flow, was measured by volumetric technique.
  
  
  RESULTS
  Resting forearm blood flow, heart rate and blood pressure were similar in diabetic patients and controls. Basal plasma noradrenaline was reduced in the diabetics compared with controls (0.75 +/- 0.06 vs. 1.09 +/- 0.10 pmol L-1, P < 0.05), but the increase in plasma noradrenaline in response to LBNP was similar in the two groups. The haemodynamic responses to LBNP in the two groups were equal, showing a reduction of pulse pressure, an increase in heart rate and in peripheral resistance with a concomitant blood flow reduction. The transcapillary fluid absorption (mL 100 mL-1 min-1) was significantly reduced in the diabetic patients: LBNP 15 cmH2O, 0.024 +/- 0.004 vs. 0.036 +/- 0. 002; 30 cmH2O, 0.041 +/- 0.003 vs. 0.056 +/- 0.005; and 60 cmH2O, 0. 057 +/- 0.007 vs. 0.091 +/- 0.008 (diabetic patients vs. controls, P < 0.001).
  
  
  CONCLUSIONS
  The transcapillary fluid absorption from tissue to blood during hypovolaemic circulatory stress in type 1 diabetic patients is reduced by one-third compared with controls, which indicates impaired plasma volume regulation. This basic mechanism for plasma volume control is affected before clinical microcirculatory complications are found and could be one of the causes of the increased cardiovascular morbidity and mortality in IDDM.
authors.affiliation: Department of Endocrinology, Lund University, Malmö University Hospital, Malmö, Sweden. olsen@mbox337.swipnet.se
authors.forename: H
authors.initials: H
authors.lastname: Olsen
authors.forename: U L
authors.initials: UL
authors.lastname: Hulthén
authors.forename: T
authors.initials: T
authors.lastname: Länne
mesh_terms: D000328:Adult; D001132:Arm / Q000098:blood supply; D001783:Blood Flow Velocity; D001794:Blood Pressure; D002199:Capillary Permeability; D003922:Diabetes Mellitus, Type 1 / Q000378:metabolism*; D018495:Fluid Shifts; D006339:Heart Rate; D006801:Humans; D020896:Hypovolemia / Q000378:metabolism*; D008150:Lower Body Negative Pressure; D008297:Male; D018482:Muscle, Skeletal / Q000378:metabolism*; D012867:Skin / Q000378:metabolism*; D014655:Vascular Resistance