In order to investigate the effects of thermal injury on microvascular hemodynamics and permeability, hindpaw arterial (PA), venous (PV), and capillary (PC) pressures, blood (QB) and lymph (QL) flows, and lymph (CL) and plasma (CP) total protein concentrations were measured before and for 3 hr after a 10-sec 100°C scald burn in 11 dogs. Prior to injury in eight experiments (Group I-permeability analysis) venous pressure was elevated by outflow restriction until the minimal CL CP was obtained. In three experiments (Group II-hemodynamic analysis) outflow was not restricted. Lymph and plasma protein fractions ranging in size from 37 to 120 Å were measured using gradient gel electrophoresis and capillary equivalent pore sizes were calculated. In the early postburn period, PC increased from 24 ± 2 (mean ± SE)to 47 ± 5 mm Hg (P < 0.05) and precapillary resistance (RA) decreased from 6.6 ± 0.2 to 2.5 ± 0.2 mm Hg/ml/min/100 g (P < 0.05) while postcapillary resistance (RV) remained unchanged. Pre- to postcapillary resistance ( RA RV) fell by 74%. The reflection coefficient for total proteins (calculated as σ = 1 - CL CP) decreased from 0.87 ± 0.01 to 0.45 ± 0.02 (P < 0.01). Permeability of the postburn capillary endothelium was described by using two populations of equivalent pores. Preburn pore radii were 50 and 300 Å with 13% of the capillary filtrate passing through the large pores. Pore radii increased after injury to 70 and 400 Å with 49% of the filtrate passing through the large pores. The postburn total tissue filtration coefficient (Kf) increased to 2.4 times the control. Over the first 3 hr postburn, 53% of the increase in capillary filtration was attributable to increased capillary pressure and 47% to increased permeability. We conclude that the early rapid edema formation following thermal injury is the result of marked increases in both capillary filtration pressure and filtration through large nonsieving pores.
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