The electrical potential difference (PD) in the rat proximal convoluted tubule was investigated in vivo as a function of distance from the glomerulus. The PD was found to be invariably negative (up to -4.5 mV) in the earliest segments (less than 0.5 mm from the glomerulus) and rose to positive values (+2 to +4) in the later segments (1 mm beyond the glomerulus). This change in PD correlated with the bubule fluid-to-plasma (TF/P) chloride ratios, which rose from unity in the early segments to approximately 1.3 in the late. Corresponding changes in PD and chloride ratios could be elicited by single-nephron stop-flow techniques in the early segments. Luminal perfusion techniques demonstrated a direct relationship between PD and tubule fluid chloride concentration. Acetazolamide was found to significantly reduce both late proximal PD (less than +2 mV) and TF/P chloride ratios (less than 1.06). Split-drop studies demonstrated that the negative PD in the early proximal tubule was dependent on the presence of glucose and alanine and the absence of a chloride gradient, whereas in the late proximal tubule under the same conditions the PD was not significantly different from zero. In this segment of the nephron the positive PD in free flow appeared to result from the chloride diffusion potential generated by preferential HCO3 reabsorption. These results provide further demonstration of intrinsic differences in the transport properties along the length of the proximal convoluted tubule.

No abstract

Galactosamine-induced fulminant hepatic failure rats have been used as a model for statistical assessment of liver support systems. The present study reports in detail the biochemical, hematological and histological changes in these animals. They have been used to study statistically the effects of ACAC charcoal hemoperfusion, cross-circulation and liver perfusion on long-term survival in fulminant hepatic failure.

Control trials and statistical analysis were carried out to assess the effects of albumin‐collodion microencapsulated activated charcoal (ACAC) hemoperfusion on fulminant hepatic coma. A rat model of galactosamine induced fulminant hepatic coma was used. Rats which did not recover died at 3.0 0.6 days after galactosamine injection. Those which survived this period recovered. Forty‐eight hours after galactosamine injection, a test group of 21 rats were treated with 1 hour hemoperfusion and compared with an untreated group of 23 rats. 71.4% of the treated group survived as compared to 30.4% of the untreated rats. Statistical analysis (t test) shows a significant increase in recovery for the treated group (<0.01). Biochemical and histological results will be discussed.

ACAC hemoperfusion was used in series with a small fluid removal system for a clinical trial in the treatment of uremia. A 22‐month trial included a pretest control period, test period and a post‐test control period. The most significant observations from this trial are: 1) the predialysis body weight of the patient could be maintained closer to the patient's dry weight; 2) there was a significant increase in hematocrit; and 3) there was insufficient removal of urea. With the development of an effective urea removal system, a more compact artificial kidney than any presently available will become feasible.