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This study investigated the relationship between urinary sodium excretion and liver function, as assessed by the aminopyrine breath test (ABT) and conventional parameters, in 62 patients with cirrhosis kept on a constant salt diet. Urinary sodium excretion was related non-linearly to the ABT (r = 0.76). Less significant correlations were observed to the Child-Pugh score (r = -0.65), cholinesterase (r = 0.58), bilirubin (r = -0.56), albumin (r = 0.51) and prothrombin time (r = 0.49). When patients were arbitrarily divided into 6 groups according to the ABT, sodium excretion balanced the sodium intake up to a 50% reduction in ABT. In groups with more than a 50% reduction sodium retention occurred. When patients were grouped according to the Child-Pugh score, urinary salt output was balanced in patients with scores of 5 and 6 and decreased in patients with scores greater six. However, the change in sodium output from normal salt excretion to sodium retention was less pronounced in patients grouped according to the Child-Pugh score than in patients grouped according to the ABT. The results suggest a non-linear relationship between the impairment in hepatic and renal function in cirrhosis. They are compatible with the concept of a threshold of hepatic function necessary to maintain normal renal function.

The method of Pattern Flash elicited P300 (PFP300) has been applied to evaluate the dynamic alterations in cognitive function of a 58 year old woman (H. C.) presenting with hepatic failure due to fulminant hepatitis Non-A-Non-B. At the time of the first investigation she complained about slight memory deficits and revealed signs of hepatic encephalopathy grade I according to Parson-Smith et al. (bilirubin 26.0 mg/dl, NH3 102 micrograms/dl, electrolytes and blood sugar normal). Psychometric tests: Number connection test (NCT): 54 s (28-53 s, greater than 2sd); Syndrom-Kurz-Test (SKT): total score = 9 (0-4), compatible with a slight "organic brain syndrome". PFP300: N250 latency 343.5 ms (276.4 +/- 14.7 ms, greater than 4sd); PFP300-latency: 442.5 ms (326.9 +/- 14.7, greater than 7sd); PFP300 amplitudes: 16.0 microV (14.4 +/- 8.4, +/- 1sd), indicating severe disturbance in visual discrimination without visual attention deficits. Due to progressive deterioration of liver function the patient had to undergo orthotopic liver transplantation. The patient was reinvestigated four weeks later. The clinical and laboratory status were normal and no signs of hepatic encephalopathy could be detected clinically or by means of the psychometric tests. The parameters of the PFP300 complex had also completely returned to normal: N250-latency: 273.0 ms (less than 1sd); PFP300-latency: 348.0 ms (less than 1sd). This observation suggests that the analysis of P300 can help to detect and follow minor cognitive deficits in cases of acute hepatic encephalopathy. It further underscores the hepatic etiology as well as the potential reversibility of this type of encephalopathy.

20 healthy male subjects with a mean age of 24 +/- 2.7 years were intravenously administered a mean total dose of ethanol of 1.33 +/- 0.04 g ethanol/kg body weight using a perfusor device. The ethanol kinetic resulted in a "rising phase" of 90.2 +/- 0.9 min. in average. The PFP300 parameter in this phase of acute alcohol intoxication showed the following changes: Along with the increasing blood alcohol level the N250- and PFP300a-latencies of both the A- and B-potentials are progressively prolonged and the ascending PFP300-amplitudes are progressively reduced. The N250-latency of the B-potentials is shown to be the most sensitive parameter of the PFP300-complex already changing at a blood alcohol concentration (= b.a.c.) of 0.59 +/- 0.11% with a mean linear prolongation of 2.5 ms per 0.1 g ethanol/kg body weight. This prolongation reflects the increasing disability of the subjects to discriminate between task-relevant and task-irrelevant stimuli at b.c.a.-levels much below that being presently permitted for driving in the Federal Republic of Germany.

For studying the relationship between the PFP300 (Pattern Flash elicited P300) and age we investigated 73 healthy subjects - 34 males, 39 females - between 18 and 60 years of age by presenting randomly two different checkerboards A (16 X 16 caskets visual angle = 50') and B (64 X 64 caskets visual angle = 12.5') to them (A:B = 80:20). The subjects' task was to keep a running count in their heads of the infrequent B-stimuli only. The resulting A- and B-responses were derived from Oz to Fz (Cz was ground). The results were as follows: 1. Comparing the PFP300-parameters between age group I (N = 46, 18-30 years) and age group II (N = 27, 31-60 years) we found that in the elder group both the N250-latencies (in B-potentials) and the PFP300a-latencies (in A-potentials) are significantly prolonged (p less than or equal to 0.01). The ascending PFP300a-amplitudes, however, remain (still?) unchanged. 2. Regression analyses between the PFP300-parameters and age for the total group revealed significant relationships for both the N250- (r = 0.35, P less than or equal to 0.01) and PFP300a-latencies (r = 0.78, P less than or equal to 0.01) and PFP300a-latencies (r = 0.78, P less than or equal to 0.01). In contrast to this, we could only find a zero correlation for the ascending PFP300a-amplitudes. 3. The coefficient of the regression line was 0.71 ms/year for the N250-latency and 1.09 ms/year for the PFP300a-latency. These findings indicate that one has to build age-matched control groups for applying PFP300 to pathophysiological processes.