Factors affecting long-term outcomes after thromboembolectomy for acute lower limb ischemia.

AIM: The aim of this study was to analyze factors influencing outcomes of surgical management for lower limb acute ischemia. METHODS: A retrospective analysis of 490 thromboembolectomies performed in 468 patients was conducted. Perioperative and follow-up results were analyzed. Univariate and multivariate analysis of clinical variables and patients' characteristics for the risk of reocclusion, amputation and mortality at 2 years were performed. Statistical significance was defined as a P value <0.05. RESULTS: Cumulative reocclusion, amputation and mortality rates at 24 months were 22.6%, 14.3% and 42.8%, respectively. At univariate analysis, the factors associated with increased 2-year reocclusion rate were severity of clinical presentation, current smoking habit, arterial thrombosis rather than embolism, atrial fibrillation and the avoidance of completion angiography. All these factors except clinical presentation maintained significance at multivariate analysis. Factors associated with increased 2-year amputation rate at univariate analysis included severity of clinical presentation, smoke, arterial thrombosis, atrial fibrillation and valvulopathy. All these factors except clinical presentation and valvular defects maintained significance at multivariate analysis. Factors associated with increased 2-year mortality rate at univariate analysis included age >80 years, arterial thrombosis, history of peripheral arterial disease and antiplatelet drugs. The same factors, except antiplatelet treatment, were found to be significant at multivariate analysis. CONCLUSION: Surgical intervention for lower limb ischemia is associated with high 2-year mortality but offers good 2-year limb salvage. The pattern of risk factors for reocclusion and amputation rates is quite different from those affecting mortality. Only thrombotic aetiology is a significant risk factor for all the three outcomes.

Lower extremity traumatic vascular injury at a level II trauma center: an analysis of limb loss risk factors and outcomes.

AIM: The objectives were to review in our series the risk factors, management and outcomes of patients who sustained vascular injuries in the lower limbs and to determine the effect of risk factors and treatment on the outcome of the injured extremity. METHODS: Fifty-six patients submitted to surgical treatment were retrospectively reviewed. Results were analysed in terms of type of operation and reconstruction, intraoperative and 30 day complications, reconstruction occlusion, major amputation and mortality. RESULTS: The mechanism of trauma was blunt in 30.4% and penetrating in 69.6%. The overall primary amputation rate was 5.4%, the overall secondary amputation rate was 1.8%. The overall intraoperative and postoperative mortality were 1.8% and 5.4% respectively. At univariate analysis, the presence of compartment syndrome and ischemia time >6 hours were associated with a significantly higher risk of early reconstruction thrombosis (both P=0.03). It showed also that the number of patent vessels (P=0.0000) and the presence of a MESS score >7 (P=0.0000) significantly affected primary amputation, and that the occurrence of postoperative deep wound infection or sepsis (P=0.0000), of tibio-peroneal trunk injury (P=0.003) and of a MESS score >7 (P=0.004) significantly affected secondary amputation. CONCLUSION: The number of patent arteries (0-1), the presence of a MESS score >7, the incidence of tibio-peroneal trunk injury and the occurrence of postoperative deep wound infection are significant independent factors for limb loss. The presence of compartment syndrome and of ischemia time >6 hours are associated with a significantly higher risk of early reconstruction thrombosis.

Comparison of dipyrone/propofol versus fentanyl/propofol anaesthesia during surgery in rabbits.

In this study, the investigation of the intraoperative effects of dipyrone (metamizol) on heart rate (HR), mean arterial pressure (MAP) and analgesic efficacy in rabbits is described for the first time. This was carried out to evaluate the cardiovascular stability achieved using dipyrone compared with fentanyl. In this prospective study, 17 female New Zealand White rabbits were randomly allocated to either one of two groups: dipyrone/propofol (DP) or fentanyl/propofol (FP). Anaesthesia was induced in both groups using propofol to effect (4.0-8.0 mg/kg intravenously) until the swallowing reflex was lost for intubation. After induction, anaesthesia was maintained with continuous infusion of propofol 1.5-1.7 mg/kg/min intravenously. Analgesics were then injected in defined boluses of either dipyrone 65 mg/kg or fentanyl 0.0053 mg/kg. After surgical tolerance, defined as loss of the ear pinch reflex and loss of the anterior and posterior pedal withdrawal reflex, was achieved, two surgical procedures were performed. The surgical procedures (implantation of either a pacemaker or an electrocardiogram transmitter), both require a comparable level of analgesic depth. During and after surgery, clinical variables, such as MAP, HR, peripheral arterial oxygen saturation (SpO2) and end-tidal CO2 (P(E')CO2) were recorded simultaneously every 2 min. Eight time points were chosen for comparison: baseline, surgical tolerance (ST), values at 10, 20 and 30 min after reaching ST, values at the end of propofol infusion (EI) and data at 10 and 20 min after EI. Both FP and DP combinations provided effective anaesthesia and analgesia in rabbits. In both groups a significant decrease of HR and MAP was measured. The results of this study indicate that the non-opioid drug dipyrone produces similar analgesic and even better cardiovascular effects by trend in rabbits. Therefore we conclude that dipyrone in combination with propofol can be used as an alternative to FP for intraoperative analgesia.

Partial antagonization of midazolam-medetomidine-ketamine in cats--atipamezole versus combined atipamezole and flumazenil.

Two different methods, administered both subcutaneously and intravenously, to reverse intramuscular midazolam-medetomidine-ketamine, are evaluated. Eighteen cats were anaesthetized twice each 5 min after premedication with atropine 0.04 mg/kg using midazolam 0.5 mg/kg, medetomidine 0.02 mg/kg and ketamine 2.0 mg/kg intramuscularly in one syringe. Because this study was conducted in co-operation with a dental prophylaxis project, cats had to be immobilized for approximately 1 h. Therefore, anaesthesia was prolonged with propofol to effect, if necessary. After 68+/-11 min on average, immobilization was partially reversed by either atipamezole 0.05 mg/kg subcutaneously (group A/SC, n=7) or intravenously (group A/IV, n=10), or by atipamezole 0.05 mg/kg and flumazenil 0.05 mg/kg subcutaneously (group AF/SC, n=10) or intravenously (group AF/IV, n=9), respectively. These four groups were additionally compared with a non-reversed group. Recovery time and total time of immobilization (until cats regained a standing position) were not significantly shortened using the antagonists. However, unconsciousness and sedation (expressed through parameters like the time taken to head lifting, crawling, sitting and the return of righting reflex) were significantly shortened by the antagonists, especially if administered intravenously. Abnormal behaviour, such as vocalization, licking, hyperaesthesia, restlessness or salivation, was observed in all groups. However, excitation and hyperaesthesia were not observed in group AF/IV, whereas in this group only intensified salivation occurred. The addition of flumazenil showed no significant difference to atipamezole alone, but subcutaneous administration of atipamezole alone was not sufficient in the dosage used to show an advantage compared to non-reversed cats.

A comparative clinical study of three different dosages of intramuscular midazolam-medetomidine-ketamine immobilization in cats.

A low dose of midazolam-medetomidine-ketamine (MMK) combination was evaluated in three increasing dosages. Each of the 18 cats was randomly allocated for several times to one of four groups. Five minutes after premedication with intramuscular (IM) 0.04 mg/kg atropine, group A (n = 43), B (n = 40) and C (n = 28) all were anaesthetized with 0.5 mg/kg midazolam, combined with 10, 20 or 30 microg/kg medetomidine, and 1.0, 2.0 or 3.0 mg/kg ketamine, respectively, IM in one syringe. Group D (n = 11) received the established combination of 50 microg/kg medetomidine and 10.0 mg/kg ketamine for comparison. Because this study was in cooperation with a project on dental prophylaxis, cats had to be immobilized for approximately 1 h. Therefore, anaesthesia was prolonged with propofol to effect, if necessary. Duration of MMK anaesthesia was between 30 +/- 15, 45 +/- 19 and 68 +/- 28 min in groups A, B and C respectively. A significant decrease of respiratory rate was observed with increasing dosage, but venous carbon dioxide (pCO(2)) and pH values in combination with arterial oxygen saturation (SpO(2)) values were not alarming. The diastolic blood pressure particularly showed an increase. MMK combination A showed the best cardiovascular results, but it cannot be recommended due to disadvantages like a long induction time sometimes accompanied by excitations and the short duration of surgical immobilization. Dosage C in contrast had fewer side effects but less favourable cardiovascular results and a longer recovery period. However, either dosage B or C was suitable as a repeatable IM immobilization method for non-invasive procedures in healthy cats.

Comparison of long-term papilla healing following sulcular full thickness flap and papilla base flap in endodontic surgery.

AIM: To compare long-term loss of papilla height when using either the papilla base incision (PBI) or the standard papilla mobilization incision in marginal full thickness flap procedures in cases with no evidence of marginal periodontitis. METHODOLOGY: Twelve healthy patients, free of periodontal disease, who had intact interdental papillae were referred for surgical treatment of persisting apical periodontitis and included in the study. The flap design consisted of two releasing incisions connected by a horizontal incision. The marginal incision involved the complete mobilization of the entire papilla in one interproximal space but in the other interproximal space the PBI was performed. Further apically a full thickness flap was raised. Following flap retraction, standard apical root-end resection and root-end filling was performed. Flap closure was achieved with microsurgical sutures. The PBI was sutured with two to three interrupted sutures (size 7/0), the elevated papilla was reapproximated with vertical mattress sutures (size 7/0), which were removed 3-5 days after the surgery. The height of the interdental papilla was evaluated preoperatively and postoperatively after 1-, 3- and 12-month recall using plaster replicas. The loss of papilla height was measured using a laser scanner. Papilla paired sites were evaluated and statistically analysed. RESULTS: Most papilla recession took place within the first month after the surgery in the complete elevation of the papilla. Further small increase in loss of papilla height resulted at 3 months. After 1 year the loss of height diminished to 0.98 +/- 0.75 mm, but there was no statistical difference between the various recall intervals. In contrast, after PBI only minor changes could be detected at all times. There was a highly significant difference between the two incision techniques for all recall appointments (P < 0.001). CONCLUSIONS: In the short as well as long-term the PBI allows predictable recession-free healing of the interdental papilla. In contrast, complete mobilization of the papilla displayed a marked loss of the papilla height in the initial healing phase although this was less evident 1 year postoperatively. In aesthetically relevant areas the use of the PBI is recommended, to avoid opening of the interproximal space, when periradicular surgical treatment is necessary.

Comparison of papilla healing following sulcular full-thickness flap and papilla base flap in endodontic surgery.

AIM: To compare the loss of papilla height when using the papilla base incision (PBI) or the standard papilla mobilization incision in marginal full-thickness flap in cases with no evidence of marginal periodontitis. METHODOLOGY: Twelve healthy patients referred for surgical treatment of persisting apical periodontitis, who were free from periodontal disease and had intact interdental papillae, were included in the study. The preoperative papilla height was recorded by measuring the distance between a reproducible coronal point on the tooth and the most coronal point of the papilla. The flap design consisted of two releasing incisions connected by a horizontal incision. The marginal incision involved the complete mobilization of the entire papilla in one interproximal space, and the PBI in the other interproximal space. The PBI consisted of a shallow first incision at the base of the papilla and a second incision directed to the crestal bone creating a split thickness flap in the area of the papilla base. Further, apically, a full-thickness flap was raised. In the other interproximal space, the buccal papilla was carefully incised and elevated completely. Following flap retraction, standard root-end resection and root-end filling were performed. Flap closure was achieved with microsurgical sutures. The PBI was sutured with two to three interrupted sutures (size 7/0) and the elevated papilla was reapproximated with vertical mattress sutures, which were removed 3-5 days after the surgery. The height of the interdental papilla was evaluated preoperatively and postoperatively after 1 month and at the 3-month recall, using plaster replicas. The loss of papilla height was measured using a laser scanner. Twelve papilla-paired sites were evaluated. The results were statistically analysed using the t-test. RESULTS: Complete closure of the wound was achieved in all treated sites followed by uneventful healing in all patients. The total mobilization of the papilla resulted in loss of papilla height of 1.10 +/- 0.71 mm at 1 month and 1.25 +/- 0.81 mm at the 3-month recall. At the 3-month recall, the retraction had increased in nine sites, whereas in three sites, the loss of height had slightly diminished compared to 1 month. In contrast, after the PBI, only minor changes could be detected: 0.07 +/- 0.09 mm at 1 month and 0.10 +/- 0.15 mm at 3 months. There was a significant difference between the two incision techniques studied (P < 0.007). CONCLUSIONS: In patients with healthy marginal periodontal conditions, the PBI allows rapid and predictable recession-free healing, whereas complete mobilization of the papilla led to a marked loss of the papilla height. In aesthetically relevant areas, the use of the PBI is recommended, to avoid opening of the interproximal space, when periradicular surgical treatment is necessary.

Angular limb deformity in a calf treated by periosteotomy and wedge osteotomy.

A carpus valgus deformity was diagnosed in a five-week-old Brown Swiss calf. The 45 degrees deformity was caused by the malaligned healing of a fracture of the left metacarpus after birth trauma. The deviation improved to 25 degrees after being treated with a semicircular lateral periosteotomy above the distal physis of the radius. A complete correction was made by means of a wedge osteotomy five months after the first treatment. A 20 degrees wedge of bone was removed. The metacarpus was stabilised with a seven-hole dynamic compression plate which was removed 12 weeks later. Thirty months later the calf was sold as a pregnant heifer at an auction of breeding cattle.

Carbohydrate type and amount alter intravascular processing and catabolism of plasma lipoproteins in guinea pigs.

To test the effects of exchanging dietary complex and simple carbohydrate for fat calories on lipoprotein metabolism, guinea pigs were fed two different fat/carbohydrate ratios: 2.5:58% (w/w) or 25:29% (w/w) with either sucrose or starch as the carbohydrate source. Animals fed high-fat had higher plasma low-density lipoprotein (LDL) and hepatic cholesterol concentrations than animals fed low-fat diets (P < 0.01). The cholesteryl ester content per particle was higher, and the number of triacylglycerol (TAG) molecules was lower in very low density lipoprotein (VLDL) and LDL from animals fed high-fat diets. Intake of high-fat/sucrose resulted in higher plasma LDL concentrations than intake of high-fat/starch, and animals fed low-fat/starch had the highest plasma TAG concentrations associated with VLDL particles containing more TAG molecules, as well as a TAG-enriched LDL. The activity of plasma lecithin cholesteryl:acyl transferase (LCAT) was highest in animals fed high-fat/sucrose, and heart lipoprotein lipase (LPL) activity was higher in animals fed high-fat diets. Hepatic apoprotein B/E (apo B/E) receptor number (Bmax) was increased 21% with low-fat diets (P < 0.01). These results suggest that the hypercholesterolemia induced by high-fat and by sucrose intake are associated with a higher plasma LCAT activity which results in a cholesteryl ester-enriched VLDL which, by the action of LPL, might be more readily converted to LDL through the delipidation cascade leading to downregulation of hepatic apo B/E receptors. The hypertriglyceridemia associated with low-fat intake may result from increased production of VLDL TAG, which would explain the increased TAG content and the higher TAG/CE ratio of VLDL from animals fed the low-fat/starch diet.

[Subgingival plaque due to gingivitis and inactive periodontitis sites in the adult periodontitis patient]. / Subgingivale Plaque aus Gingivitis- und inaktiven Parodontitisstellen beim erwachsenen Parodontitispatienten.

There are several discrepancies with respect to the composition of subgingival plaque in gingivitis and in inactive adult periodontitis (AP). In this study we compared subgingival plaque samples taken from gingivitis sites to those from inactive periodontitis sites of the same patients. Of 44 patients plaque samples from 86 gingivitis sites and 92 periodontitis sites were analysed. Darkfield microscopy showed a higher proportion of spirochetes and mobile rods in the periodontitis sites. Analysis of cultures revealed a higher and statistically significant number of anaerobes in the periodontitis sites (1.7 x 10(7) vs 3 x 10(6), p = 0.006). The following bacterial species were isolated more frequently from periodontitis sites than from gingivitis sites: Actinobacillus actinomycetemcomitans (18% vs 10%), as well as the black-pigmented Prevotella intermedia (68% vs 48%) and Porphyromonas gingivalis (48% vs 28%). On the one hand, these small differences in the bacteriological parameters can be explained by the fact that both gingivitis and periodontitis plaque samples were taken from the same periodontitis patients. An infection of the gingivitis sites from the parodontitis sites within the same patient could not be excluded. On the other hand, the mean probing depth of the gingivitis sites was relatively high, 3.6 mm (measuring point interdental plus pseudo-pocket) which may favor the growth of anaerobic bacteria.

[Cauda equina syndrome in a Fleckvieh bull after a pathological fracture of the first sacral vertebra caused by a spindle cell sarcoma]. / Cauda-equina-Syndrom bei einem Fleckviehstier nach pathologischer Fraktur des ersten Sakralwirbels infolge eines Spindelzellsarkoms.

A 9 month old Simmental fattening bull was presented with signs of a cauda equina syndrome. An epidurographic examination was made after thorough clinical, neurological and routine radiographic examination. The cause of the cauda equina compression--a spindle cell sarcoma--was revealed by the pathologic-histologic examination. This tumor caused the compression of the cauda equina and pathologic transverse fracture of the body of the first sacral vertebra and cranial epiphyseal fracture of the 1st and the 3rd sacral vertebra as well as the separation of the arcus from the first and second sacral vertebral bodies. Some other diseases which can cause cauda equina syndrome are mentioned.

Evaluation of 9-(2-phosphonylmethoxyethyl) adenine therapy for feline immunodeficiency virus using a quantitative polymerase chain reaction.

To determine the efficacy of 9-(2-phosphonylmethoxyethyl)adenine (PMEA) as a prophylactic chemotherapeutic agent for the treatment of lentivirus infections, three groups of specific pathogen free cats were treated with 0, 3, or 6 mg kg-1 twice daily doses of PMEA beginning 24 h prior to virus challenge with feline immunodeficiency virus Petaluma strain. Treatment was continued for 7 weeks post challenge. During this time cats were monitored for drug toxicity, virus specific antibody response, circulating viral antigen and infectious recoverable virus. To determine the long-term influence of PMEA therapy the cats were monitored for 1 year following the cessation of treatment. The low levels of infectious virus present in blood prompted the development of quantitative polymerase chain reaction assay to enumerate viral DNA burdens in the peripheral blood mononuclear cells of the infected cats and thereby assess drug efficacy. The results indicate that, although prophylactic PMEA did not prevent infection, it did substantially limit feline immunodeficiency virus replication. Furthermore, viral DNA levels remained low in the cats receiving drug a full year (the duration of the study) after cessation of treatment.

Early therapy of feline leukemia virus infection (FeLV-FAIDS) with 9-(2-phosphonylmethoxyethyl)adenine (PMEA).

Cats infected with molecularly cloned FeLV-FAIDS develop an immunodeficiency syndrome characterized by persistent antigenemia, decline in circulating CD4+ T lymphocytes, and impaired T-cell-dependent immune responses and opportunistic infection. We evaluated the capacity of PMEA to inhibit the replication of FeLV-FAIDS in vitro and to inhibit the progression of FeLV-FAIDS infection in vivo. We found that PMEA inhibited replication of FeLV-FAIDS by greater than or equal to 50% at concentrations of greater than or equal to 0.5 microgram/ml (1.63 microM) in feline fibroblasts and prevented T lymphocyte killing at concentrations of 3 micrograms/ml. PMEA administered to cats at dosages of greater than or equal to 6.25 mg/kg/day from 0 to 49 days after FeLV-FAIDS infection prevented the development of persistent antigenemia and the induction of immunodeficiency disease. In contrast to placebo treated controls, cats successfully treated with PMEA contained viral infection, developed neutralizing antibody, and resisted a second virulent virus challenge without further therapy. Manifestations of PMEA toxicity produced by higher dosages (25 or 12.5 mg/kg/day) were anemia, leukopenia, and diarrhea. These results indicate PMEA to be a potent antiretroviral agent effective in aborting fatal progression of FeLV-FAIDS infection when therapy is initiated at the time of virus exposure.

Cerebral glutamine metabolism: study of modulatory effects of glutamine on gamma-aminobutyric acid-ergic neurotransmission.

Glutamine is one major precursor of gamma-aminobutyric acid (GABA) and glutamate, the most important inhibitory and excitatory neurotransmitters in the mammalian brain, respectively. Changes in cerebral glutamine concentrations occur in various metabolic encephalopathies including hyperammonemia and liver failure. As glutamine inhibits the specific binding of GABA to its postsynaptic receptor at physiologic concentrations, in this study the effects of glutamine on various components of the GABAA-benzodiazepine receptor complex were studied. Glutamine dose dependently inhibited the stimulation of flunitrazepam binding by GABA. This inhibition occurred already at concentrations of 10 mumol/L glutamine. Glutamine had no effects on basal or GABA-stimulated synaptoneurosomal chloride uptake. It is concluded that glutamine is not a modulator of the GABAA-benzodiazepine neurotransmitter system. Thus, changes of cerebral glutamine concentrations are unlikely to contribute to the activation of GABA-ergic neurotransmission in liver failure.

Hepatic encephalopathy in thioacetamide-induced acute liver failure in rats: characterization of an improved model and study of amino acid-ergic neurotransmission.

An imbalance of excitatory and inhibitory amino acid-ergic neurotransmission has been suggested to play a role in the pathogenesis of hepatic encephalopathy. For further evaluation of this hypothesis, several parameters of amino acid-ergic neurotransmission were studied in rats with acute liver failure induced by the administration of 300 mg per kg thioacetamide by gavage on two consecutive days. By appropriate supportive care, hypoglycemia, renal failure and hypothermia were avoided. Rats were monitored clinically and neurologically. Hepatic encephalopathy evolved in four distinct, easily recognizable stages. Light and electron microscopic examination of brains of rats with hepatic encephalopathy revealed only a slight swelling of nuclei of neurons and astrocytes without signs of neuronal degeneration or brain edema. In rats with hepatic encephalopathy, the concentrations of GABA, glutamate and taurine were decreased in the cerebral cortex, the hippocampus and the striatum, whereas those of aspartate and glycine were unchanged or increased. GABAA and benzodiazepine receptors were studied as parameters for the postsynaptic GABAA-benzodiazepine receptor complex, glutamic acid decarboxylase as parameter for presynaptic GABA-ergic neurons and stimulation of benzodiazepine binding by GABA as a parameter for a GABA-mediated postsynaptic event. None of these parameters was different in hepatic encephalopathy as compared to controls. Similarly, Ca++/Cl(-)-dependent and -independent glutamate receptors as parameters for glutamatergic neurons were unchanged in rats with hepatic encephalopathy. Thus, in rats with thioacetamide-induced liver failure and hepatic encephalopathy, changes of the concentrations of neurotransmitter amino acids occur in the brain. Other neurochemical parameters, however, failed to identify alterations of GABA-ergic or glutamatergic neurotransmission in hepatic encephalopathy.

Uptake and catabolism of gamma-aminobutyric acid by the isolated perfused rat liver.

Serum concentrations of gamma-aminobutyric acid (GABA) are increased in liver failure, possibly because of decreased hepatic GABA catabolism. To study in detail the role of the liver in GABA metabolism, uptake and catabolism of GABA by isolated perfused liver from normal rats and rats with galactosamine- or carbon tetrachloride-induced liver failure were measured. Hepatic GABA uptake was almost complete at GABA concentrations of up to 10 microM and approached saturation at a concentration of 50 microM. The apparent affinity of hepatic GABA uptake was 38 microM and the apparent maximal velocity was 158 nmol/g.min. Hepatic GABA uptake was sodium-dependent. gamma-Aminobutyric acid taken up by the liver was rapidly catabolized as measured by 14CO2 formation from [U-14C]GABA. Aminooxyacetic acid, a GABA transaminase inhibitor, completely and irreversibly inhibited hepatic GABA catabolism and thereby also inhibited hepatic GABA uptake. Although uptake of GABA by livers of carbon tetrachloride- or galactosamine-treated rats was decreased (apparent maximal velocity, 103 and 98 nmol/g.min, respectively), at physiologic GABA concentrations in the perfusate GABA uptake and catabolism was not different from that of untreated controls. The observed impairment of hepatic GABA uptake or catabolism by the diseased liver would be expected to contribute to increased GABA levels in peripheral blood plasma in liver failure. However, the magnitude of the observed impairment would be insufficient to account for a 10-fold increase in such levels.

Overestimation of serum concentrations of gamma-aminobutyric acid in patients with hepatic encephalopathy by the gamma-aminobutyric acid-radioreceptor assay.

Sera of patients with hepatic encephalopathy strongly inhibit the specific binding of gamma-aminobutyric acid to synaptic membranes. In a previous study, this inhibition of specific gamma-aminobutyric acid binding was attributed to gamma-aminobutyric acid itself, and it was assumed that serum gamma-aminobutyric acid is increased 5- to 30-fold in patients with hepatic encephalopathy. The findings of that study, however, were not confirmed by other analytical methods. Therefore, the validity of the gamma-aminobutyric acid-radioreceptor assay was tested. In view of the increased serum concentrations of several amino acids in hepatic encephalopathy, the effects of L-alpha-amino acids on the assay were studied. Five amino acids inhibited specific gamma-aminobutyric acid binding at a concentration of 0.5 mM or lower: glutamine; glutamate; taurine; proline, and OH-proline. Equimolar amounts of aminooxyacetate prevented the inhibition of specific gamma-aminobutyric acid binding by glutamine and glutamate but had no effect on that of gamma-aminobutyric acid, taurine, proline and OH-proline. Aminooxyacetate had no effect on specific gamma-aminobutyric acid binding itself. The inhibitory activity of a serum sample from a patient with hepatic encephalopathy was inhibited by 0.5 mM aminooxyacetate. The gamma-aminobutyric acid binding inhibitory activity of a serum sample of a patient with hepatic encephalopathy was purified by gel chromatography and contained several amino acids at concentrations of about 0.1 mM, 3.5 mM glutamine but no detectable gamma-aminobutyric acid. Accordingly, the gamma-aminobutyric acid binding inhibitory activity is not mediated by gamma-aminobutyric acid alone and is most likely due to glutamine.(ABSTRACT TRUNCATED AT 250 WORDS)