Changes in the reticuloendothelial phagocytic function after partial hepatectomy

The changes in the phagocytic function of the reticuloendothelial (RE) system after 67% hepatectomy in rats were studied by use of 51Cr-endotoxin as the phagocytable material. The humoral opsonic index was significantly increased to approximately 1.2 to 1.8 (control, 1.0 +/- 0.2, mean +/- SD) until the fourteenth postoperative day. In contrast, the phagocytic index was decreased to 0.068 +/- 0.016 (control, 0.103 +/- 0.015) on the first day, then returned to the normal level on the second day. In this early postoperative period, uptake rates of 51Cr-endotoxin in the liver were remarkably decreased to about 50% to 70% of control, whereas those in the spleen and lung were increased two- to threefold of control. From the third to the fourteenth day, the phagocytic index was significantly increased compared with the preoperative level. During this period, the uptake rates in the liver and spleen were within the normal range. These results suggest that the increases in the opsonic index of 67% hepatectomized rats represent the homeostatic response for maintaining or stimulating RE system phagocytic function, and that high or normal phagocytic index, concomitant with the increase in the opsonic index, implies an enhanced or compensatory stage, respectively. The decrease in the phagocytic index despite the high opsonic index is assumed to represent a compromised stage of the RE system.     

Quantitative reticuloendothelial function of liver and spleen in man

Summary. A method for separate determinations of liver and spleen reticuloendothelial function, using a small-size ⁹⁹Tc^m-antimony sulphide colloid and gamma camera technique, is described. Several methods for achieving blood-background correction are examined, and it is shown that, by a three-compartment model, the use of a specific blood pool tracer can be dispensed with. Hepatic and splenic uptake of the colloid can be described by first order kinetics, and can be calculated to an error less than 5%. In a reference material (n=13), hepatic and splenic clearance was 262 ml/min (100412) and 22 ml/min (0–62), respectively. In cirrhosis (n=7), hepatic clearance was decreased and splenic clearance increased. The results indicate that this method, which is well suited for clinical studies and which is based on a reasonable physiologic model, in cirrhosis of the liver demonstrates a decreased hepatic reticuloendothelial function with (compensatory?) increase in that of the spleen.     

Effects of methylprednisolone on the Fc-receptor function of human reticuloendothelial system in vivo

Abstract. To determine whether the Fc-receptor function of reticuloendothelial system (RES) is modified by corticosteroid administration, we studied the spleen to liver uptake ratios of autologous, ⁹⁹Tc-labelled heatdamaged or IgG-coated erythrocytes, injected intravenously into 10 normal volunteers, 4 h after receiving a single dose of 32 mg of methylprednisolone by mouth.
In standard conditions, quantitative scans indicated that the spleen to liver uptake ratios, calculated per unit area 40 min after the injection of labelled erythrocytes, were 13·4 ± 0·6 and 31·2 ± 1·5 (mean values ± -SEM), for the heat-damaged ( n = 7) and IgG-coated red cells ( n = 5) respectively. Four hours after corticosteroid administration, the spleen to liver uptake ratios were significantly reduced in five of ten volunteers. Abnormal ratios correlated with the Fc-receptor function of monocytes measured in vitro using IgG-coated erythrocytes. Indeed, 2–6 h after methylprednisolone was given, the Fc-receptor binding activity of monocytes isolated from the same five subjects was reduced by at least 50%, spontaneously returning to a rather normal value 4–6 h later. The C3-receptor binding activity of these monocytes remained normal, after otherwise identical experimental conditions.
These results show a transient, specific impairment of the Fc-receptor function of RES after methylprednisolone administration, and may therefore explain, in part, the infectious complications occurring in some patients treated by corticosteroids.     

The significance of activation of reticuloendothelial function on hepatectomy

The prognosis of patients after massive hepatectomy is poor in certain cases whose hepatic reserve, including reticuloendothelial function, is deteriorated. We administered OK-432 before 70% hepatectomy on rats to activate the reticuloendothelial function and studied its effect on postoperative course. The elevations in plasma endotoxin, GOT and GTP were attenuated, and the deterioration of the complement activity after hepatectomy was greatly improved by OK-432 treatment. The RNA content in the liver was significantly increased by OK-432 administration. These findings suggest that activation of the reticuloendothelial function at the time of massive hepatectomy enhances endotoxin clearance from blood and thereby contributes in lessening the magnitude of hepatic injury, maintaining the serum complement, and improving liver protein synthesis.     

Significance of activation of reticuloendothelial function after hepatectomy in cirrhotic rats

Effect of hepatectomy on the prognosis of cirrhotic rats prepared by oral administration of thioacetamide was studied from the standpoint of the reticuloendothelial function and energy metabolism of the liver. OK-432, a streptococcal preparation, was used to activate reticuloendothelial functions. Administration of OK-432 to cirrhotic rats prior to 70% hepatectomy significantly prevented the elevation of serum GOT, GPT and LDH, the prolongation of blood coagulation and the decrease of serum complement level. Hepatic ATP synthesis and RNA content were significantly increase by the use of OK-432. These findings suggest that activation of reticuloendothelial functions at the time of massive hepatectomy in cirrhotic rats may diminish hepatic injury, maintain serum complement level, and improve protein synthesis of the liver.     

Stimulation of the phagocytic activity of the reticuloendothelial system in adjuvant arthritis in the rat.

The administration of mycobacterial adjuvant produced a stimulation of the reticuloendothelial system (RES) phagocytic function. The degree of such a stimulation was greater in Lewis than in AVN inbred strain of rats. There was no relationship between the degree of RES stimulation and clinical signs of adjuvant-induced arthritis.     

Plasma lysozyme level and reticuloendothelial system function in human liver disease

Plasma lysozyme levels have been reported to reflect the functional status of the reticuloendothelial system (RES). We measured plasma lysozyme levels in 22 patients with acute hepatitis and 21 patients with cirrhosis and a mesocaval shunt. In 17 of these patients RES function was assessed by measuring the disappearance rate (t/2) of radio-labelled sulphur colloid. In acute hepatitis plasma lysozyme levels and colloid t/2 were significantly lower than in healthy controls and cirrhotics. In the acute hepatitis patients, the plasma lysozyme levels rose significantly two weeks after admission as the hepatitis improved. The colloid t/2 of the 17 patients with liver disease was significantly correlated with the plasma lysozyme level (r = +0.66, p = 0.005).These results suggest that in human liver disease, in comparison with animal experiments, plasma lysozyme is dependent on RES functional status in the sense that a more active RES will result in a lower lysozyme level.     

Influence on plasma beta-N-acetyl-D-glucosaminidase of reticuloendothelial stimulation and depression: an experimental study in rats

Plasma levels of the lysosomal enzyme, beta-N-acetyl-D-glucosaminidase (EC 3.2.1.30; 2-acetamido-2-deoxy-beta-D-glucoside acetamidodeoxyglucohydrolase ) were estimated 120 minutes after intravenous injection of zymosan in rats. Different groups of animals were investigated according to pretreatment with agents influencing reticuloendothelial activity. Pretreatment for two days with the reticuloendothelial stimulating agent, zymosan, or the reticuloendothelial suppressing agent, methyl palmitate, did not influence the basal plasma levels of beta-N-acetyl-D-glucosaminidase. In all groups after zymosan injection, plasma beta-N-acetyl-D-glucosaminidase activity was increased in comparison with basal levels. The increase of enzyme activity was most pronounced after pretreatment with zymosan and differed significantly from enzyme activity after pretreatment with methyl palmitate. Alcohol administration in combination with zymosan did not cause a further rise of beta-N-acetyl-D-glucosaminidase activity in normal rats nor in rats pretreated with zymosan. The observations suggest that plasma levels of beta-N-acetyl-D-glucosaminidase in rats after a standardized zymosan injection are related to the functional status of the reticuloendothelial system (RES).     

Activation of reticuloendothelial function for prevention of endotoxemia after hepatectomy in cirrhotic patients

In order to prevent endotoxemia after hepatectomy in cirrhotic patients, we administered OK-432 before and after hepatectomy to activate the reticuloendothelial function and studied its effect on postoperative endotoxemia. In the cirrhotic group without OK-432 administration (7 patients), the value of endotoxin increased significantly after hepatectomy, compared to the cirrhotic group which received OK-432 administration (5 patients) and the non-cirrhotic group (12 patients), and the endotoxin level was still higher than the preoperative value even on the 14th day. On the other hand, the cirrhotic group with OK-432 administration and the non-cirrhotic group showed minimal increases of endotoxin levels at the first day, which returned to the preoperative values at the third day. Base on these findings, it is suggested that activation of the reticuloendothelial function bears substantial significance as one of the therapeutic modalities for prevention of endotoxemia after hepatectomy in cirrhotic patients.     

Chronic liposome administration in mice: effects on reticuloendothelial function and tissue distribution

Liposomes have a pronounced tendency to localize in the reticuloendothelial (RE) system, a major host defense system. We have examined, in mice, the effect of chronic i.v. administration of low to moderate liposome doses on drug metabolism, phagocytic index and spleen and liver size. Little effect on the rate of pentobarbital metabolism was noted, except when mice received 80 mg/kg of sphingomyelin-containing liposomes in a series of 10 injections over 3.5 weeks. Impairment of RE phagocytic function was found to be related to liposome size and composition, size and frequency of liposome dose and the presence of lipid peroxides. The effects on tissue distribution of liposome-entrapped [14C]sucrose was also determined in mice receiving chronic liposome injections. In RE blockaded mice there was a consistent trend in favor of decreased liver uptake and increased spleen uptake. No significant uptake of liposome contents was seen in non-RE tissues even in mice with severe RE blockade, indicating that the induction of RE blockade by predosing with empty liposomes may not be a successful strategy for increasing liposome uptake to non-RE tissues. Liver to spleen ratios of [14C]sucrose appeared to be a sensitive method for quantitating RE blockade. Sphingomyelin-containing liposomes produced the greatest RE blockade, distearoylphosphatidylcholine-cholesterol liposomes were intermediate and egg phosphatidylcholine-cholesterol liposomes produced the least impairment in RE function. Liposomes which contained 1% vitamin E as an antioxidant had slightly less effect on RE function than liposomes not containing vitamin E.(ABSTRACT TRUNCATED AT 250 WORDS)