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Biomedical subjects

T M Saba

Publications and source records attributed to T M Saba.

At least 163 records · Page 9Linked to original sources
PubMed1975

Hepatic reticuloendothelial host defense failure following surgical trauma.

We evaluated potential pituitary-adrenal influences on postoperative reticuloendothelial (RE) function. Male dogs, 13 to 18 kg (28.6 to 39.6 lb), were used and the operative procedure was hemicolectomy. The RE function was evaluated by a colloid clearance technique and circulating opsonin levels were quantified by bioassay. Normal animals manifested RE depression three hours following incision (49 percent decline in the global phagocytic index K and an associated 30 percent decline in the circulating opsonic activity). Dexamethasone sodium phosphate pretreatment over a three-day preoperative period prevented the postoperative RE clearance failure (control K = 0.69; postoperative k = 0.79) however, a slight (18 percent) but not significant decrease in opsonic activity occurred. Cortisone acetate or adrenocorticotropic hormone over a wide-dosage range manifested no depressing effect on in vitro phagocytosis. These studies, in conjunction with our previous findings of Kupffer cell activation following adrenalectomy, as well as the demonstration of opsonin depletion and RE phagocytic depression following surgery in the absence of the adrenal glands suggest that the pituitary-adrenal system modulates postoperative RE phagocytosis.

Animals↗
PubMed1975

Humoral mediated macrophage response during tumour growth.

Reticuloendothelial (RE) phagocytic and circulating plasma opsonic activity was evaluated in rats transplanted with the Walker 256 carcinoma tumour in an attempt to evaluate the role of opsonic protein in governing the functional state of the macrophage system. Animals transplanted intramuscularly with 2 X 10(4) viable tumour cells manifested 2 peaks of RE stimulation at 6 and 14 days post-transplantation with a subsequent decline in the phagocytic activity over the 14-30 day period. Increased phagocytic activity as determined by colloid clearance was primarily a reflection of hepatic Küpffer cell hyperphagocytosis while the decline in phagocytic activity was related to a decrease in Küpffer cell function. The initial peak of RE stimulation was associated with an elevation in the blood opsonin level and no significant enlargement of the liver and spleen. In contrast, the second peak of RE stimulation at 14 days was associated with both an elevation in opsonin levels and an associated hepatic and splenic enlargement. The decline in phagocytic activity over the 14-30 day interval was associated with a progressive decline in the plasma opsonic activity, a return of the spleen to its normal size in relationship to the body weight, and a persistent hepatomegaly. These findings suggest that the alterations in macrophage function during tumour growth may be mediated in part by changes in the opsonic or phagocytosis promoting capacity of plasma. Since opsonic protein contributes to the discriminatory capacity of macrophages, it is suggested that changes in the blood opsonin level may condition the anti-tumour capacity of the macrophage system with respect to host defence aginst malignant disease.

Animals↗
PubMed1975

Degradation of particulate lipid by the large-granule fraction of rat liver (38555).

Radiolabeled particulate lipid administered intravenously was cleared from the circulation and localized primarily with in the liver. The phagocytized 131I-triglyceride was degraded with the subsequent release of free 131I-triglyceride emulsion in vitro with different hepatic subcellular fractions revealed that the lysosome rich large-granule fraction contained the highest specific deiodinative activity. This observation coupled with the findings on latency of activation and an acid findings on latency of activation and an acid pH optimum, support the concept that the lysosomes are critically involved in the degradation of the particulate phagocytized lipid in the liver.

Animals↗
PubMed1975

Serum calcium and hepatic Kupffer cell phagocytosis.

Serum calcium can markedly influence the phagocytic activity of the hepatic Kupffer cell. Specifically, depletion of calcium by chelator induced impairment of phagocytosis but elevation of serum calcium levels above normal leads to a progressive inhibition of phagocytosis. The findings suggest that alterations of serum calcium may induce significant R.E.S. functional changes which may produce a state of altered host resistance. The relationship of these observation to disturbances of the macrophage system during mealignancy, which is known for its ability to alter dramatically the serum calcium concentration warrants further investigation.

Animals↗