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Biomedical subjects

D J Loegering

Publications and source records attributed to D J Loegering.

At least 73 records · Page 4Linked to original sources
PubMed1979

Depression of the reticuloendothelial system following graded isoproterenol-induced myocardial injury.

The effect of experimental myocardial injury on reticuloendothelial system (RES) phagocytic function was investigated. Graded myocardial injury was produced in rats by the subcutaneous injection of isoproterenol in doses of 5, 50 or 500 mg/kg. Phagocytic index, determined from the clearance rate of gelatinized lipid emulsion at six hours after isoproterenol injection, showed a progressive depression with increasing severity of myocardial injury. The depression in phagocytic index was due primarily to a depression of hepatic phagocytosis. RES blockade induced with colloidal carbon prior to isoproterenol injection (650 mg/kg) increased the mortality rate from 20% to 87%. It was concluded that the depression of RES function during this form of myocardial injury may hasten the deterioration of the organism and that it may be important to consider the role of RES function during clinical cardiogenic shock.

Animals↗
PubMed1978

Reticuloendothelial system function and humoral factor deficiency following acute hemorrhage.

The present study has shown that following acute hemorrhage (equivalent to 3% body weight withdrawn over 20 min) in the rat, there is a large reduction (56% of control) in circulating alpha-2-glycoprotein opsonic activity. The reduction in this plasma opsonic activity was near maximal by the completion of blood withdrawal and was maintained throughout a 2-h hypotension period. There was no trend toward recovery of the opsonic activity when evaluated 15 min following reinfusion of shed blood in animals that were hypotensive for 0, 30, and 120 min. Reticuloendothelial system (RES) phagocytic function, as assessed from the carbon clearance rate (phagocytic index) following reinfusion of the shed blood, was depressed in animals that were hypotensive for 0, 30, and 120 min. Thus, phagocytic index followed a time course similar to the depression of opsonic activity. The observed close temporal relationship between alpha-2-glycoprotein opsonic deficiency and depression of RES clearance further supports the possible role of a humoral opsonic deficiency in mediating the RES phagocytic depression during circulatory shock.

Animals↗
PubMed1978

Reticuloendothelial system blockade-induced humoral factor depletion and susceptibility to hemorrhagic shock.

This study was carried out to determine if reticuloendothelial system (RES) blockade-induced depletion of circulating alpha-2-glycoprotein opsonic activity resulted in increased susceptibility to hemorrhagic shock. RES blockade induced by the injection of gelatinized lipid emulsion was associated with a 45.9% decrease in phagocytic index and a 85.7% decrease in plasma alpha-2-glycoprotein opsonic activity. Animals subjected to RES blockade 30 min prior to hemorrhagic shock showed a decrease in time to decompensation and a decrease in maximum shed volume. These results are consitent with the concept that circulating levels of this opsonic protein are important in modulating RES phagocytic function and in host defense to shock.

Animals↗
PubMed1978

The effect of indomethacin on cardiovascular and lysosomal mechanisms during experimental myocardial ischemia.

The present study evaluated the effects of indomethacin (INDO) on cardiovascular and lysosomal mechanisms during experimental myocardial ischemia (MI). INDO (5 mg/kg) was infused IV prior to MI, and the results were compared to vehicle-treated and sham-operated dogs. INDO induced a slight hypertension after MI. Additionally, INDO attenuated the decline in coronary blood flow in the non-ischemic myocardium after MI. Myocardial lysosomes (biopsied three hours post-MI) were more labile in ischemic than in nonischemic tissue, and INDO had a stabilizing effect on lysosomes from ischemic tissue. Plasma activity of cathepsin was increased following MI, and INDO attenuated this increase. In the myocardium (biopsies three hours post-MI) prostaglandin A + E levels were suppressed 60% in both ischemic and nonischemic tissue with INDO treatment; prostaglandin F2 alpha levels were lower with INDO treatment but not significantly so. These results suggest that INDO has a stabilizing effect on lysosomes in vivo, possibly involving an endogenous prostaglandin mechanism, and this protective effect may attenuate lysosomal damage to the cardiovascular system during MI.

Animals↗
PubMed1978

Plasma cathepsin activity and reticuloendothelial phagocytic function during hemorrhagic shock.

The present study evaluated two forms of hemorrhagic shock in terms of changes in plasma lysosomal enzyme activity, reticuloendothelial system (RES) phagocytic function, and plasma opsonic activity. Hemorrhagic shock was induced in rats by withdrawal of a fixed volume of blood equivalent to 3% body weight or by maintaining the arterial blood pressure at 40--45 mm Hg. Plasma cathepsin activity did not increase until after one hour of hypotension, and was increased 2.7-fold two hours after a 3% body weight hemorrhage and 11-fold after two hours at a blood pressure of 40--45 mm Hg. Phagocytic index and plasma opsonic activity were decreased in animals reinfused at 0, 30, or 120 minutes following a 3% body weight hemorrhage and in animals reinfused 0, 30, and 90 minutes following hemorrhage to a blood pressure of 40 mm Hg. There was a strong temporal relationship between the changes in phagocytic index and plasma opsonic activity; however, the decrease in RES function occurred earlier than the increase in plasma lysosomal enzyme activity. These results suggest that the depression of RES function during shock may be mediated, in part, by a deficit in circulating opsonic activity and that RES depression occurs prior to shock-induced cellular injury during hemorrhagic shock.

Animals↗
PubMed1978

Cardiac output and regional blood flow following trauma.

The changes in cardiac output (Q), regional blood blow (Qr) and regional vascular resistance, and arterial pressure were studied in rats subjected to moderate (LD0) or severe (LD50) traumatic shock. Q and Qr were determined using microspheres at 15, 60 and 180 min posttrauma. Arterial pressure decreased in both groups at 15 min and recovered by 3 hr after sublethal (LD0) trauma, while arterial pressure did not return to control levels after LD50 trauma. Q decreased in both groups at 15 min and returned to control only in the LD0 trauma group by 3 hr. Cerebral, coronary, and hepatic arterial flows and resistances were maintained in both groups. Renal, intestinal, and splenic flows decreased and resistances increased in both groups by 15 min and returned to control levels by 3 hr only in the LD0 trauma group. Total hepatic and hepatic portal flows decreased at 60 min and returned to control levels at 3 hr after LD0 trauma, while there was significant depression in these parameters 3 hr after LD50 trauma. Therefore, sublethal and severe trauma resulted in early redistribution of flow favoring the coronary, cerebral, and hepatic arterial beds. However, renal, intestinal, splenic, and portal flows remained depressed only in severely traumatized rats, suggesting that continued hypoperfusion is a factor in the multiple organ failure and death following severe traumatic injury.

Animals↗
PubMed1977

Humoral factor depletion and reticuloendothelial depression during hemorrhagic shock.

Circulating opsonic activity and reticuloendothelial system (RES) phagocytic function were determined in anesthetized rats subjected to hemorrhagic shock. Animals were hemorrhaged to and maintained at 40 mmHg arterial blood pressure until they spontaneously took back 5% or 40% of the maximum bled volume. The phagocytic index, as determined by colloid clearance kinetics, was decreased in both groups following reinfusion of the shed blood. The reduction in phagocytic index was associated with decreased liver, unchanged spleen, and increased lung test colloid localization. Plasma opsonic activity, as determined by liver slice bioassay, was decreased 50-60% at 5% and 40% uptake of the maximum shed volume, decreased further 15 min after reinfusion in both groups, and tended to recover 1 h after reinfusion in the 5% uptake group. In vitro hepatic phagocytic activity of liver slices from shocked animals in the presence of normal rat plasma was decreased only in the 40% uptake animals after reinfusion when the arterial blood pressure had decreased to 50 mmHg. These data indicate that the depression of RES phagocytic function during hemorrhagic shock is associated with and may be mediated, in part, by decreased circulating opsonic activity.

Animals↗
PubMed1977

Effects of prolonged hemorrhagic hypotensive stress on catecholamine concentration of mesenteric blood vessels.

Norepinephrine (NE) and epinephrine (E) concentrations were determined fluorometrically as an index of functional adrenergic innervation in small mesenteric arteries, veins, and superior mesenteric arteries of dogs and rats subjected to a period of prolonged hemorrhage at a constant mean arterial pressure of 35 mm Hg. In nonhemorrhaged animals, highest catecholamine concentrations were found in the small principal arteries, next highest in the small veins, and least in superior mesenteric arteries. A significant decrease occurred in the NE and E concentrations of all three vessel types in the dog during the decompensatory phase of the hypotensive stress (defined as the hypotensive period beyond the time at which maximum bleedout volume occurred). In the rat significant decreases were detectable only in the NE concentrations of the small arteries and veins during this phase. It is concluded that the increase in neurogenic vascular tone accompanying severe hemorrhagic stress is lost simultaneously on the arterial and venous sides of compensatory vascular beds. Such loss is closely related to transmitter depletion at the adrenergic neuromuscular junction and, if allowed to continue uncorrected, can contribute significantly to irreversible cardiovascular collapse.

Animals↗
PubMed1975

Changes in plasma levels of lysosomal and non lysosomal enzymes during hemorrhagic hypotension.

In a study of 4-hr hemorrhagic hypotension in dogs, the plasma levels of the lysosomal enzymes, cathepsin (CATH) and acid phosphatase (AP) showed early and progressive increases in activity. The plasma levels of the intestinal fraction of alkaline phosphatase (IAkP) and aspartate aminotransferase (AAT) were increased after 2 hr of hypotension and the liver specific enzyme, ornithine carbamyltransferase (OCT), and creatine phosphokinase (CPK), after 3 hr. All of the enzymes showed large increases after 4 hr of hypotension. The plasma levels of CATH showed the earliest and largest relative increase indicating that with the shock model used, this enzyme was the most sensitive indicator of shock severity. The increase in plasma enzyme levels was probably the result of tissue damage in the splanchnic region but the elevation of plasma CPK, a muscle specific enzyme, indicates some muscle cell damage as well. While the increase in the plasma enzyme activity is probably due, in large part, to cellular damage, it is likely that a decreased enzyme removal rate--resulting from a hypofunctional RES--also contributes to the elevated plasma enzyme levels during hemorrhagic hypotension.

Acid Phosphatase↗