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PubMed1996

Anion gap in turpentine-induced pleural effusions. Correlation with pH and protein level.

Since the pleural fluid proteins and lactate are unmeasured anions, the pleural fluid anion gap (Na+K-Cl-total CO2) should vary with the protein level and should be high in acidic effusions (which have high lactate levels). The anion gap is also convenient and inexpensive to measure, and less subject to artifact than the pH measurement. To test the hypothesis that the anion gap correlates with the pH, protein level, and other traditional pleural fluid measurements, we used a well-described model of turpentine-induced effusions in nine New Zealand white rabbits. Nonacidic exudative effusions were induced by an intrapleural injection of turpentine; acidic exudative effusions were induced by a second injection. Pleural fluid and blood were obtained just before (0 h) and 9, 24, 48, and 72 h after the second injection. We found the anion gap correlated with pH, the glucose, protein, and lactate dehydrogenase levels, pleural-fluid/plasma protein and lactate dehydrogenase ratios, and WBC count (all p < 0.001). The pH and protein ratio together accounted for 95% of all anion gap variation within individual subjects. We also found the influence of the PCO2 level on pH was not significant after taking into account the influence of the anion gap. These results suggest the anion gap may be useful in the clinical evaluation of pleural effusions and could potentially replace the pH measurement.

Acid-Base Equilibrium↗
PubMed1983

Response of transcortin and alpha 2u-globulin to turpentine-induced inflammation in the rat: influence of corticosteroids and prolactin.

Evidence is presented that (transcortin and alpha 2u-globulin react as negative acute-phase proteins in the rat. Thirty-six hours after turpentine injection, the serum concentration of these proteins showed a two- to threefold decrease. Thereafter, transcortin rapidly returned to normal values, whereas alpha 2u-globulin remained low. This reaction pattern was still present after adrenalectomy, adrenalectomy and administration of glucocorticoids, and after treatment with bromocriptine, a suppressor of prolactin secretion. It is concluded that changes in the secretion of glucocorticoids and prolactin are not required for the observed turpentine-induced decrease of transcortin and alpha 2u-globulin.

Adrenalectomy↗
PubMed1995

Increase in antilipoperoxidant activity of plasma as a consequence of an inflammatory reaction induced by subcutaneous turpentine in the rabbit.

In the rabbit, an acute inflammatory reaction triggered by the subcutaneous administration of turpentine induces in hepatic tissues an oxidative stress, as well as a decrease in activity of enzymatic scavengers of reactive oxygen species (ROS). The objective of this study was to investigate, the repercussions of a local inflammatory reaction on the antioxidant capacity and markers of systemic oxidative stress in plasma. To this purpose, rabbits received a.s.c. injection of turpentine (5 mL/kg) or NaCl 0.9% (w/v). Blood samples were collected at different times during the 48 hours of the experiment to evaluate: firstly, the antilipoperoxidant activity of plasma by measuring the inhibition of autoxidation of brain homogenate, and the concentrations of tocopherol and ascorbic acid; secondly, the severity of oxidative stress in plasma by assaying the concentration of thiobarbituric acid reactive substances (TBARS), and the concentration of ascorbyl radical. The results show that the antilipoperoxidant capacity of plasma gradually increased to be 167% higher than baseline values (p < 0.05) after 48 hours of experiment. alpha-Tocopherol and ascorbic acid levels increased by 49% and 80%, respectively (p < 0.05) during the first 24 hours. Lipid peroxidation continuously increased to be 98% higher than baseline values (p < 0.05) at 48 hours, while ascorbyl radical levels were not modified (p < 0.05). In summary, an acute local inflammatory reaction causes a steady progression of oxidative stress, while it stimulates the antilipoperoxidant activity of plasma, to which alpha-tocopherol and ascorbic acid appear to contribute, essentially early in the inflammation.

Animals↗
PubMed1995

Polyacrylamide gel electrophoretic patterns of chicken serum in acute inflammation induced by intramuscular injection of turpentine.

To develop a method to detect hidden inflammation using serum protein in chickens, changes in serum proteins with acute inflammation were analyzed using a turpentine-induced inflammation model. Inflammation in the pectoral muscle of a 14-wk-old White Leghorn became apparent 3 h after the injection of turpentine and became more severe thereafter. Coincident with the development of inflammation, changes in serum proteins were analyzed by electrophoresis on polyacrylamide gradient gels. The electrophoretic patterns were divided into 21 segments. Two of these segments increased remarkably. These were located near the center of the electrophoretic pattern and were identified as transferrin due to iron staining, correlation of movement against a commercial transferrin sample in SDS-PAGE, and immunoblotting. These results suggest that transferrin may serve as a marker for inflammation in chicken.

Acute-Phase Reaction↗
PubMed1985

Relation between 67Ga uptake and the stage of inflammation induced by turpentine oil in rats.

For the establishment of the experimental system to judge easily the effect of anti-inflammatory drug, 67Ga-citrate was used. The weight of granuloma tissues induced by inflammable agent, turpentine oil, gradually increased and reached a maximum at 6 days after the administration of turpentine oil. Gallium-67 accumulation in the inflammatory lesions showed also a maximum at 6 days after that. Both patterns were closely similar each other. These results showed that the processes and/or stages of inflammation could be indicated by the pattern of 67Ga uptake.

Animals↗
PubMedDate not supplied

[Application of yellow turpentine baths in patients with chronic prostatitis complicated by sexual dysfunctions].

Patients with chronic prostatitis complicated by sexual dysfunction took turpentine baths with yellow solution in concentration rising from 5 to 55 ml solution per 200 l water, temperature 35-40 degrees C, duration 5-16 min, daily, 12-15 procedures. Yellow turpentine baths raise efficacy of treatment of patients with copulative dysfunction to 64% due to intensive arterial blood inflow to the sexual organs including the cavernous bodies of the penis.

Baths↗
PubMed1991

Rat liver eicosanoid synthesis during turpentine-induced inflammation.

Subcellular liver fractions from rats receiving a subcutaneous injection of turpentine, which causes a local inflammation, show an increased synthesis of Prostaglandin E2 and Prostaglandin F2 alpha which reaches a peak 90 minutes and 3 hours after treatment, respectively. Stimulation of phospholipase A2 activity of liver cell preparations seems to be responsible for the supply of arachidonic acid necessary to feed PG synthesis: this stimulation is accompanied by unchanged levels of diacylglycerol lipase, diacylglycerol kinase and protein kinase C activities and by an unchanged content of diacylglycerol in the liver tissue. This picture does not favour the hypothesis of an involvement of phospholipase C in the early stages after turpentine treatment. Determinations of GTP-ase activity in plasma membrane-rich liver preparations give ambiguous results, which do not allow any conclusion on the possible role of G-proteins in phospholipase A2 activation.

Animals↗
PubMed1985

Evidence that production of platelet fibrinogen is synchronous with platelet production in the turpentine-induced acute phase response.

Fibrinogen is synthesized by both hepatocytes and megakaryocytes, and available evidence indicates that cellular production of this protein is controlled by a single gene. We evaluated platelet and plasma fibrinogen production in rats injected with turpentine to induce the acute phase response. After turpentine injection, plasma fibrinogen levels, as expected, rose to more than double the baseline values within 48 hours and then declined to the upper limit of the normal range in 6 days. When levels were expressed as a percentage of total plasma protein, a rise form 4.2% to 10.0% occurred. Thrombocytosis was not observed until day 4; platelet counts returned to the normal range by day 8. The mean fibrinogen content per platelet did not change significantly (P greater than 0.05) during this period of observation. Thus, in contrast to the abrupt rise in the level of plasma fibrinogen, changes in the blood level of platelet fibrinogen paralleled changes in the platelet count. We interpret these findings to indicate that platelet fibrinogen production is synchronized with platelet production by megakaryocytes and thus suggest that fibrinogen production is regulated differently in these cells than it is in hepatocytes.

Acute-Phase Proteins↗
PubMed1986

Modulation of alpha 2-acute phase globulin serum concentration in turpentine- and immune complex-challenged rats by dexamethasone and adrenaline: evidence for a synergistic mode of action.

The acute phase response (APR) induced by immune complexes or turpentine and modulated by dexamethasone as well as adrenaline was investigated in intact, sham-adrenalectomized and adrenalectomized rats. The serum level of alpha 2-acute phase globulin was examined by means of electroimmunodiffusion, and the complex serum protein profile was studied using the crossed-IE. Dexamethasone administration increased the alpha 2-acute phase globulin concentration weakly over a wide dose range whereas rats dosed with adrenaline responded strongly over a small dose range. Turpentine but not immune complex challenge provoked an almost complete acute phase protein profile as well as a moderate alpha 2-acute phase globulin elevation in adrenalectomized rats. After combined administration of the prophlogistic agents and dexamethasone or adrenaline a remarkably high alpha 2-acute phase globulin level was found (up to 14 mg/ml with about 0.05 mg/ml as base level). From these results a synergistic mode of action can be suggested. With crossed-IE some of the proteins could by divided in proteins responding in a glucocorticoid-dependent (e.g. alpha 2-acute phase globulin, haptoglobin) and -independent fashion (alpha 1-acute phase globulin), respectively. It can be concluded that glucocorticoids, catecholamines as well as cytokines are the main candidates for triggering the acute phase response; however, additional factors may also be of importance.

Adrenalectomy↗
PubMed1988

Bovine acute phase response following turpentine injection.

The serum levels of five proteins, alpha 1 antitrypsin, ceruloplasmin, fibrinogen, haptoglobin and seromucoid, were measured daily in calves after the subcutaneous injection of oil of turpentine. Raised concentrations were detected on the second and third days after injection with peak levels occurring on the fourth to seventh days and returning to normal by the 17th day. Levels of four of these proteins, alpha 1 antitrypsin, ceruloplasmin, haptoglobin and seromucoid were compared in the same calves following three different doses of turpentine. Levels of haptoglobin and seromucoid varied with the dose whereas ceruloplasmin and alpha 1 antitrypsin levels did not.

Acute-Phase Proteins↗
PubMed1989

Action of blood serum from rats with turpentine sterile inflammation on the development of CFU erythrocyte colonies. Possible role of erythropoietin.

Bone marrow CFUe mice cultures were prepared in Petri dishes and the number of full developed erythrocyte colonies were counted under various experimental conditions. In certain experiments, erythropoietin (EP = 0.4 U x ml-1 in the suspending medium) or sera from normal rats (100 microliters) or from animals with chronic turpentine sterile abscesses (60 or 100 microliters), were delivered to the CFUe colonies. The number of colonies in the group without EP was almost 5 times smaller than in the group with EP. Inasmuch as some few colonies are still able to develop, even in absence of added EP, the suggestion is advanced holding that the phenomenon may represent the effect of EP already bound to the group of cells initiating differentiation. Comparisons among all experimental groups indicate that the delivery of sera from turpentine rats to cultures containing added EP, reduced significantly the number of CFUe colonies seen in controls with EP but without inflammatory serum. It is suggested that the present findings could be explained assuming an inhibition of the influence of exogenous EP, subserved by the inflammatory serum, or alternatively that this kind of rat serum induces a partial blockade of EP at receptor sites whose activation is a mandatory step for the adequate and full development of cultured erythrocytes.

Abscess↗
PubMed1983

Synthesis and secretion of some plasma proteins by tissue slices of Morris hepatoma 7777 and liver from control and turpentine-injected rats.

Slices of Morris hepatoma 7777 or rat liver isolated from control or turpentine-injected rats were incubated for 2 h with 14C-leucine. Radioactivities incorporated into albumin, alpha-fetoprotein, fibrinogen, alpha 1-AP-globulin, haptoglobin and alpha 1-acid glycoprotein were determined after the proteins had been isolated from the incubation medium or tissue homogenate by immunoprecipitation with monospecific antisera. It was found that hepatoma synthesizes fibrinogen, alpha 1-AP-globulin and alpha 1-acid glycoprotein in the amounts comparable to rat liver, whereas formation of albumin and haptoglobin is reduced 5- to 10-fold. Local inflammation elicited by injection of turpentine to tissue donors increased formation of acute-phase protein in liver slices but had no effect on synthesis of these proteins in preparations of Morris hepatoma, although certain ultrastructural changes in the Golgi complex were observed not only in the liver but also in the tumour.

Animals↗
PubMed1981

Increased serum antibacterial activity after turpentine-induced acute inflammation.

An acute inflammatory response was induced in rabbits by an intramuscular injection of turpentine. After this injection serial serum samples were obtained and serum haptoglobin levels were monitored. In addition, increased antibacterial activity was measured using a viable plate and photometric growth assay. As early as 4 hrs after turpentine challenge an increase was noted in serum antibacterial activity towards Staphylococcus aureus. At 48 hrs pronounced killing activity was demonstrated against S. aureus and S. epidermidis but not against Escherichia coli or other gram negative bacilli. By five days another serum bactericidal activity was present against Bacillus subtilis. Enhanced serum antibacterial activity persisted for 2 weeks. Partial characterization of these factors indicates that they are probably beta lysins.

Animals↗
PubMed1982

[Systemic reactions in rats following the initiation of a local inflammatory process by subcutaneous administration of spirits of turpentine].

Local inflammation was induced in rats by single (1 x 4 ml/kg) or multiple (14 X 0.2 ml/animal) infections of turpentine. The induction of inflammatory processes in both groups resulted in anemia and granulocytosis following an initial leukopenia. Thrombopenia on the second day, followed by thrombocytosis, was also observed in both groups. Studies on blood chemistry parameters revealed a decline in serum albumin; elevation of alkaline phosphatase in serum was observed only after multiple injection of turpentine. In these animals an elevation in the weights of spleen and adrenals and a reduction in the weight of thymus were also found.

Animals↗
PubMed1976

Fibrinogen response to turpentine and endotoxin in busulfan-treated rabbbits.

The response of the plasma fibrinogen level to the subucutaneous injection of turpentine and to the intravenous injection of endotoxin was measured in normal rabbits and in rabbits made granulocytopenic and thrombocytopenic with busulfan. Plasma fibrinogen levels rose sharply in both normal and busulfan-treated rabbits and the extent of the rise in fibrinogen level after turpentine. As discussed herein, these data are consistent with the hypothesis that material from granulocytes plays a pathophysiologic role in the stimulation of fibrinogen synthesis in inflammation and after tissue trauma.

Agranulocytosis↗
PubMed1991

The effect of endotoxin and turpentine administration on intestinal permeability in the rat.

Intestinal permeability in 4-week-old rats has been assessed by the dual sugar (lactulose/mannitol) permeability test before and for two days after induction of systemic inflammation by various endotoxins and turpentine. Evidence of an inflammatory response to these agents was provided by marked reductions in food consumption and growth rate, hypoalbuminaemia, and a large increase in the plasma concentration of the acute-phase protein alpha-2-macroglobin. Abnormal values for intestinal permeability occurred only in animals which had been injected with E. coli 0111:B4 endotoxin. Neither turpentine nor the other endotoxins produced any detectable effect. Within 2-7h of the first exposure to a low dose, (3mg/kg) of either phenol or trichloroacetic extracts of E. coli 0111:B4 endotoxin, the lactulose:mannitol (L M ) ratio was elevated by 32% and 50% respectively (p < 0.05), but the rise was not sustained despite continued twice-daily injections of endotoxin. Administration of a higher dose, (10 mg/kg twice daily, phenol extract) resulted in diarrhoea, and a greater more persistent increase in the L M ratio; 115% (p < 0.05) 2-7h after the first injection, and 49% above control values, (p < 0.01) 24h later. The increase in L M ratio appeared to be due to a decrease in mannitol excretion. Total urinary lactulose also tended to fall, especially in rats given the high dose of endotoxin. It is concluded that a systemic inflammatory response does not necessarily lead to a change in intestinal permeability as measured by the dual sugar permeability test. The transient permeability changes observed following E. coli 0111:B4 administration may be a specific reaction to this material rather than to a more general systemic stimulus.

Journal Article↗
PubMed1951

The effect of adrenocorticotropic hormone on inflammation due to tuberculin hypersensitivity and turpentine and on circulating antibody levels.

The treatment with adrenocorticotropic hormone of guinea pigs sensitized with heat-killed tubercle bacilli caused suppression of their skin reactivity to tuberculin. Similar animals treated with saline did not show this change. Normal guinea pigs treated with adrenocorticotropic hormone showed suppression of inflammation, but not necrosis, produced by intracutaneous oil of turpentine. There was slight, but probably not significant, diminution of inflammation during saline administration. Tuberculin complement-fixing antibody titers were not altered by either adrenocorticotropic hormone or saline administration. Adrenocorticotropic hormone produced marked eosinopenia and lymphopenia in guinea pigs.

Adrenocorticotropic Hormone↗