Histological study of increased vascular permeability in the sheep in turpentine-induced inflammation of skin and pleura.
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Relationship between changes in seromucoid concentrations and the rate of oxidation or acetylation of several substrates.
This study was carried out to assess the relationship between turpentine-induced elevation of seromucoids and drug metabolism. Six groups of rats were used; one of them received 1 ml of turpentine sc, another received 1 ml of turpentine by gavage (po), and a third group received, ip, 80 mg/kg of phenobarbital daily for 3 days. Three control groups received saline instead of turpentine. Forty-eight hr later, the serum seromucoids were assayed and the rates of N-demethylation of aminopyrine, O-dealkylation of 7-ethoxycoumarin, and hydroxylation of aniline and total cytochrome were determined in liver microsomes. When turpentine was administered sc, seromucoids increased from 3.15 +/- 0.18 to 16.13 +/- 0.84 g/dl (mean +/- SE) (p less than 0.01), but the rates of N-demethylation (p less than 0.01), of O-dealkylation (p less than 0.01) and of hydroxylation (p less than 0.05) were all decreased. In the rats receiving turpentine po, seromucoids remained unchanged, but the rates of N-demethylation and O-dealkylation as well as the concentration of total cytochrome increased (p less than 0.01). Phenobarbital enhanced significantly the rates of N-demethylation, O-dealkylation, and hydroxylation and the total concentration of cytochrome, without modifying the concentration of seromucoids. In another set of experiments we assessed whether turpentine-induced inflammation would affect the in vivo rate of acetylation of sulfamethazine; the results show that inflammation does not affect the rate of acetylation, despite an important increase in seromucoids. It is concluded that, under the present experimental conditions, there is no direct relationship between changes in seromucoids and the rate of drug metabolism.
Acetylation↗
A study of cutaneous myiasis in Sri Lanka.
BACKGROUND AND OBJECTIVES: Cutaneous myiasis (CM) due to Diptera fly larvae shows different patterns in different regions. Many modalities of treatment have been described. The objectives of our study were to identify the species causing CM in Sri Lanka, the common sites of infestation, and the contributory factors, and to assess some treatment modalities, in particular mineral turpentine and certain herbal preparations. METHODS: All patients with CM admitted or referred to the Dermatology Unit at the General Hospital, Kalutara, over 18 months starting from July 1997, and all patients with CM from the orthopedic and surgical wards of the National Hospital of Sri Lanka in Colombo over 6 months from July 1997, were studied. Details of the history and examination were recorded on specially designed forms. Maggots extracted were identified at the Department of Parasitology, Faculty of Medicine, University of Colombo. The modalities of treatment employed in the patients were recorded. In the Department of Parasitology, a colony of Chrysomya megacephala was maintained. Homogenized leaf extracts of Azadirachta indica (neem) and Pongamia pinnata (Indian beech) and mineral turpentine (active ingredient--low aromatic white spirits) were tested for efficacy in killing C. megacephala larvae in vitro. Leaf extracts were not used directly on patients. RESULTS: There were 16 patients (10 males and five females; the sex of one patient was not recorded). The mean age was 58.5 years (range, 11-94 years). Identification of larvae revealed C. bezziana in 14 (87.5%) and C. megacephala in two (12.5%) patients. The foot was affected in 15 (93. 7%) and the scalp in one patient. The immediate predisposing factor for CM in dermatology patients was infected dermatitis. The other relevant associated factors were: diabetes mellitus, psychiatric illness, leprosy, and mental subnormality. Turpentine was a useful adjunct in the removal of maggots manually. There were no side-effects to turpentine. In the in vitro testing, turpentine was 100% effective in killing maggots. Some patients required surgical removal under anesthesia. Indian beech and neem leaf extracts were not effective against Chrysomya larvae in vitro. CONCLUSIONS: All cases of CM were due to larvae of Chrysomya species. The commonest was C. bezziana. C. megacephala larvae causing CM have been reported for the first time in Sri Lanka. The foot was the site of predilection. Dermatitis, psychiatric illness, leprosy, diabetes, and mental subnormality were some contributory factors. Topically instilled mineral turpentine, followed by manual removal of maggots, was effective in most cases. The plant extracts tested in vitro were ineffective. As C. bezziana is an obligatory parasite capable of penetrating deeply, the importance of preventive measures is emphasized.
Adolescent↗
Involvement of the acute phase protein alpha 1-acid glycoprotein in nonspecific resistance to a lethal gram-negative infection.
Resistance to gram-negative infection can be induced by pretreating animals with several agents such as turpentine and interleukin (IL)-1. Because these agents are powerful inducers of acute phase proteins, we wondered whether these proteins, more particularly alpha(1)-acid glycoprotein (alpha(1)-AGP), are involved in nonspecific resistance to infection. Turpentine and IL-1 protect completely against a lethal challenge of Klebsiella pneumoniae when given 48 and 12-48 h before the challenge, respectively. alpha(1)-AGP induction in the serum reached peak values 48 h after turpentine and 12-48 h after IL-1 injection. Administration of alpha(1)-AGP, 2 h before a challenge of K. pneumoniae, significantly increased the survival. Numbers of bacteria cultured from blood and organs were significantly lower in mice pretreated with a protective dose of turpentine, IL-1, or alpha(1)-AGP. These data suggest that alpha(1)-AGP is a possible mediator in turpentine- or IL-1-induced protection because time points of maximal induction of alpha(1)-AGP by turpentine or IL-1 and of optimal protection by alpha(1)-AGP coincide. Transgenic overexpression of rat alpha(1)-AGP protected mice from a K. pneumoniae infection. Bacterial counts in blood and organs were significantly lower in transgenic mice, and only in control mice were large necrotic areas, apoptosis, and blood clots observed in the spleen. Our data suggest that alpha(1)-AGP prevents gram-negative infections and may be an essential component in nonspecific resistance to infection.
Animals↗
Hepatic gene expression and cytokine responses to sterile inflammation: comparison with cecal ligation and puncture sepsis in the rat.
Inflammatory stimulation of hepatic acute phase protein expression is, in part, modulated by tumor necrosis factor-alpha (TNFalpha), interleukin-1beta (IL-beta), and IL-6. These cytokines also may mediate some aspects of the persistent inflammation and metabolic dysregulation of sepsis. Cecal ligation and puncture (CLP) sepsis in male Sprague-Dawley rats inappropriately decreases hepatocellular transcription of phosphoenolpyruvate carboxykinase (PEPCK), glucose-6-phosphatase (G6Pase), carnitine palmitoyltransferase II (CPTII), acetyl CoA acyltransferase (ACA), and ornithine transcarbamylase (OTC). We hypothesize that 1) transcriptional reprogramming does not occur after simple inflammation induced by subcutaneous turpentine injection, 2) the pattern of acute phase gene expression after CLP differs from that following turpentine injection, and 3) the different responses reflect differences in the intrahepatic activity of TNFalpha/IL-1beta or IL-6. Gene expression, transcription factor activity, and cytokine abundance were determined after either a subcutaneous injection of turpentine or CLP. After turpentine injection, PEPCK, G6Pase, CPTII, ACA, and OTC expression were unchanged, different from previously reported data following CLP. Both turpentine injection and CLP increased expression of TNFalpha/IL-1beta-regulated alpha1-acid glycoprotein, and IL-6-regulated alpha2-macroglobulin and decreased expression of transthyretin (a negative acute phase protein). However, the magnitude and temporal pattern of expression differed. Turpentine injection increased the activity of the TNFalpha/IL-1beta-linked transcription factor NF-kappaB and the intrahepatic abundance of TNFalpha in a manner similar to that observed after CLP but only slightly altered the activity of the IL-6-linked transcription factor Stat-3 and intrahepatic IL-6 abundance. This differed significantly from observations after CLP. We conclude that CLP-induced alterations in hepatic gene expression may reflect differences in IL-6 activity.
Acute-Phase Reaction↗
Quantification of ocular inflammation with technetium-99m glucoheptonate.
Histological and morphometric evaluation of ocular inflammation is difficult, particularly when there is extensive ocular involvement with abscess formation and necrosis. A quantitative imaging procedure applicable to humans would be important clinically. To establish such a procedure, turpentine-induced ocular inflammation was obtained by subconjunctival injection in the right eye of 55 rabbits. The left eye was used as control and injected with a volume of saline equal to the volume of turpentine in the right eye. Volumes of turpentine or saline were 0.02, 0.04, 0.06, 0.2 and 0.6 ml, and the rabbits were divided into groups 1-5, according to these volumes. Imaging was performed 48 h after turpentine injection and 6 h after intravenous injection of 10 mCi of technetium-99m glucoheptonate (99mTc-GH). An inflammatory reaction index (IRI), defined as the ratio of counts of the right eye divided by counts of the left eye, was used. IRIs were proportional to the degree of inflammation and allowed the distinction of 3 subgroups: one represented by group 4, one by group 5 and one by groups 1, 2 and 3. This method of quantification of ocular inflammatory processes using 99mTc-GH is original, rapid, non-invasive, reproducible and safe, although unable to differentiate inflammatory processes caused by doses of turpentine which are very small and close to each other. It is conceivable that its application to humans will bring new insight into the ocular inflammatory process and response to therapy.
Animals↗
Polyamines in rat liver during experimental inflammation.
The effect of turpentine, a chemical inflammatory agent, on polyamine synthesis has been studied. Ornithine decarboxylase activity is markedly increased in liver 6 hrs after subcutaneous injection of turpentine, and then decreases. No significant modification is observed in S-adenosylmethionine decarboxylase. Putrescine injected prior to turpentine prevents this increase. Putrescine, spermidine and spermine concentrations are all increased following turpentine, but with different patterns: spermidine alone keeps increasing for 50 hours. Putrescine and spermidine injected prior to turpentine partially counteract the increase of serum alpha 2-macroglobulin, which is believed to be a marker of inflammation.
Adenosylmethionine Decarboxylase↗
Mechanisms of activation of the pituitary-adrenal axis by tissue injury in the rat.
To characterize the mechanisms of the pituitary-adrenal (P-A) response to tissue injury, rats were injected intramuscularly (IM) with turpentine. This resulted in marked elevations in the plasma concentrations of ACTH and corticosterone within the first hour after injection, which were attenuated by either total deafferentation of the medial basal hypothalamus (MBH) or neonatal capsaicin pretreatment. The plasma concentrations of corticosterone remained elevated for 18 h in the turpentine-injected rats, despite a return of ACTH toward control values (by 2-4 h). Bioactive concentrations of interleukin-6 (IL-6) in plasma rose markedly after turpentine, and its concentrations were significantly correlated with plasma corticosterone concentrations 4-8 h after turpentine. Pretreatment with IL-1 receptor antagonist (IL-1ra) attenuated the release of IL-6 and had a marginal effect on the corticosterone response 6 h after turpentine. These results suggest that the early and late phase of the P-A response to tissue injury are mediated by different mechanisms.
Acute-Phase Reaction↗
Signal transduction pathways implicated in the decrease in CYP1A1, 1A2 and 3A6 activity produced by serum from rabbits and humans with an inflammatory reaction.
Incubation of serum from rabbits with a turpentine-induced inflammatory reaction and from humans with an upper respiratory viral infection with hepatocytes from rabbits with a turpentine-induced inflammatory reaction for 4h reduces total cytochrome P450 content and activity of cytochrome P450 isoforms CYP1A1/1A2 and 3A6 without affecting the expression of these proteins. To document the signal transduction pathways implicated in the decrease in CYP1A1/1A2 and 3A6 activity, hepatocytes from rabbits with a turpentine-induced inflammatory reaction were incubated with serum from rabbits with a turpentine-induced inflammatory reaction, serum from individuals with a viral infection and interleukin-6 for 4h in presence of inhibitors of protein kinases. The sera-induced decrease in CYP1A1/1A2 and 3A6 activity was partially prevented by the inhibition of Janus-associated protein tyrosine kinase, double-stranded RNA-dependent protein kinase, protein kinase C, and p42/44 mitogen-activated protein kinase. The serum from rabbits with a turpentine-induced inflammatory reaction increased the phosphorylation of Erk1/2, effect prevented by PD98059 but not by bis-indolylmaleimide, a specific inhibitor of protein kinase C. The results demonstrated that the decrease in total cytochrome P450 content and in CYP1A1/1A2 and 3A6 activity by sera and interleukin-6 involves the activation of protein tyrosine kinases, p42/44 mitogen-activated protein kinase and protein kinase C. Indirect evidence supported that nitric oxide is implicated in the decrease in activity of these enzymes.
Animals↗
IL-6 and IL-1 beta in fever. Studies using cytokine-deficient (knockout) mice.
Previous data support the hypothesis that during inflammation, interleukin (IL)-1 beta and IL-6 are involved in fever, in activation of the hypothalamic-pituitary-adrenal (HPA) axis, and in the induction of eicosanoids. Most of the pathophysiologic effects of IL-1 beta and Il-6 are mediated by prostaglandins (PGs), modulated by other cytokines, and antagonized by glucocorticoids (GC), a final product of the HPA axis. To further test these relationships, we measured changes in body temperature using biotelemetry in mice deficient in genes for IL-1 beta and/or IL-6 (IL-1 beta knockout [KO] and IL-6 KO) following injection with lipopolysaccharide (LPS) to induce systemic inflammation or turpentine to induce local abscess. Circulating IL-6, tumor necrosis factor alpha (TNF-alpha), GC, and PGE2 were measured in these mice after treatment. IL-1 beta KO mice responded with reduced fever and IL-6 KO mice with normal fever to a high dose of LPS. In contrast, neither type of KO mice produced fever to turpentine. PGE2 levels (measured in the circulation) were suppressed in both types of KO mice injected with turpentine. IL-1 beta KO mice showed deficiency in IL-6 following turpentine, but not LPS, injection. LPS-induced increases in TNF-alpha did not differ between IL-1 beta KO mice and their wild-type counterparts, whereas IL-6 KO mice showed exacerbated LPS-induced circulating TNF-alpha. No differences were noted in plasma elevations of GC between KO and wild-type mice following injection of LPS or turpentine, indicating that IL-1 beta and IL-6 are not required for activation of the HPA axis during inflammation. Our data demonstrate that in the mouse, IL-1 beta and IL-6 are critical for the induction of fever during local inflammation, whereas in systemic inflammation they appear only to contribute to fever.
Animals↗
Effect of inflammation and proadifen on the disposition of antipyrine, lignocaine and propranolol in rat isolated perfused liver.
The effect of inflammation, induced in rats by injection of turpentine oil, on drug disposition has been evaluated in rat isolated perfused livers. The drugs studied were a low extraction drug, antipyrine, and two high extraction drugs, lignocaine and propranolol. Turpentine significantly increased the half-life of antipyrine and of propranolol, but not that of lignocaine. Proadifen (SKF 525A) significantly increased the half-life of all three drugs. Turpentine decreased the clearance of antipyrine significantly by about 50% and that of propranolol non-significantly by about 20%, but did not affect the clearance of lignocaine. Proadifen significantly decreased the clearance of all three drugs, but this was most pronounced for antipyrine. In both turpentine- and proadifen-treated rats a significant increase in volume of distribution of propranolol was observed. The results show that, as with proadifen, turpentine-induced inflammation affects the hepatic clearance of antipyrine in the rat isolated perfused liver. With both high extraction drugs, the effect of inflammation on their clearance was low or absent, in contrast to the effect of proadifen. This suggests that a possible effect of inflammation on intrinsic clearance is not large enough to influence the hepatic clearance of the high extraction drugs.
Animals↗
IL-1 beta mediates leptin induction during inflammation.
Interleukins (IL) are key mediators of the host response to infection and inflammation. Leptin is secreted by adipose tissue and plays an important role in the control of food intake. Administration of lipopolysaccharide (LPS), tumor necrosis factor (TNF), or IL-1 acutely increases leptin mRNA and protein levels. To investigate the role of IL-1 beta and IL-6 in leptin expression during inflammation, we used IL-1 beta-deficient (-/-) and IL-6 -/- mice. Mice were injected intraperitoneally with LPS or subcutaneously with turpentine, as models of systemic or local inflammation, respectively. In IL-1 beta +/+ mice, both LPS and turpentine increased leptin mRNA and circulating leptin. In contrast, neither LPS nor turpentine increased leptin levels in IL-1 beta -/- mice. In IL-6 +/+ or IL-6 -/- mice, turpentine increased leptin protein to comparable levels. We conclude that IL-1 beta is essential for leptin induction by both LPS and turpentine in mice, but IL-6 is not.
Animals↗
Transplacental transport of alpha 2-macroglobulin (alpha 2M) and induction of alpha 2M in maternal and neonatal rats with acute inflammation.
The aims of this study were to investigate transplacental transport of alpha 2-macroglobulin (alpha 2M) in rats in rats and to examine the degree of alpha 2M induction in maternal and neonatal rats with acute inflammation. Serum was collected from healthy pregnant CD (IGS) rats, neonates of the pregnant rats and their cord blood. Additional serum samples were obtained from pregnant rats inoculated with an inflammatory agent, turpentine oil, their neonates and cord blood, and neonates inoculated with turpentine oil. The serum levels of alpha 2M were measured by means of an enzyme-linked immunosorbent assay. The average serum levels of alpha 2M in healthy neonates and cord blood were about 380 micrograms/ml. Serum a2M level in neonates inoculated with turpentine oil averaged about 580 micrograms/ml. Serum alpha 2M levels in maternal rats inoculated with turpentine oil, neonates from those rats and their cord blood were elevated, the values being 2,000 micrograms/ml or higher. It was demonstrated that induction of alpha 2M in neonatal rats was lower than in maternal rats when inoculated with turpentine oil. These results suggest that alpha 2M is transplacentally transported from maternal rats to fetal ones.
Animals↗
Cyclooxygenase system contributes to the maintenance of post convulsive period of epileptic phenomena in the genetically epileptic El mice.
Recent studies have shown that cytokines and cyclooxygenase (COX)-2 are up-regulated in the brain of human epilepsy patients and animal models of epilepsy. We investigated the effect of inflammatory responses induced by intramuscular injection of turpentine on the epileptic phenomenon in genetically epileptic El mice. As parameters of epileptic seizure, seizure threshold (number of toss-ups to induce convulsion), duration of actual convulsion and duration of post actual convulsive period (period from the offset of convulsion to full recovery) were evaluated. The post actual convulsive period was prolonged without any change of seizure threshold or duration of actual convulsion 24 h after turpentine injection. Although pretreatment with indomethacin for one week did not change the seizure parameters, indomethacin suppressed the prolongation of the post actual convulsive period induced by turpentine. The mRNA expression of IL-1beta, IL-6 and COX-2 in the cerebral cortex was detected by RT-PCR. There was no difference in the mRNA expression in the cerebral cortex before and 24 h after seizure. The mRNA levels of IL-1beta, IL-6 and COX-2 in the cerebral cortex were up-regulated 24 h after turpentine injection. On the other hand, the up-regulated mRNA levels of IL-1beta, IL-6 and COX-2 in the cerebral cortex after turpentine treatment were not suppressed by indomethacin. These results suggest that prostaglandins induced with COX-2 in the cerebral cortex seem to play an important role in the maintenance of the post convulsive period, but not in induction and maintenance of the actual convulsive state.
Animals↗
Comparison of the effects of four hyperplastic agents on hamster cheek pouch mucosa.
Hyperplasia in the hamster cheek pouch was examined using 4 different hyperplastic agents: oil of turpentine 50% v/v in liquid paraffin; vitamin A palmitate 10% w/v in liquid paraffin; 12-O-tetradeconyl-phorbol-13-acetate 16nM in acetone; and ethylphenylpropiolate 0.04mM in acetone. Acetone, paraffin and untreated control groups were also examined. Cheek pouches were painted 3 times a week for up to 4 weeks with each solution. Samples were removed and prepared for light microscopy 24 hours after 2 weeks of painting and 24 hours, 6, 12 and 18 weeks after 4 weeks of painting. Hyperplasia was produced by application of turpentine, vitamin A and TPA after 2 weeks of application. Further increases in epithelial width occurred after 4 weeks of painting in the turpentine and vitamin A groups but a decrease was seen in the TPA group. Six weeks (vitamin A and TPA groups) or 12 weeks (turpentine group) after the completion of treatment the epithelium had a normal histological appearance. No differences between the control or EPP treated cheek pouch mucosa could be detected. Turpentine and vitamin A can be used as models of reversible hyperplasia in the hamster cheek pouch.
Alkynes↗
c-PKC-dependent modulation of plasma fibrinogen levels during the acute-phase response in young and old rats.
The expression and subcellular distribution of liver cPKC alpha and beta, nPKC delta and aPKC zeta isoenzymes and the plasma levels of fibrinogen were measured in young, 2- and 6-month-old, and aged, 24-month-old, normal and turpentine-treated rats, to induce an aseptic inflammatory condition and the acute-phase response. In young and old rats a down-regulated expression of cPKC alpha and, to a lesser extent, beta isoenzymes, was observed 8 h after turpentine administration, i.e. at times preceding the maximal expression of fibrinogen mRNA. Under these conditions, the plasma fibrinogen levels peaked by 24 h in young animals, being up to 7-fold over the values of untreated controls at 72 h. By contrast, old untreated control rats showed 4-fold increases of basal plasma fibrinogen levels compared with young controls, with down-regulated expression of cPKC alpha. In old rats, treatment with turpentine increased up to 1.9-fold over the basal control values the fibrinogen concentration within 72 h. Levels similar to those of young turpentine-treated animals were reached at this time. The results of this study suggest a prominent role for cPKC alpha in eliciting the synthesis of fibrinogen after inducing an acute-phase response with turpentine administration in young as well as old rats. This isoform may act by regulating the serine phosphorylation of Stat3 transcription factor, whose activation is under IL-6 control, a multifunctional cytokine that is proving to be a major contributor to the acute-phase response. No evidence for a role of aPKC zeta or of nPKC delta was demonstrated under these conditions.
Acute-Phase Reaction↗
Inhibition of liver RNA breakdown during acute inflammation in the rat.
Liver RNA- and protein-degradation rates were measured after the induction of acute inflammation in the rat. A preliminary study determined changes in hepatic RNA and protein content 12, 18 and 24 h after a turpentine oil injection. The RNA content in turpentine-treated rats compared with pair-fed animals increased significantly and sharply from 12 h (+ 11%) to 18 h (+ 32%) and slightly thereafter (+ 37% at 24 h). The liver protein content was significantly enhanced only at 24 h (+ 11%) in response to inflammation. RNA-degradation rates were determined in livers perfused cyclically in situ for 15 min by measuring the accumulation of radioactive cytidine in the medium 60 h after in vivo labelling of RNA by [5-3H]cytidine instead of [6-14C]orotic acid, the most commonly used radioactive marker. Several validation procedures showed that the method employed was a valid alternative to the use of radioactive orotic acid. RNA-degradation rates, which mainly reflect rRNA breakdown, were significantly lower in the turpentine-treated rats than in respective pair-fed animals at 18 and 24 h (57 and 45% decrease respectively). Proteolysis rates measured at 24 h together with RNA breakdown by valine accumulation in the perfusion medium were not modified after turpentine treatment. The main factors known to regulate RNA degradation (amino acids, insulin/glucagon ratio) were measured in the portal blood 24 h after induction of acute inflammation. Of the known regulatory amino acids, only glutamine and to a lesser extent methionine were increased in the turpentine-treated rats as compared with their pair-fed counterparts. The insulin/glucagon molar ratio was similar in both groups. In conclusion, the reduced breakdown of RNA, especially rRNA, is largely responsible for the accumulation of hepatic RNA during acute inflammation. This inhibition of RNA degradation could possibly be related to the increase in glutamine.
Amino Acids↗
Inhibitory effect of neurogenic and immune stressors on testosterone secretion in rats.
OBJECTIVE: We investigated the ability of foot shocks, endotoxemia and turpentine-induced tissue injury, to interfere with luteinizing hormone (LH) and testosterone (T) secretion, and the putative role of beta-adrenergic, opiate- and corticotropin-releasing factor (CRF) receptors in these responses. METHODS: Adult male rats were exposed to mild intermittent foot shocks for 1 h, administered endotoxin [lipopolysaccharide (LPS)] intravenously (i.v., 5 microg/kg), or injected with turpentine intradermally (i.m., 400 microl/kg), prior to injection with human chorionic gonadotropin (hCG, 1 U/kg i.v.). In some cases, antagonists to CRF, adrenergic or opiate receptors, or their vehicle were administered prior to the stressors. Levels of LH, T, tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), adrenocorticotropin (ACTH) and/or corticosterone were measured in serial blood samples. RESULTS: All three challenges significantly lowered basal LH and T levels and blunted the T response to hCG, though the magnitude of this inhibition was significantly (p < 0.01) smaller in shocked rats (42%), compared to animals injected with LPS (92%) or turpentine (78%). Shocks, LPS and turpentine all significantly stimulated ACTH and corticosterone release, and the magnitude and time course of these responses were also stressor specific. While turpentine only increased circulating IL-6 concentrations, shocks and LPS both significantly increased circulating TNF-alpha and IL-6 levels, but the effect of shocks was markedly smaller. Pretreatment with propranolol did not restore T responses, while naloxone produced small and inconsistent effects. However, the CRF antagonist Astressin B, which significantly prevented stressor-induced increase in circulating levels of ACTH and corticosterone, partially reversed the inhibitory effect of LPS on hCG-induced T release. CONCLUSION: (1) Both neurogenic and systemic stressors lower basal plasma LH and T levels and blunt the T response to hCG. (2) LPS, whose ability to release ACTH and corticosterone was similar to that of shocks, but caused increases in circulating TNF-alpha and IL-6 levels that were significantly larger than those due to the other stressors, was the most potent inhibitor of the T response to hCG. (3) Neither beta-adrenergic nor opiate receptors play a major role in the ability of the stressors we used to inhibit T release.
Adrenergic beta-Antagonists↗