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Biomedical subjects

H Harbach

Publications and source records attributed to H Harbach.

7 recordsLinked to original sources

Minimal immunoreactive plasma beta-endorphin and decrease of cortisol at standard analgesia or different acupuncture techniques.

BACKGROUND AND OBJECTIVE: Acupuncture has been claimed to be associated with activation of the endogenous antinociceptive system. The analgesic effects of acupuncture have been ascribed to beta-endorphin interacting with opioid receptors. However, firstly, the release of beta-endorphin into the blood has been proven to be induced by stress, i.e. under dysphoric conditions, and, secondly, if released under stress, beta-endorphin has been shown not to be analgesic. Our aim was to test whether beta-endorphin immunoreactive material is released into the cardiovascular compartment during acupuncture comparing the most frequently used types of acupuncture with standard pain treatment under apparently low stress conditions. METHODS: This prospective study included 15 male patients suffering from chronic low back pain. beta-Endorphin immunoreactive material and cortisol were measured in the plasma of patients who underwent, in random order, therapy according to a standard pain treatment, traditional Chinese acupuncture, sham acupuncture, electro acupuncture and electro acupuncture at non-acupuncture points before, at and after the treatment. Statistical analysis was performed using two-way ANOVA with repeated measures. RESULTS: A decrease in plasma cortisol concentration measured over the five treatment protocols was highly significant (P < 0.001). The beta-endorphin immunoreactive material concentrations in plasma were minimal at all times and in all treatment conditions. The influence of treatments by various acupuncture procedures on cortisol and beta-endorphin immunoreactive material plasma concentrations over the three time points was not significantly different. CONCLUSIONS: beta-endorphin immunoreactive material in blood is not released by any type of acupuncture as tested under low stress conditions.

Acupuncture Analgesia↗

Pathways involved in alanyl-glutamine-induced changes in neutrophil amino- and alpha-keto acid homeostasis or immunocompetence.

We examined the effects of DON [glutamine-analogue and inhibitor of glutamine-requiring enzymes], alanyl-glutamine (regarding its role in neutrophil immunonutrition) and alanyl-glutamine combined with L-NAME, SNAP, DON, beta-alanine and DFMO on neutrophil amino and alpha-keto acid concentrations or important neutrophil immune functions in order to establish whether an inhibitor of *NO-synthase [L-NAME], an *NO donor [SNAP], an analogue of taurine and a taurine transport antagonist [beta-alanine], an inhibitor of ornithine-decarboxylase [DFMO] as well as DON could influence any of the alanyl-glutamine-induced effects. In summary, irrespective of which pharmacological, metabolism-inhibiting or receptor-mediated mechanisms were involved, our results showed that impairment of granulocytic glutamine uptake, modulation of intracellular glutamine metabolisation and/or de novo synthesis as well as a blockade of important glutamine-dependent metabolic processes may led to significant modifications of physiological and immunological functions of the affected cells.

Adult↗

Surfactant protein C mutations in sporadic forms of idiopathic interstitial pneumonias.

Interstitial pneumonias have recently been associated with mutations in the gene encoding surfactant protein C (SFTPC). In particular, SFTPC mutations have been reported in a number of familial forms of pulmonary fibrosis and in infants with interstitial lung diseases. The present study searched for SFTPC mutations in adult patients with sporadic idiopathic interstitial pneumonia. In total, 35 adult patients with sporadic idiopathic interstitial pneumonia and 50 healthy subjects were investigated for SFTPC mutations by direct DNA sequencing. Of the patients with sporadic idiopathic interstitial pneumonia, 25 suffered from idiopathic pulmonary fibrosis and 10 patients from nonspecific interstitial pneumonia. Only two frequent nonsynonymous variants, T138N and S186N, were detected. Allele frequencies of both variations as well as of other identified noncoding alterations did not differ significantly between the diverse patient groups and control subjects. In conclusion, mutations in the gene encoding surfactant protein C are not common in sporadic cases of idiopathic pulmonary fibrosis and nonspecific interstitial pneumonia, suggesting that the mutated gene does not play an important role in the pathogenesis of these forms of idiopathic interstitial pneumonia.

Adult↗

Nitric oxide and polyamine pathway-dependent modulation of neutrophil free amino- and alpha-keto acid profiles or host defense capability.

We have examined the effects of N(omega)-nitro-L-arginine-methylester-hydrochloride [L-NAME; inhibitor of nitric oxide synthase], S-nitroso-N-acetyl-penicillamine [SNAP; nitric oxide donor], alpha-difluoro-methyl-ornithine [DFMO; inhibitor of ornithine decarboxylase] arginine or ornithine as well as the combination of arginine or ornithine with L-NAME, SNAP or DFMO on intracellular free amino- and alpha-keto acid profiles and the immune function markers superoxide anion and hydrogen peroxide generation as well as released myeloperoxidase activity in neutrophils (PMN). Although the underlying mechanisms still remain unclear, we believe from our results that nitric oxide as well as polyamine-dependent pathways are involved in the signal transmission of free radical molecule, beneficial nutritional therapy or maleficient pharmacological stress-induced alterations in PMN nutrient composition. Relevant changes in intragranulocyte free amino- and alpha-keto acid homeostasis and metabolism, especially, may be one of the determinants in PMN nutrition that positively or negatively influences and modulate neutrophil host defence capability and immunocompetence.

Adult↗

Impact on postoperative pain of long-lasting pre-emptive epidural analgesia before total hip replacement: a prospective, randomised, double-blind study.

Clinical studies on pre-emptive analgesia have produced inconsistent results. We conducted a clinical study investigating the effect of long-lasting pre-emptive epidural analgesia on consumption of analgesics and acute pain. Forty-two patients scheduled for elective hip replacement for osteo-arthritis were randomly assigned to receive, on the day before operation, either 5 ml.h(-1) ropivacaine 0.2% (study group, n = 21) or 5 ml.h(-1) saline (control group, n = 21). Postoperative analgesia was achieved in both groups by patient-controlled epidural analgesia (PCEA) with ropivacaine 0.2%. The main outcome measure was consumption of local anaesthetics. Additional parameters included visual analogue pain scale (VAS) scores, consumption of rescue analgesics, requests for PCEA boluses, and side-effects. The pre-operative parameters and pain scores were similar in the two groups. Epidural blocks provided sufficient operative analgesia in all patients. Pre-emptive analgesia was continued for 11-20 h and led to significantly decreased pain scores before surgery. The consumption of local anaesthetics was decreased postoperatively in the study group (194 mg vs. 284 mg in the postoperative period). Furthermore, bolus requests occurred more frequently in the control group. VAS scores did not differ significantly between groups. Long-lasting "pre-emptive" epidural analgesia decreases postoperative pain with improved pain control.

Adult↗

Beta-endorphin (1-31) in the plasma of male volunteers undergoing physical exercise.

beta-Endorphin is an opioid peptide representing the C-terminal 31 amino acid residue fragment of proopiomelanocortin (POMC). The release of beta-endorphin from the pituitary into the cardiovascular compartment under physical or emotional stress has been frequently reported. However, besides beta-endorphin (1-31), nine acetylated or non-acetylated beta-endorphin analogues exist - in addition to N-terminally elongated beta-endorphin derivatives such as beta-lipotropin (beta-LPH). Since conventional radioimmunoassays (RIAs) and even commercially available two site-RIAs pick up at least some of those beta-endorphin derivatives, only "beta-endorphin immunoreactive materials" and not authentic beta-endorphin have been determined in those studies. We have developed a highly specific two site-RIA for beta-endorphin (1-31), which does not cross-react with all beta-endorphin derivatives known to occur as yet. Using this RIA as well as further assays for determination of beta-endorphin (1-31), beta-endorphin immunoreactive material (IRM), ACTH and Cortisol in the plasma of 14 volunteers upon intensive physical exercise, we found authentic beta-endorphin only in about 50% of the plasma samples, representing therein only a minor portion of the beta-endorphin IRM.

Adrenocorticotropic Hormone↗

beta-Endorphin immunoreactive material and authentic beta-endorphin in the plasma of males undergoing anaerobic exercise on a rowing ergometer.

Adrenocorticotropic hormone (ACTH), beta-endorphin immunoreactive material (beta-endorphin IRM), and authentic beta-endorphin (1 -31) have been determined in the plasma of 23 volunteers undergoing anaerobic exercise on a rowing ergometer. The volunteers had different histories of training from occasional physical activities up to intensive preparation for international rowing competitions. ACTH and beta-endorphin-IRM were determined using commercially available immunometric assays; for determination of beta-endorphin (1-31) a highly specific two-site fluid phase immunoprecipitation radioimmunoassay was developed, which did not cross-react with any beta-endorphin derivative or any other opioid peptide tested. In agreement with reports from the literature ACTH and beta-endorphin-IRM concentrations in the plasma rose upon anaerobic exercise in all 23 subjects; this increase in the ACTH and beta-endorphin IRM levels was significantly correlated with the increase of lactate levels observed upon anaerobic exercise. Authentic beta-endorphin (1-31) was only found in two plasma samples containing minor concentrations of the peptide. We conclude that the beta-endorphin immunoreactive material released into blood under anaerobic exercise is identical with authentic beta-endorphin (1-31) only to a minor extent and thus should not be called "beta-endorphin". The major part of the material in fact released into the blood upon anaerobic exercise is probably identical with beta-lipotropin and further components so far unknown.

Adrenocorticotropic Hormone↗