Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A method for determining the vocalization response to algesic agents in conscious guinea pigs is described. Retrograde injection of small amounts of algesic agents into the femoral artery caused transient but obvious vocalization response in a dose-dependent manner. The vocal sound was converted into electrical signals and the envelope of the sound obtained by a peak detector circuit was recorded on an ink-writing oscillograph. The area of the vocalization response circumscribed by a base line and the envelope tracing of the vocal sound was also recorded. Bradykinin, kallidin, acetylcholine (ACh) and nicotine caused the vocalization response, while substance P, histamine, bethanechol, methacholine, serotonin, kallikrein and prostaglandins E1 and E2 caused no or little response. No detectable tachyphylaxis to bradykinin, ACh and nicotine was observed. The pretreatment with hexamethonium abolished the response induced by ACh or nicotine but not the response induced by bradykinin. These results suggest that the paravascular pain receptor of the femoral artery excited by ACh is nicotinic in character. Subcutaneous injection of morphine, pentazocine, diclofenac and aminopyrine inhibited the vocalization response induced by bradykinin in a dose-dependent manner.
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PMID:Vocalization response to close-arterial injection of bradykinin and other algesic agents in guinea pigs and its application to quantitative assessment of analgesic agents. 43 Mar 71

Kinins, the biologically active peptides, potentiate the central stimulatory effects of NA and depressant action of acetylcholine as have been shown by the authors previously. The aim of the work has been to study the effects of these peptides on the central action of 5-HT. For experiments female Wistar rats were used. 5-HT given ivc to the animals and 5-HTP applied ip resulted in an increase of the pain threshold to the electrical stimuli and in a worse motor coordination. Bradykinin injected ivc or kallikrein ip to some extent abolished these effects. The biochemical tests revealed that bradykinin ivc lead to a significant decrease in 5-HT content in the midbrain. In experiments in vitro this peptide increased markedly the release of the platelets 5-HT and inhibited the uptake of this mediator to platelets. The results have shown that kinins can attenuate the central action of 5-HT. This effect can be ascribed, at least in part to a kinin-induced changes of 5-HT concentration in some structures of the central nervous system.
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PMID:Effect of kinins on the central action of serotonin. 108 29

Bradykinin (BK), an important mediator of allergic reactions and pain induction, is released by the activation of the plasma kallikrein-kinin (K-K) cascade. Neurotropin is a biological material obtained from inflamed rabbit skin inoculated with vaccinia virus and is widely used clinically in Japan as an effective agent for these disorders. Since its mechanism of action is not clearly known, we have investigated the effects of Neurotropin on the human plasma K-K system. In dextran sulfate-activated plasma, Neurotropin inhibited the formation of BK, the cleavage of high molecular weight kininogen (HK) and the formation of kallikrein-C1 inhibitor and activated coagulation factor XII (FXIIa)-C1 inhibitor complexes. Experiments using purified enzyme of the K-K cascade indicated that Neurotropin inhibited surface-mediated activation of coagulation factor XII (FXII) and the activation of prekallikrein by FXIIa. Neurotropin also inhibited the binding of FXII and HK to the activating surface. These data suggest that the ameliorating effects of Neurotropin in allergic disorders and pain syndromes may be related to this ability to inhibit activation of the K-K cascade and consequently the formation of BK.
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PMID:Effect of Neurotropin on the activation of the plasma kallikrein-kinin system. 156 87

Bradykinin, a nine-amino-acid peptide formed from a large precursor polypeptide (kininogen) by the action of the enzyme kallikrein (kininogenase), is the initial mediator of inflammation, and, in particular, bradykinin induces pain and alters vascular permeability. Bradykinin is one of the first compounds produced at the site of tissue injury and subsequently initiates a cascade of reactions that produce the cardinal features of inflammation. We will explore the role that bradykinin plays in various types of neuronal injury. In particular, we will focus on the role that bradykinin and other kinins play in brain and spinal cord trauma, in the pathophysiology of subarachnoid and intraparenchymal hemorrhage and ischemia, and in the initiation of nociceptive pain. This role suggests that bradykinin antagonists may be clinically useful in the therapeutic management of neurosurgical patients.
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PMID:Bradykinin and neuronal injury. 158 16

Recent evidence suggests an important role for kinins in the generation of pain, swelling and the cellular damage associated with inflammatory joint disease. Kinins are considered to be pro-inflammatory peptides for a variety of reasons. They stimulate c fibres in the synovium to cause pain and increase extravasation of fluid to produce swelling. Kinins possess the capacity to release neurotransmitters (substance P, acetylcholine) and a second wave of mediators (interleukin-1, tumour necrosis factor, interleukin-8, prostaglandins, leukotrienes). The steady levels and turnover of kinins is regulated by formation (enzymic action of kininogenases on endogenous substrates called kininogens) and by metabolism (kininases, peptidases that hydrolyse kinins). These components of the kinin system can enter the synovial joint space either by transudation from the plasma or from degranulating neutrophils chemotactically attracted into the synovium from which they migrate into the synovial fluid. If kinins are involved, one would expect neutrophil derived mediators of the system to dominate in rheumatoid arthritis and psoriatic arthritis and plasma derived products to be more important in osteoarthritis and gout. But, the question whether any of the functions attributed to each component of the system can be considered to be a primary factor in the cellular pathology of inflamed joints remains to be established. Future investigations, including therapeutic trials with kinin antagonists and kallikrein inhibitors, will need to address the differential role of the kallikreins and kinins in the different types of synovitis, on symptoms of inflammation and on any remedial effects on the progression of tissue damage within the joint.
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PMID:Kinins--key mediators in inflammatory arthritis? 164 49

Kallikrein (Padutin-Depot) was administered to 20 patients with obliterative atherosclerosis of the lower limbs of the II degree (19 patients) and IV degree (1 patient). The drug was given in the daily dose of 40 U i.m. for 28 days. An effect of kallikrein on the distance in intermittent claudication, rate of pain relieve after walking the maximal distance, blood flow in the lower limbs, and on the index of circulating aggregates have been determined. Clinical improvement has been noted after a 4-week therapy with kallikrein. The drug in a single dose of 40 U activates plasma fibrinolytic system for 5 hours and decreases the number of circulating aggregates (2-5 h). The authors explain kallikrein action as the release of endogenous bradykinin, which subsequently releases two epithelial mediators, i.e. PFG1 and EDRF.
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PMID:[Kallikrein in the treatment of patients with obliterative atherosclerosis of the lower limbs and its mechanism of action]. 166 40

Potentialities of current chemotherapy of chronic pancreatitis are delineated. An individual approach is advocated for patients with the primary and secondary disease varying in etiology, for those with and without external and internal pancreatic insufficiency. Indications are validated for application of drugs distinct from each other by mechanism of action and intended for pain relief, of kallikrein-protease and other trypsin inhibitors, replacement polyenzymatic therapy, stimulators of pancreatic exocrine secretion, antihistamine drugs, parenteral feeding, vitamins, detoxicating, immunomodulating and psychopharmacological agents. Approaches to management of chronic pancreatitis and its complications as well as associated diseases are detailed. Chronic pancreatitis sufferers must be followed up and undergo prophylactic treatment.
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PMID:[Drug therapy of chronic pancreatitis]. 187 77

In recent years, numerous agents have been recognized as inflammatory mediators. In this review, however, we discuss only those having direct relevance to human inflammatory diseases These mediators are clinically important due to their proinflammatory properties such as vasodilatation, increased vascular permeability, pain and chemotaxis. They may lead to the fifth cardinal sign, loss of function in inflammatory diseases. Agonists and non-specific antagonists are used as pharmacological tools to investigate the inflammatory role of PGs, LTs, PAF, IL-1, histamine, complement, SP, PMN-leukocytes, and kallikrein-kininogen-kinin systems. Unfortunately, no compound is known which concurrently abolishes all actions and interactions of inflammatory mediators. Therefore it would be highly useful to promote efforts in developing selective and competitive antagonists against proinflammatory actions of these chemical mediators. This may help to a better understanding of the pathogenesis of inflammatory reactions, and it may also be useful for the therapy of inflammatory diseases.
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PMID:The role of chemical mediators in the pathogenesis of inflammation with emphasis on the kinin system. 197

Amben (fibrinolysis inhibitor) and parmidin (bradykinin inhibitor) were used as pathogenetic treatment of 38 and 36 patients with hemorrhagic erysipelas respectively. Early amben treatment proved clinically rather effective and was accompanied by normalization of fibrinolysis and kallikrein-kinin system. Parmidin treatment resulted only in pain control, other subjective signs, normalization of the kallikrein-kinin system while fibrinolysis activity was maintained at former levels.
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PMID:[The treatment of patients with the hemorrhagic form of erysipelas by using amben and parmidine]. 227 46

The release of glandular kallikrein into the interstitium of the parotid gland appears to play an important role in the occurrence of the inflammatory interstitial edema in chronic recurrent parotitis. This provides fresh impetus for the treatment of this parotid disease with a kallikrein inhibitor. In our present study, seven patients with acute exacerbated chronic recurrent parotitis were treated with the kallikrein inhibitor aprotinin (Trasylol, Bayer AG, Leverkusen). With this therapy all patients were free of pain 12 h after the start of the therapy and most salivary gland function had returned to normal by 48 h after beginning treatment. Within this period of time, concomitant swelling of the affected parotid gland disappeared completely in five patients and resolved in the other two patients after 1 week.
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PMID:New concepts in the treatment of chronic recurrent parotitis. 241 5


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