13 résultats
BACKGROUND
Increase in SP release as a function of hypoxia of the rat carotid body is a tissue response to ischemia that leads to neurogenic inflammation and cognitive deficits. Substance P-mediated inflammation is reported to attenuate the neuroprotective PPAR-γ. This study was undertaken to
This basic review is intended to summarize the current knowledge of methemoglobinemia as an important cause of secondary headache with the hope of generating a growing interest in studying this phenomenon.We describe the pathological underpinnings of No current experimental model on migraine is fully satisfactory, and constructing a single model which takes into account all the various clinical and pharmacological aspects does not seem feasible. A critical review of the large number of experimental approaches developed over the past 20 years to
To characterize the tachykininergic effects in fire smoke (FS)-induced acute respiratory distress syndrome (ARDS), we designed a series of studies in rats. Initially, 20 min of FS inhalation induced a significant increase of substance P (SP) in bronchoalveolar lavage fluid (BALF) at 1 h and
Pain is a major comorbidity of sickle cell disease (SCD). Opioids are the mainstay for pain treatment but remain suboptimal. We discuss mechanism-based treatable targets devoid of opioids to prevent and/or treat SCD pain.Understanding the pathogenesis of The tachykinin NK1 receptor is widely distributed in both the central and peripheral nervous system. In the CNS, NK1 receptors have been implicated in various behavioural responses and in regulating neuronal survival and degeneration. Moreover, central NK1 receptors regulate cardiovascular and
Secretoneurin (SN) represents a 33 amino acid neuropeptide, which is highly conserved between mammals, reptiles, birds, amphibians and fish. It is specifically expressed in endocrine, neuroendocrine and neuronal tissues. In brain, the pattern of SN expression is widespread and unique, partially
The mechanisms underlying complex regional pain syndrome (CRPS) have been increasingly studied over the past decade. Classically, this painful and disabling disorder was considered to emerge from pathology of the central nervous system. However, the involvement of additional peripheral disease
BACKGROUND
Blau theorized that migraine triggers are exposures that in higher amounts would damage the brain. The recent discovery that the TRPA1 ion channel transduces oxidative stress and triggers neurogenic inflammation suggests that oxidative stress may be the common denominator underlying
Sickle cell anemia (SCA) is an inherited disorder associated with severe lifelong pain and significant morbidity. The mechanisms of pain in SCA remain poorly understood. We show that mast cell activation/degranulation contributes to sickle pain pathophysiology by promoting neurogenic inflammation
Migraine is a debilitating illness that has no exact bio molecule to explain its pathology. After reviewing the neurophysiological and biochemical basis of the research findings of nitric oxide and migraine, I present to the best of my knowledge the first para sinus nitric oxide mediated
Hydrogen sulfide (H(2)S) is an important gasotransmitter in the mammalian respiratory system. The enzymes that produce H(2)S - mainly cystathionine-β-synthase and cystathionine-γ-lyase - are expressed in pulmonary and airway tissues. Endogenous H(2)S participates in the regulation of the respiratory
Complex regional pain syndrome type I (CRPS-I) is a common and disabling disorder affecting a peripheral limb, usually developing after a trauma to an extremity. CRPS-I is characterised by presence of spontaneous pain, allodynia and hyperalgesia, disproportionate to the inciting event and by a