Canadian journal of physiology and pharmacology
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Can. J. Physiol. Pharmacol. · Aug 2013
ReviewCardioprotection against myocardial reperfusion injury: successes, failures, and perspectives.
The past few decades have witnessed an enormous number of research strategies aimed at protecting the heart against myocardial ischemia-reperfusion injury. Several randomized clinical trials are nowadays in progress testing whether promising therapeutic strategies aimed at preventing lethal reperfusion injury can be translated from bench to bedside. ⋯ These limitations include clinical setting, patient profile, drug administration, and methods for evaluating treatment efficacy. Identifying potential mechanistic and methodological pitfalls in the field may improve future translational research.
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Breast cancers are the most common source of metastases to bone, of which cancer-induced bone pain is a frequent pathological feature. Cancer-induced bone pain is a unique pain state with multiple determinants that remains to be well understood and managed. Current standard treatments are limited by dose-dependent side effects that can reduce the quality of life of patients. ⋯ In cancer cells, glutamate release is understood to be a side effect of the cellular response to oxidative stress that upregulates the expression and activity of system x(c)(-) to promote the increased import of cystine. Attenuation of glutamate release from cancer cells has been demonstrated to result in reductions in associated cancer-induced bone pain in animal models. This review examines the clinical implications of attenuating cystine uptake and glutamate release in the treatment of cancer-induced bone pain.
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Can. J. Physiol. Pharmacol. · Feb 2009
ReviewTransient receptor potential: a large family of new channels of which several are involved in cardiac arrhythmia.
The transient receptor potential (TRP) family of ion channels comprises more than 50 cation-permeable channels expressed throughout the animal kingdom. TRPs can be grouped into 7 main subfamilies according to structural homology: the TRPC (canonical), TRPV (vanilloid), TRPM (melastatin), TRPP (polycystin), TRPML (mucolipin), TRPA (ankyrin), and TRPN (NO mechanopotential). ⋯ The later part of this review focuses on the potential contribution of TRPs to cardiac rhythm and their potential proarrhythmic effects. Furthermore, several neurotransmitters that activate the formation of diacylglycerol could modulate cardiac rhythm or, like ATP, induce arrhythmia.
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Can. J. Physiol. Pharmacol. · Jan 2007
ReviewSmooth muscle molecular mechanics in airway hyperresponsiveness and asthma.
Asthma is a respiratory disorder characterized by airway inflammation and hyperresponsiveness associated with reversible airway obstruction. The relative contributions of airway hyperresponsiveness and inflammation are still debated, but ultimately, airway narrowing mediated by airway smooth muscle contraction is the final pathway to asthma. Considerable effort has been devoted towards identifying the factors that lead to the airway smooth muscle hypercontractility observed in asthma, and this will be the focus of this review. ⋯ Increased smooth muscle rate of shortening via altered signaling pathways or altered contractile protein expression has been demonstrated in asthma and in numerous models of airway hyperresponsiveness. Increased rate of shortening is implicated in counteracting the relaxing effect of tidal breathing and deep inspirations, thereby creating a contracted airway smooth muscle steady-state. Further studies are therefore required to understand the numerous mechanisms leading to the airway hyperresponsiveness observed in asthma as well as their multiple interactions.
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Can. J. Physiol. Pharmacol. · Mar 2001
ReviewTherapeutic implications of hypothermic and hyperthermic temperature conditions in stroke patients.
Brain temperature is an important variable in determining the outcome of cerebral ischemia; increases in core temperature escalate neural damage whereas decreases in core temperature reduce damage. Fever induction often occurs in patients prior to or as a direct or indirect result of the ischemic insult, with a worsened stroke outcome, compared with non-febrile ischemic patients. Most importantly, post-ischemic hypothermia reduces long term neural damage and associated behavioral deficits in animals studied for up to a year after the ischemic insult. This review discusses the importance of monitoring the brain temperature of stroke patients and implemention of therapeutic thermoregulatory strategies to reduce the temperature of ischemic patients.