Journal of physiology and pharmacology : an official journal of the Polish Physiological Society
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J. Physiol. Pharmacol. · Sep 2005
Nitric oxide mediates the interleukin-1beta- and nicotine-induced hypothalamic-pituitary-adrenocortical response during social stress.
We investigated the role of nitric oxide (NO) in the interleukin 1beta (IL-1beta) and nicotine induced hypothalamic-pituitary-adrenal axis (HPA) responses, and a possible significance of CRH and vasopressin in these responses under basal and social stress conditions. Male Wistar rats were crowded in cages for 7 days prior to treatment. All compounds were injected i.p., nitric oxide synthase (NOS) inhibitors, alpha-helical CRH antagonist and vasopressin receptor antagonist 15 min before IL-1beta or nicotine. ⋯ These results indicate that NO plays crucial role in the IL-1beta-induced HPA axis stimulation under basal and social stress conditions. CRH and vasopressin of the hypothalamic paraventricular nucleus may be involved in the nicotine induced alterations of HPA axis activity. NO generated by eNOS, but not nNOS, is involved in the stress-induced alterations of HPA axis activity by nicotine.
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In the contemporary bioethics, patient's autonomy is often recognized as the most important issue. This autonomy is interpreted as the right to self-determination regarding all medical-related decisions. An essential condition of autonomous decisions is the adequate knowledge of the issues involved. ⋯ The results clearly show the multiplicity and variety of meanings that assume breathing-related linguistic expressions. All of them are classified in four main groups. In conclusion, the author submits that an improvement in the understanding of different meanings of words used in the doctor-patient relationship can contribute to maintaining ethical standards in medical practice.
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J. Physiol. Pharmacol. · Sep 2005
Ultrastructure of immediate microvascular lung injury induced by bacterial endotoxin in the isolated, no-deficient lung perfused with full blood.
NOS-2-derived NO is involved in hypotension, vasoplegia, metabolic disorders and lung injury in endotoxic shock. On the other hand, NOS-3-derived NO protects against LPS-induced lung injury. We have previously shown that NO limits lung injury in the isolated blood-perfused rat lung. ⋯ Mechanisms of immediate lung response to LPS in presence of NO and those leading to acute microvascular lung injury in response to LPS in absence of NO are summarized. In our view, immediate lung response to bacterial endotoxin represents a phylogenetically ancient host defence response involving complement-dependent activation of platelets and neutrophils and subsequent production of lipid mediators. This response is designed for a quick elimination of bacterial endotoxin from the circulation and is safeguarded by endothelial NO.
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Genomic studies provide scientists with methods to quickly analyse genes and their products en masse. The first high-throughput techniques to be developed were sequencing methods. A great number of genomes from different organisms have thus been sequenced. ⋯ Genomics and integrated biology are huge tasks and no single lab can pursue this alone. We are probably at the end of the beginning rather than at the beginning of the end because Genomics will probably change Biology to a greater extent than previously forecasted. In addition, there is a great need for more information and better understanding of genomics before complete public acceptance.
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J. Physiol. Pharmacol. · Jun 2005
Superoxide- and nitric oxide-derived species mediate endothelial dysfunction, endothelial glycocalyx disruption, and enhanced neutrophil adhesion in the post-ischemic guinea-pig heart.
The study was aimed at testing the hypothesis that a toxic product of the reaction between superoxide (O(2)(-)) and nitric oxide (NO) mediates, not only endothelial dysfunction, but also endothelium-glycocalyx disruption, and increased neutrophil (PMN) accumulation in the heart subjected to ischemia/reperfusion (IR) injury. Accordingly, we studied if scavengers of either O(2)(-) or NO, or a compound that was reported to attenuate cardiac production of peroxynitrite, would prevent endothelial injury and subsequent PNM adhesion in IR heart. Langendorff-perfused guinea-pig hearts were subjected to 30 min ischemia/35 min reperfusion, and infusion of PMN between 15 and 25 min of the reperfusion. ⋯ These alterations were prevented by superoxide dismutase (150 U/ml), NO synthase inhibitor, L-NAME (10 microM), NO scavenger, oxyhemoglobin (25 microM), and NO donor, SNAP (1 microM), and were not affected by catalase (600 u/ml). The glycocalyx-protective effect of these interventions preceded their effect on PMN adhesion. The data imply that PMN adhesion in IR guinea-pig heart is a process secondary to functional and/or structural changes in coronary endothelium, and that a toxic product of the reaction between superoxide and NO mediates these endothelial changes.