Journal of physiology and pharmacology : an official journal of the Polish Physiological Society
-
The available data supporting the role of oxygen radicals (OR0) as fundamental--though not unique--mediators in the pathogenesis of sepsis and septic shock are reviewed. The main questions are 1) Are there any signs of OR0 overgeneration during sepsis and septic shock? 2) Are there any indirect signs of OR0 damage during sepsis and septic shock? 3) Does OR0 inactivation affect the evolution and severity of sepsis and septic shock? 4) May the pathophysiology of sepsis and septic shock be viewed as a consequence of OR0 overgeneration? All these questions might receive affirmative answers; thus the relationships of OR0 with other mediators of sepsis and septic shock are discussed. ⋯ There are also very close relationships with nitric oxide, another free radical. The data in favour of an antioxidant therapy of sepsis and septic shock in humans are too few to be conclusive.
-
J. Physiol. Pharmacol. · Dec 1997
ReviewMechanisms of acute respiratory distress syndrome: role of surfactant changes and mechanical ventilation.
Acute respiratory distress syndrome (ARDS) is a condition characterized by a high permeability oedema due to loss of the integrity of the alveolo-capillary barrier with impairment of normal surfactant function, resulting in an increased collapse tendency of the alveoli. Mechanical ventilation on such alveoli with repeated alveolar collapse and subsequent reexpansion results in severe lung parenchymal injury and may induce further surfactant impairment. ⋯ Recent evidence from experimental studies has shown that ventilator modes which allow end-expiratory collapse can induce bacterial translocation from the lung into the bloodstream and trigger the release of inflammatory mediators, which can also be presented by maintaining end-expiratory alveolar volume. These data suggest that the interaction between surfactant changes and mechanical ventilation may play a role in the transition of ARDS into the systematic inflammatory disease process of multiple system organ failure (MSOF).
-
J. Physiol. Pharmacol. · Dec 1997
ReviewPhysiologic, metabolic and mediator responses in posttrauma ARDS and sepsis: is oxygen debt a critical initiating factor?
Posttrauma adult respiratory distress syndrome (ARDS) and sepsis initiate complex humoral and cellular inflammatory responses that initially effect the microvascular system, but rapidly extend to involve and modulate the solid organ metabolic response. It is discussed whether the interaction between these cellular processes and the organs which they involve appear to be initiated by the trauma induced oxygen debt.
-
J. Physiol. Pharmacol. · Jun 1997
Mediation by nitric oxide of the carbachol-induced corticosterone secretion in rats.
Nitric oxide synthase, an enzyme responsible for nitric oxide (NO) formation has been found in the hypothalamic paraventricular nucleus and median eminence, structures closely associated with regulation of the pituitary activity, and the pituitary gland itself. Nitric oxide modulates the stimulated release of CRH from the rat hypothalamus in vitro, which suggests its role in regulating the secretion of ACTH from the pituitary corticotrops and of corticosterone from the adrenal cortex. The purpose of the present study was to elucidate the yet unknown role of endogenous NO in the HPA response to central cholinergic stimulation in conscious rats. ⋯ L-NAME is a weak inhibitor of neuronal NOS itself, and must first be de-estrified to N omega-nitro-L-arginine to potently inhibit this enzyme. Systemic (10 mg/kg) and icv (1 microgram) pretreatment with L-NNA enhanced more effectively the carbachol-induced rise in corticosterone secretion than did pretreatment with L-NAME by either route. These results are the first direct evidence that endogenous NO significantly inhibits the HPA response to central cholinergic, muscarinic receptor stimulation under in vivo conditions.
-
J. Physiol. Pharmacol. · Jun 1997
Clinical Trial Controlled Clinical TrialEndogenous nitric oxide in the control of esophageal motility in humans.
Recent animal studies have suggested that nitric oxide (NO) plays an important role in the regulation of esophageal motility, being partly responsible for latency period and latency gradient between the onset of a swallow and contractions of esophageal circular smooth muscles. The aim of this study was to evaluate whether endogenous NO is responsible for physiological timing of forthcoming contractions in the human esophageal body after swallowing. Eight male volunteers (age 21-25 years, weight 67-82 kg) were involved in this placebo controlled study on the effects of increasing doses of the NO synthase blocker, NG-monomethyl-L-arginine (L-NMMA 1.0-4.0 mumol/min i.v.), and/or L-arginine (L-arg) (30 mumol/kg-min i.v.) on the peristalsis of esophageal body in response to wet swallows (5 ml of water) and lower esophageal sphincter (LES) resting pressure. ⋯ The mean BP significantly increased during infusion of L-NMMA (control 97.0 +/- 5.7 vs. L-NMMA 4.0 mumol/min: 116.4 +/- 3.1 mm Hg) and this was also reversed by L-arg. We conclude that in humans endogenous NO is involved, at least in part, in the physiological regulation of motility patterns of the distal esophageal body and LES.