Propofol proportionally decreased CBF and CMRO2 without affecting a-vDO2 in humans, suggesting that normal cerebral circulation and metabolism are maintained.

The aim of the current study was to elucidate the synergism of dietary calcium restriction and exhaustive exercise in the antioxidant enzyme system of rat soleus muscle, and to investigate the involvement of neutrophils in exercise-induced muscle damage. Forty-eight male Wistar rats were assigned to the following groups: control (C) or calcium-restricted [1 month (1 M) or 3 months (3 M)]. Each group was subdivided into acutely exercised or non-exercised groups. Soleus muscle from each rat was analysed to determine the levels of antioxidant enzymes [Mn-superoxide dismutase (SOD), Cu, Zn-SOD, glutathione peroxidase (GPX), and catalase (CAT)]. Dietary calcium restriction resulted in calcium deficiency and upregulated the antioxidant enzymes examined except GPX. Conversely, exhaustive exercise significantly decreased GPX and CAT, but not SODs activities in the calcium-restricted (1 M and/or 3 M) rats. Contents of immunoreactive Mn-SOD and Cu,Zn-SOD were only increased in the 3 M rats. During calcium restriction, the mRNA expression of both forms of SOD showed initial upregulation, followed by downregulation. Exhaustive exercise significantly increased the mRNA expressions only in the 3 M rats. Moreover, exhaustive exercise markedly increased myeloperoxidase activity in soleus muscles from the 1 M and 3 M rats compared with the C rats, and significantly enhanced the ability of neutrophils to generate superoxide in the 3 M rats. The results demonstrate that dietary calcium restriction upregulates certain antioxidant enzyme activities in rat soleus muscle, indicating an enhanced resistance to potential increases in intracellular reactive oxygen species. The results also suggest that exhaustive exercise may cause oxidative damage in soleus muscle of calcium-deficient rats through the activation of neutrophils.

We have assessed if fentanyl interacts with the endothelium to affect vessel tone. In the presence or absence of endothelium, fentanyl in concentrations greater than 10(-7) mol litre-1 decreased the sensitivity of the rat aortic rings to phenylephrine, but fentanyl in smaller concentrations had no significant effect. Rings, with or without endothelium, and pre-contracted by phenylephrine were relaxed by fentanyl, and this relaxation was not inhibited by the opioid receptor antagonist, naloxone. Pretreatment of the rings with either fentanyl or phentolamine protected alpha-adrenoceptors from block by the alpha-adrenoceptor antagonist, phenoxybenzamine. We conclude that, in the rat aorta, fentanyl-induced relaxation was mediated by alpha-adrenergic receptors, and that the endothelium modulated, but did not mediate, this relaxation.

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