We studied the relation of perioperative blood transfusion and the outcomes in 175 patients with hepatocellular carcinoma (HCC) who underwent hepatic resection from 1986 to 1994 in our hospital. Hepatectomy was performed in 23 (13.1%) patients with and 152 (86. 9%) without blood transfusions. The cumulative cancer-free survival rates for patients who had received blood transfusion was significantly lower than that for patients who had not received blood transfusions (p = 0.003). Further examinations revealed a significant difference in cancer-free survival rates for stage I-II patients (n = 75) of HCC (p = 0.02) but not for stage III-IV patients (n = 56) (p = 0.06). Cox regression analysis for recurrence revealed that blood transfusion was the most significant prognostic indicator (p = 0.001) for recurrence in stage I-II patients but not in stage III-IV patients (p = 0.99). These results suggest that a perioperative blood transfusion may be a significant prognostic indicator for patients with HCC who had underwent hepatectomy, especially in stage I-II patients of HCC.

Tactile sensory abnormalities, such as tactile hypoesthesia and mechanical allodynia, are frequently present in patients with chronic pain. A growing body of evidence indicates that hyperesthetic phenomena, like mechanical allodynia, are at least in part due to altered processing by neurons in the CNS. We propose that the hyperesthesia is associated with a functional tactile hypoesthesia that is similarly mediated by altered processing by CNS neurons, and that this association is characterized by a particular topography that may be related to the receptive field organization of somatosensory CNS neurons. Moreover, we propose that the hyperesthetic-hypoesthetic association is dynamically modulated in tandem by pain input.

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Abstract. Cannabinoids have been reported to have analgesic properties in animals of acute nociception or of inflammatory and neuropathic pain models, but the mechanisms by which they exert such alleviative effects are not yet fully understood. We investigated whether the CB 1 -cannabinoid-receptor agonist HU210 modulates the capsaicin-induced 45 Ca 2+ influx and substance P like-immunoreactivity (SPLI) release in cultured rat dorsal root ganglion (DRG) cells. HU210 attenuated the capsaicin-induced 45 Ca 2+ influx and this effect was reversed by the CB 1 antagonist AM251. Treatment of DRG cells with 100 nM bradykinin for 3 h potentiated capsaicin-induced SPLI release accompanied with the induction of cyclooxygenase-2 mRNA expression. The potentiation of SPLI release by bradykinin was reversed by HU210 or the protein kinase A (PKA) inhibitor H-89. HU210 also reduced forskolin-induced cyclic AMP production and forskolin-induced potentiation of SPLI release. These results suggest that CB 1 could inhibit either the capsaicin-induced Ca 2+ influx or the potentiation of capsaicin-induced SPLI release by a long-term treatment with bradykinin through involvement of a cyclic-AMP-dependent PKA pathway. In conclusion, CB 1 -receptor stimulation modulates the activities of transient receptor potential vanilloid receptor 1 in cultured rat DRG cells.

Objective-The present study was designed to examine in the human omental artery whether high concentrations of D-glucose inhibit the activity of ATP-sensitive K ϩ channels in the vascular smooth muscle and whether this inhibitory effect is mediated by the production of superoxide. Methods and Results-Human omental arteries without endothelium were suspended for isometric force recording.Changes in membrane potentials were recorded and production of superoxide was evaluated. Glibenclamide abolished vasorelaxation and hyperpolarization in response to levcromakalim. D-glucose (10 to 20 mmol/L) but not L-glucose (20 mmol/L) reduced these vasorelaxation and hyperpolarization. Tiron and diphenyleneiodonium, but not catalase, restored vasorelaxation and hyperpolarization in response to levcromakalim in arteries treated with D-glucose. Calphostin C and Gö6976 simultaneously recovered these vasorelaxation and hyperpolarization in arteries treated with D-glucose. Phorbol 12-myristate 13 acetate (PMA) inhibited the vasorelaxation and hyperpolarization, which are recovered by calphostin C as well as Gö6976. D-glucose and PMA, but not L-glucose, significantly increased superoxide production from the arteries, whereas such increased production was reversed by Tiron. Key Words: ATP-sensitive K ϩ channels Ⅲ high glucose Ⅲ human artery Ⅲ protein kinase C Ⅲ superoxide I ncreasing evidence suggests that ATP-sensitive K ϩ channels play important roles in physiological and pathophysiological vasodilation. 1 Previous studies on the diabetic animal models suggest that hyperglycemia impairs the activity of ATP-sensitive K ϩ channels in the vascular smooth muscle cells. 2,3 Although a recent study on coronary arterioles from the diabetic patients has documented the reduction of vasorelaxation mediated by ATP-sensitive K ϩ channels, 4 the acute effect of high glucose on the activity of K ϩ channels has not been studied in the human blood vessels. Conclusions-TheseStudies using several diabetic animal models indicate that superoxide reduces the activity of ATP-sensitive K ϩ channels in the vascular smooth muscle cells. 5 However, the evidence showing that hyperglycemia-induced formation of reactive oxygen species modulates the activity of ATP-sensitive K ϩ channels is scarce. Recent studies on the rat as well as the rabbit demonstrated that protein kinase C activation inhibits ATP-sensitive K ϩ channels expressed on vascular smooth muscle cells. 6,7 In animal models, hyperglycemia is reportedly capable of increasing the activity of protein kinase C, whereas this has not been well-documented in the human vasculature. 8 In addition, it is unclear whether in the human blood vessels the activation of protein kinase C via acute exposure of high glucose may induce increased production of superoxide, resulting in the inhibitory effect on the function of K ϩ channels. Therefore, the present study was designed to examine in the human omental artery, whether high concentrations of D-glucose inhibit the activity of ATP-sensitive K ϩ channels, and wh...

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The present study was designed to examine whether in the human artery, synthetic peroxisome proliferator-activated receptor (PPAR)-␥ agonists restore vasorelaxation as well as hyperpolarization via ATP-sensitive K ϩ channels impaired by the high concentration of D-glucose and whether the restoration may be mediated by the antioxidant capacity of these agents. The isometric force and membrane potential of human omental arteries without endothelium were recorded. The production rate of superoxide was evaluated using a superoxide-generating system with xanthine-xanthine oxidase in the absence of smooth muscle cells. Glibenclamide abolished vasorelaxation and hyperpolarization in response to levcromakalim. Addition of D-glucose (20 mM) but not L-glucose (20 mM) reduced this vasorelaxation and hyperpolarization. Synthetic PPAR-␥ agonists (troglitazone and rosiglitazone) and/or an inhibitor of superoxide generation (4,5-dihydroxy-1,3-benzene-disulfonic acid, Tiron), but not a PPAR-␣ agonist (fenofibrate), restored vasorelaxation and hyperpolarization in response to levcromakalim in arteries treated with D-glucose. Troglitazone and rosiglitazone, but not fenofibrate, decreased the production rate of superoxide without affecting uric acid generation. These findings suggest that synthetic PPAR-␥ agonists recover the function of ATP-sensitive K ϩ channels reduced by the high concentration of glucose in human vascular smooth muscle cells and that the effect of these agonists may be mediated in part by their antioxidant capacity.