[Efficacy and safety of sugammadex (Org 25969) in reversing moderate neuromuscular block induced by rocuronium or vecuronium in Japanese patients].

BACKGROUND: Efficacy and safety of sugammadex in reversing neuromuscular block induced by rocuronium or vecuronium were investgated in Japanese patients. METHODS: We studied 98 Japanese patients undergoing surgery requiring general anesthesia. Patients were allocated randomly to receive intubation dose of rocuronium or vecuronium. During surgery, patients received additional doses of rocuronium or vecuronium for maintenance of moderate block. At T2 reappearance sugammadex 0-4.0 mg . kg-1 was administered. The neuromuscular block was monitored with acceleromyography using TOF stimuli. Sevoflurane was administered to all treatment groups after intubation. RESULTS: For the rocuronium-induced neuromuscular block, the mean recovery time of the T4/T1 ratio to 0.9 decreased from 82.1 min in the placebo group to 1.8 min in the 4.0 mg . kg-1 sugammadex group. For the vecuronium-induced neuromuscular block, it decreased from 83.2 min in the placebo group to 2.1 min in the sugammadex 4.0 mg . kg-1 group. Plasma concentrations of sugammadex were approximately dose proportional over the dose range of 0.5 to 4.0 mg . kg-1 and independent of the neuromuscular blocking agents used. No clinical evidence of recurarization or residual curarization was observed. CONCLUSIONS: The efficacy and safety of sugammadex were confirmed in Japanese surgical patients.

Sevoflurane inhibits angiotensin II-induced Rho kinase-mediated contraction of vascular smooth muscle from spontaneously hypertensive rat.

PURPOSE: Angiotensin II (Ang II)-induced vasoconstriction is mediated by changes in intracellular free Ca(2+) concentration ([Ca(2+)](i)) and myofilament Ca(2+) sensitivity. Protein kinase C- and Rho kinase-mediated signaling pathways are proposed for the regulation of the Ca(2+) sensitization mechanisms. We have demonstrated that sevoflurane inhibits Rho kinase-mediated contraction of isolated rat aortic smooth muscle. A recent study demonstrated that Rho-kinase mediated Ca(2+) sensitization was involved in the pathophysiology of hypertension. This study was designed to investigate the effects of sevoflurane on Ang II-induced Rho kinase-mediated vascular contraction in spontaneously hypertensive rats (SHR). METHODS: The effects of sevoflurane on vasoconstriction, increase in [Ca(2+)](i), and membrane translocation of Rho kinase in response to Ang II were investigated in normotensive Wistar-Kyoto rats (WKY) and SHR, using an isometric force transducer, a fluorometer, and Western blotting, respectively. RESULTS: The inhibitory effects of sevoflurane on Ang II (10(-7)M)-induced contraction were greater (P < 0.05) in SHR than in WKY at the highest concentration of sevoflurane (5.1%). Y27632 (3 × 10(-7)M), a specific inhibitor of Rho kinase, inhibited the Ang II-induced contraction in SHR, but not in WKY. Sevoflurane did not affect the increases in [Ca(2+)](i) in response to Ang II in either strain. Ang II stimulated Rho kinase activity in SHR, which was almost abolished by sevoflurane at a concentration of 5.1% (P < 0.05). CONCLUSIONS: These findings suggest that the inhibition of the Ang II-induced contraction by sevoflurane in SHR may be, at least in part, due to the attenuation of the Rho kinase-mediated signaling pathway.

High-dose remifentanil suppresses sinoatrial conduction and sinus node automaticity in pediatric patients under propofol-based anesthesia.

BACKGROUND: We sought to determine the effect of remifentanil on sinus node function and the atrial-His (AH) interval in pediatric patients undergoing radiofrequency catheter ablation. METHODS: Sixty pediatric patients with Wolff-Parkinson-White syndrome were prospectively enrolled in this study. General anesthesia was induced and maintained with a continuous infusion of propofol. We recorded the calculated sinoatrial conduction time (CSACT), corrected sinus node recovery time (CSNRT), and AH interval when the patients were in a stable anesthetic state and compared the values before and during remifentanil administration at a moderate dose (0.2 µg · kg(-1) · min(-1)) or a high dose (0.4 µg · kg(-1) · min(-1)). Data are expressed as mean (95% confidence interval). RESULTS: At the moderate dose, remifentanil prolonged CSNRT (from 177 [117-237] milliseconds to 245 [167-322] milliseconds after administration; P=0.016), but had no effect on either CSACT (P=0.59) or AH interval (P=0.11). However, high-dose remifentanil prolonged both CSNRT (from 201 [144-260] milliseconds to 307 [232-382] milliseconds after administration; P=0.019) and CSACT (from 48 [31-65] milliseconds to 78 [59-96] milliseconds after administration; P=0.038), but had no effect on the AH interval (P=0.058). The interaction in CSNRT between remifentanil administration and its dose was not different (P=0.44). CONCLUSION: Remifentanil may inhibit both intraatrial conduction and sinus node automaticity, but it has no effect on conduction through the atrioventricular node. Dose dependency was not observed within the range of 0.2 to 0.4 µg · kg(-1) · min(-1) of remifentanil.

Reduction of adhesion formation by an angiotensin type 1 receptor antagonist.

PURPOSE: Adhesion formations are important causes of intestinal obstruction and can lead to infertility in women. The formation of adhesion appears to be determined by the fibrinolytic activity. Fibrinolysis itself is controlled by the plasminogen activator system, and several studies have shown that angiotensin type 1 (AT(1)) receptor antagonists can reduce plasminogen activator inhibitor-1 (PAI-1) expression, but the effect of AT(1) receptor antagonists on PAI-1 expression involved in the adhesion formation remains unclear. The aim of this study was to investigate whether an AT(1) antagonist, candesartan, can reduce PAI-1 mRNA expression using experimental model of peritoneal adhesions, which seems to reflect post-operative adhesions. METHODS: Using the experimental bowel adhesion rat model, we compared adhesion formation evaluated by the adhesion scoring system and PAI-1 mRNA expression. RESULTS: The adhesion score and PAI-1 mRNA expression were significantly increased in the experimental bowel adhesion rat model. Candesartan administration decreased adhesion score and abolished increase in PAI-1 mRNA expression. CONCLUSIONS: The AT(1) receptor antagonist, candesartan, significantly decreased the severity of intraperitoneal adhesion, which was associated with an inhibition of PAI-1 mRNA expression in the mesenterium of rats. It suggests that AT(1) receptor antagonists may be useful for the prevention of adhesion formation after surgery.

The cellular mechanisms underlying the inhibitory effects of isoflurane and sevoflurane on arginine vasopressin-induced vasoconstriction.

PURPOSE: Arginine vasopressin (AVP) is a potent vasoconstrictor that is sometimes used for the treatment of refractory vasodilatory shock. AVP constricts vascular smooth muscle by increasing both intracellular calcium concentration ([Ca(2+)](i)) and myofilament Ca(2+) sensitivity. However, the modulation of AVP-mediated vasoconstriction by volatile anesthetics remains to be determined. This study investigates the effects of isoflurane and sevoflurane on AVP-induced vasoconstriction and elucidates the underlying mechanisms, with an emphasis on the Ca(2+)-mediated pathways and Ca(2+) sensitization pathways of rat aortic smooth muscle. METHODS: The effects of isoflurane and sevoflurane on AVP-induced vasoconstriction and on the AVP-induced increase in [Ca(2+)](i) and Rho activity in rat aorta were investigated by isometric force recording, by measuring [Ca(2+)](i) using fluorescence dye, and by Western blotting techniques. RESULTS: Arginine vasopressin (10⁻7M) elicited a transient contractile response that was inhibited by isoflurane and sevoflurane in a concentration-dependent manner. AVP (10⁻7 M) induced a transient increase in intracellular Ca(2+) concentration ([Ca(2+)](i)). Isoflurane and sevoflurane also inhibited an AVP-induced increase in [Ca(2+)](i) in a concentration-dependent manner. AVP (10⁻7 M) increased the Rho activity that was attenuated by 2 minimum alveolar concentration of sevoflurane (P < 0.01), but not by an equipotent concentration of isoflurane. CONCLUSION: Arginine vasopressin-induced vasoconstriction is mediated by an increase in [Ca(2+)](i) and by the activation of the Rho-Rho kinase pathway in rat aortic smooth muscle. Although both isoflurane and sevoflurane, at clinically relevant concentrations, attenuate AVP-induced contraction, the cellular mechanisms of their inhibitory effects appear to differ.

Sevoflurane does not alter norepinephrine-induced intracellular Ca²(+) changes in the diabetic rat aorta.

PURPOSE: The effect of volatile anesthetics on the mechanism(s) of vascular contraction in diabetes mellitus (DM) has not been fully understood. The current study was designed to determine the effects of sevoflurane on the norepinephrine (NE)-induced changes in contractile state and intracellular Ca²(+) concentrations ([Ca²(+)](i)) in the spontaneously developing type 2 DM rat. METHODS: The effects of sevoflurane on NE (10⁻6M)-induced vasoconstriction and increase in [Ca²(+)](i) in the aortas from Otsuka Long-Evans Tokushima Fatty (OLETF) rats, a type 2 DM model, and from age-matched control Long-Evans Tokushima Otsuka (LETO) rats were investigated using an isometric force transducer and fluorometer with fura-2 as an indicator of [Ca²(+)](i). RESULTS: Norepinephrine-induced increases in tension and [Ca²(+)](i) in OLETF rats were 54.8%, 95% confidence interval (CI) 36.9-72.6% and 58.8%, 95% CI 51.5-66.1%, respectively, and in LETO rats they were 46.4%, 95% CI 39.0-53.7% and 53.8%, 95% CI 46.9-60.7%, respectively, when expressed as the percentage relative to that induced by KCl 30 mM. In LETO rats, sevoflurane at a concentration of 3.4% inhibited the vascular contraction (9.4%, 95% CI 6.3-12.6%; P < 0.001) and the increase in [Ca²(+)](i) (33.3%, 95% CI 27.4-39.2%; P = 0.002). In OLETF rats, however, sevoflurane failed to affect either the NE-induced contraction (43.6%, 95% CI 28.3-58.9%; P = 0.68) or the elevation in [Ca²(+)](i) (60.5%, 95% CI 56.3-64.8%; P = 0.93). CONCLUSION: Sevoflurane at clinically relevant concentrations inhibited the NE-induced increase in [Ca²(+)](i) in the aortic smooth muscle from normal rats but not in that from type 2 DM rats. Thus, a Ca²(+)- signalling pathway resistant to sevoflurane appears to exist in the type 2 DM rat aorta.

Severe methemoglobinemia after dental anesthesia: a warning about propitocaine-induced methemoglobinemia in neonates.

Methemoglobinemia is a fatal complication of local anesthesia. We describe a case report of female neonate who developed severe methemoglobinemia after extraction of neonatal teeth conducted with general anesthesia plus local injection of Citanest-Octapressin(®) (propitocaine of approximately 10 mg/kg). Central cyanosis appeared within an hour after surgery. The percentage of methemoglobin reached up to 43.9%. Not only pediatric dentists but also anesthesiologists generally agree with the idea that local anesthesia provides various benefits in painful procedures in neonates. However, this case may serve as a warning when using Citanest-Octapressin(®), which is still commercially available for neonatal patients.

The modulation of vascular ATP-sensitive K+ channel function via the phosphatidylinositol 3-kinase-Akt pathway activated by phenylephrine.

The present study examined the modulator role of the phosphatidylinositol 3-kinase (PI3K)-Akt pathway activated by the alpha-1 adrenoceptor agonist phenylephrine in ATP-sensitive K(+) channel function in intact vascular smooth muscle. We evaluated the ATP-sensitive K(+) channel function and the activity of the PI3K-Akt pathway in the rat thoracic aorta without endothelium. The PI3K inhibitor 2-(4-morpholinyl)-8-phenyl-1(4H)-benzopyran-4-one hydrochloride (LY294002) (10(-5) M) augmented relaxation in response to the ATP-sensitive K(+) channel opener levcromakalim (10(-8) to 3 x 10(-6) M) in aortic rings contracted with phenylephrine (3 x 10(-7) M) but not with 9,11-dideoxy-11alpha,9alpha-epoxy-methanoprostaglandin F(2alpha) (U46619; 3 x 10(-8) M), although those agents induced similar contraction. ATP-sensitive K(+) channel currents induced by levcromakalim (10(-6) M) in the presence of phenylephrine (3 x 10(-7) M) were enhanced by the nonselective alpha-adrenoceptor antagonist phentolamine (10(-7) M) and LY294002 (10(-5) M). Levels of the regulatory subunits of PI3K p85-alpha and p55-gamma increased in the membrane fraction from aortas without endothelium treated with phenylephrine (3 x 10(-7) M) but not with U46619 (3 x 10(-8) M). Phenylephrine simultaneously augmented Akt phosphorylation at Ser473 and Thr308. Therefore, activation of the PI3K-Akt pathway seems to play a role in the impairment of ATP-sensitive K(+) channel function in vascular smooth muscle exposed to alpha-1 adrenergic stimuli.

Differential vasodilation response to olprinone in rabbit renal and common carotid arteries.

PURPOSE: Olprinone, one of the most frequently used phosphodiesterase-3 inhibitors, exerts its positive inotropic and vasodilation effects by inhibiting the degradation of intracellular cyclic adenosine monophosphate (cAMP). The vasodilation response to olprinone is not uniform among the different vascular beds. This study was designed to compare the vasorelaxation response to olprinone between renal and common carotid arteries, and investigate its underlying mechanisms. METHODS: Isometric force measurement, enzyme immunoassay, and western blotting techniques were used to investigate the vasorelaxation action of olprinone in isolated rabbit renal and common carotid arteries. RESULTS: Olprinone inhibited the contractile response to phenylephrine (PE) both in the renal and carotid arteries in a concentration-dependent manner with IC50 values of 40 +/- 10 and 103 +/- 43 nM, respectively. The IC50 value was lower (P = 0.004) and the maximal inhibition was greater (P = 0.002) in the renal artery compared with the carotid artery. A cell-permeable cAMP analogue, 8-bromo-cAMP, also inhibited the contractile response to PE in the renal and carotid arteries with IC50 values of 581 +/- 150 and 740 +/- 179 microM, respectively; however no differences were observed both in the IC50 value and the maximal inhibition between two arteries. Olprinone (0.1 microM) increased the intracellular cAMP level in the renal arterial smooth muscle cells (ASMCs) but not in the carotid ASMCs. The expression of PDE3A was greater (P = 0.008) in the carotid ASMCs than the renal ASMCs. CONCLUSION: The enhanced vasodilator action of olprinone in the renal artery is presumably because of its ability to stimulate the cAMP production, which might be attributable to the heterogeneous expression of PDE3A.

Interactions between morphine and nitric oxide in various organs.

Nitric oxide (NO) plays obligatory roles as an important intercellular messenger in the control of physiological functions and it also participates in pathophysiological interventions. This labile, gaseous molecule is also involved in mechanisms underlying the beneficial and untoward actions of therapeutic agents. Endogenous NO is formed by endothelial and neurogenic NO synthases that are constitutively present mainly in the endothelium and nervous system, respectively, and is induced by lipopolysaccharides or cytokines mainly in mitochondria, glial cells, and vascular smooth muscle cells. NO modulates the effects of morphine on processes involving the central nervous system, such as learning, memory, convulsion, thermoregulation, and penile erection. This molecule is also involved in the modification of morphine actions on the cardiovascular, digestive, and respiratory systems. Morphine regulates NO bioavailability in various organs. NO formed by inducible NO synthase participates in some morphine actions in the immune system. Information concerning interactions between NO and morphine and other opioids in a variety of organs and tissues is quite useful in establishing new strategies for minimizing the noxious and unintended reactions that are frequently encountered during analgesic therapy.

The role of 20-hydroxyeicosatetraenoic acid in cerebral arteriolar constriction and the inhibitory effect of propofol.

BACKGROUND: We conducted this study to examine, in cerebral parenchymal arterioles, whether 20-hydroxyeicosatetraenoic acid (20-HETE) induces constrictor responses via superoxide and whether propofol reduces this constriction. METHODS: Electrical field stimulation or 20-HETE was applied to rat brain slices monitored by computer-assisted microscopy. In some experiments, a Na(+) channel antagonist tetrodotoxin, a 20-HETE synthesis inhibitor HET0016, a superoxide scavenger, Tiron, nicotinamide adenine dinucleotide phosphate (NADPH) oxidase inhibitors diphenyleneiodonium (DPI) and gp91ds-tat, or propofol was added. The superoxide level in the brain slice and the production rate in the absence of slices were evaluated by dihydroethidium fluorescence or cytochrome c reduction with a superoxide-generating system, respectively. RESULTS: Electrical stimulation induced constriction of the cerebral parenchymal arteriole, whereas this response was abolished by tetrodotoxin, HET0016, Tiron, or DPI. 20-HETE (10(-8)-10(-6) mol/L) produced arteriolar constriction, which was inhibited by Tiron or DPI. Propofol reduced the constriction induced by electrical stimulation or 20-HETE. 20-HETE induced superoxide production in the brain slice, which was reduced by Tiron, gp91ds-tat, or propofol. However, propofol did not alter the superoxide production rate in the absence of brain slices. CONCLUSIONS: Either neuronal transmission-dependent or exogenous 20-HETE seems to induce cerebral parenchymal arteriolar constriction via superoxide production resulting from NADPH oxidase activation. Propofol is likely to prevent this constriction via inhibition of NADPH oxidase, but not by its scavenging effect on superoxide.

Volatile anesthetics inhibit angiotensin II-induced vascular contraction by modulating myosin light chain phosphatase inhibiting protein, CPI-17 and regulatory subunit, MYPT1 phosphorylation.

BACKGROUND: Vascular contraction is regulated by myosin light chain (MLC) phosphorylation. Inhibition of MLC phosphatase (MLCP) increases MLC phosphorylation for a given Ca(2+) concentration, and results in promoting myofilament Ca(2+) sensitivity. MLCP activity is mainly determined by protein kinase C (PKC) and Rho kinase through the phosphorylation of both PKC-potentiated inhibitory protein (CPI-17) and myosin phosphatase target subunit (MYPT1). We have previously demonstrated that sevoflurane inhibits PKC phosphorylation and membrane translocation of Rho kinase. This study was designed to investigate the effects of sevoflurane and isoflurane on CPI-17, MYPT1, and MLC phosphorylation in response to angiotensin II (Ang II) in rat aortic smooth muscle. METHODS: The effects of sevoflurane or isoflurane (1-3 minimum alveolar concentration) on the vasoconstriction and phosphorylation of MLC, CPI-17, MYPT1 at Thr853 and MYPT1 at Thr696 in response to Ang II were investigated using isometric force transducer and Western blotting, respectively. RESULTS: Ang II (10(-7) M) elicited a transient contraction of rat aortic smooth muscle that was inhibited by both sevoflurane and isoflurane in a concentration-dependent manner. Ang II also induced an increase in the phosphorylation of MLC, CPI-17, MYPT1/Thr853 and MYPT1/Thr696. Sevoflurane inhibited the phosphorylation of MLC, CPI-17, and MYPT1/Thr853 in response to Ang II in a concentration-dependent manner. Isoflurane also inhibited MLC phosphorylation in response to Ang II, which was associated with decreases in MYPT1/Thr853, but not in CPI-17. Neither sevoflurane nor isoflurane affected the Ang II-induced phosphorylation of MYPT1/Thr696. CONCLUSION: Although both volatile anesthetics inhibited Ang II-induced vasoconstriction and MLC phosphorylation to similar extent, the mechanisms behind the inhibitory effects of each anesthetic on MLCP activity appear to differ.

Beneficial effect of propofol on arterial adenosine triphosphate-sensitive K+ channel function impaired by thromboxane.

BACKGROUND: It is not known whether thromboxane A2 impairs adenosine triphosphate (ATP)-sensitive K channel function via increased production of superoxide in blood vessels and whether propofol as a nicotinamide adenine dinucleotide phosphate (NADPH) oxidase inhibitor restores this modification. METHODS: Rat aortas without endothelium were used for isometric force recording, measurements of membrane potential, and superoxide production and Western immunoblotting. Vasorelaxation to an ATP-sensitive K channel opener levcromakalim was obtained during contraction to phenylephrine (3 x 10(-7) M) or a thromboxane A2 analogue U46619 (3 x 10(-7) M). In some experiments, aortas were incubated with an ATP-sensitive K channel antagonist glibenclamide, a superoxide inhibitor Tiron, a nonselective NADPH oxidase inhibitor apocynin, a hydrogen peroxide scavenger catalase, a xanthine oxidase inhibitor allopurinol, a thromboxane receptor antagonist SQ29548 or propofol (3 x 10(-7) to 3 x 10(-6) M). RESULTS: Levcromakalim-induced vasorelaxation was abolished by glibenclamide in rings contracted with either vasoconstrictor agent. Tiron, apocynin, and propofol, but not catalase, augmented the vasodilator response as well as the hyperpolarization by levcromakalim in aortas contracted with U46619. Tiron, apocynin, SQ29548, and propofol, but not allopurinol, similarly reduced in situ levels of superoxide within aortic vascular smooth muscle exposed to U46619. Protein expression of a NADPH oxidase subunit p47phox increased in these arteries, and this augmentation was abolished by propofol. CONCLUSIONS: Thromboxane receptor activation induces vascular oxidative stress via NADPH oxidase, resulting in the impairment of ATP-sensitive K channel function. Propofol reduces this stress via inhibition of a NADPH oxidase subunit p47phox and, therefore, restores ATP-sensitive K channel function.

Fentanyl added to propofol anesthesia elongates sinus node recovery time in pediatric patients with paroxysmal supraventricular tachycardia.

BACKGROUND: In some types of pediatric supraventricular tachycardia, reentrant mechanisms are sensitive to enhanced vagal tone. Propofol is a feasible anesthetic for pediatric electrophysiological study and radiofrequency catheter ablation. Although fentanyl and propofol infusions both enhance cardiac vagal tone, it is unclear whether the combination of propofol and fentanyl has a potential to enhance it. In this study, we evaluated the hypothesis that fentanyl combined with propofol could alter cardiac electrophysiological activities in pediatric patients undergoing electrophysiological study and radiofrequency catheter ablation. METHODS: Twenty-seven pediatric patients (9 Wolff-Parkinson-White syndrome, 7 concealed accessory pathway and 11 atrioventricular nodal reentry tachycardia) were enrolled in this study. Anesthesia was induced with propofol 2.0 mg/kg and was maintained with a continuous infusion of propofol at a rate of 100-167 microg x kg(-1) x min(-1). During a stable anesthetic state, the calculated sinoatrial conduction time and corrected sinus node recovery time (CSNRT) were measured before and after fentanyl administration. The fentanyl dose consisted of an initial 2.0 microg/kg IV bolus and subsequent continuous infusion of 0.075 microg x kg(-1) x min(-1). RESULTS: Bispectral Index scores and systemic blood pressure remained unchanged throughout the examinations. Fentanyl administration significantly prolonged CSNRT (P = 0.005) but not calculated sinoatrial conduction time (P = 0.35). CONCLUSION: Since an enhanced cardiac vagal tone is one of the causative factors for prolonged CSNRT, our findings greatly support the hypothesis that fentanyl combined with propofol has a potential to enhance cardiac vagal tone.

Prothrombotic roles of substance-P, neurokinin-1 receptors and leukocytes in the platelet-dependent clot formation in whole blood.

A number of types of non-neuronal cells including leukocytes have been confirmed to possess substance-P and its specific neurokinin-1 receptor (NK1R), while the pathophysiological roles of substance-P in these cells remain to be established. Effects of substance-P through NK1R on platelet-dependent clot formation were evaluated by using an oscillating-probe viscoelastometer. The clot signal, indicative of the clot strength in blood-derived samples, was measured after the stimulation with celite and Ca(2+). Substance-P (10 nM) increased the clot signal of whole blood obtained from healthy volunteers, especially modulating the platelet-dependent distinctive peak in traces of the signal. A NK1R antagonist Spantide (500 nM) blocked such substance-P derived change, suggesting the involvement of platelets in the action of substance-P. In contrast, substance-P did not increase the clot signal of platelet-containing but leukocyte-removed plasma. From these, we conclude that substance-P promotes platelet-dependent clot formation through NK1R, in which leukocytes appear to be involved.

Half clamping of the infrahepatic inferior vena cava reduces bleeding during a hepatectomy by decreasing the central venous pressure.

BACKGROUND AND AIMS: Bleeding from the hepatic vein is closely related to central venous pressure (CVP). To evaluate the effect of low central venous pressure during a hepatectomy, the infrahepatic inferior vena cava (IVC) was half clamped. PATIENTS AND METHODS: Between 2006 and 2007, 20 patients undergoing major hepatectomy with the IVC half clamping (half-clamping group) were compared with 58 patients undergoing hepatectomy without IVC half clamping between 2003 and 2005 (control group). The types of liver resection, amount of blood loss during the hepatectomy, volume of blood transfusion, length of hospital stay, and complications were compared between the two groups. RESULTS: In the half-clamping group, blood loss was decreased in comparison to the control group (p = 0.041) and the suprahepatic CVP was low (2.4 +/- 1.8 mmHg; p = 0.0002). The diameter at the root of the right hepatic vein was reduced in comparison to before clamping (5.8 +/- 1.6 mm; p < 0.001). There were no complications of half clamping on any hemodynamic and blood electrolytic parameters. CONCLUSION: Using the half clamping technique of the IVC, intra-operative CVP was maintained below 3 mmHg without any side effects, and the low CVP significantly reduced the bleeding from hepatic veins during a major hepatectomy.