Laparoscopy-assisted right hepatic lobectomy using a wall-lifting procedure.

This article describes a new technique for performing a laparoscopy-assisted right hepatic lobectomy using a hanger wall-lifting procedure. The patient is placed in the left semi-lateral position. A cholecystectomy and hemi-hepatic vascular inflow control are then performed through a midline incision, through which the resected liver can be removed. Next, the right lower chest and right upper abdominal wall are lifted by two wires vertical to the abdominal wall. Two ports, a 5-mm port in right lateral abdomen for forceps and a 12-mm port just right of the umbilicus for the laparoscope, are inserted. The obtained view of the operative field in the right upper abdominal cavity is thus excellent. The laparoscopy-assisted mobilization of the right hepatic lobe is done with the assistance of a hand inserted through the midline incision, including a dissection of the hepato-renal ligament, the right triangular ligament, and the right coronary ligament. A parenchymal dissection is then performed using the Cavitron Ultrasonic Surgical Aspirator (CUSA) and the resected specimen is passed through the midline incision without any morcellation of the liver. This procedure can minimize the length of the wound, while avoiding the lethal complications associated with pneumoperitoneum.

Protective effect of heme oxygenase-1 gene transfer against oxyhemoglobin-induced endothelial dysfunction.

The current study was designed to determine the effect of recombinant heme oxygenase-1 (HO-1) gene expression on endothelial function in cerebral arteries. Isolated canine basilar arteries were exposed ex vivo (30 minutes at 37 degrees C) to an adenoviral vector (10(10) PFU/mL, total volume 300 microL) encoding either the HO-1 gene (AdCMVHO-1) or the beta-galactosidase (beta-Gal) reporter gene (AdCMVbeta-Gal). Twenty-four hours after transduction, arterial rings were suspended in organ chamber for isometric force recording. Endothelium-dependent relaxations were obtained in response to bradykinin (10(-10) to 10(-6) mol/L) during contraction to uridine-5'-triphosphate (UTP; 3 x 10(-6) to 3 x 10(-5) mol/L). Certain rings were incubated with oxyhemoglobin (OxyHb; 10(-5) mol/L) overnight (16 to 18 hours of 24 hours). Expression and localization of recombinant protein were shown by Western blot analysis and immunohistochemistry. Endothelium-dependent relaxation to bradykinin and endothelium-independent relaxation to forskolin (10(-9) to 10(-5) mol/L) and DEA-NONOate (10(-10) to 10(-5) mol/L) were identical in beta-Gal- and HO-1-transduced arteries. Exposure to OxyHb caused impairment of endothelium-dependent relaxation to bradykinin (P < 0.01). In contrast, OxyHb did not affect endothelium-dependent relaxation in arteries expressing recombinant HO-1 ( P > 0.05). This protective effect of HO-1 was reversed by coincubation with tin protoporphyrin (SnPP9; 10(-5) mol/L), a selective inhibitor of HO-1 (P < 0.01). Basal levels of 3',5'-cyclic monophosphate (cGMP) in HO-1-transduced vessels were not significantly different from those in beta-Gal-transduced vessels. Pretreatment with OxyHb significantly reduced cGMP level in beta-Gal-transduced rings (P < 0.01), whereas it had no effect in HO-1-transduced rings. These results demonstrate that HO-1 gene transfer does not affect endothelial and smooth muscle function of normal arteries, and that expression of recombinant HO-1 in cerebral arteries protects vasomotor function against OxyHb-induced injury.

Inhibitory effect of valves on endothelium-dependent relaxations to calcium ionophore in canine saphenous vein.

The present study was designed to evaluate endothelium-dependent relaxation to the calcium ionophore A-23187 in isolated canine saphenous veins. Isometric force recordings and cGMP measurements using isolated veins with and without valves were performed. During contractions to U-46619 (3 x 10(-7) M), endothelium-dependent relaxations to A-23187 (10(-9)-10(-6) M) were significantly reduced in rings with valves compared with rings without valves. Endothelial removal abolished A-23187-induced relaxation. Relaxations to forskolin (FK; 10(-8)-10(-5) M) and diethylaminodiazen-1-ium-1,2-dionate; DEA-NONOate, 10(-9)-10(-5) M) were identical in rings with and without valves. In rings without valves, a nitric oxide synthase inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME; 3 x 10(-4) M), and a cyclooxygenase inhibitor, indomethacin (10(-5) M), partially reduced A-23187-induced relaxation. However, in rings with valves, L-NAME had no effect, whereas indomethacin abolished the relaxation to A-23187. A selective soluble guanylate cyclase inhibitor, 1H-[1,2,4]-oxadiazolo [4,3-a]quinoxalin-1-one (ODQ; 3x10(-6) M), had no effect on the relaxation to A-23187 in either group. In contrast, ODQ abolished the A-23187-induced increase in cGMP levels, suggesting that relaxation to nitric oxide released by A-23187 is independent of increases in cGMP. These results demonstrate that endothelium-dependent relaxation to A-23187 is reduced in regions of veins with valves compared with relaxation in the nonvalvular venous wall. Lower production of nitric oxide in endothelial cells of valvular segments appears to be a mechanism responsible for reduced reactivity to A-23187.

Functional interdependence and colocalization of endothelial nitric oxide synthase and heat shock protein 90 in cerebral arteries.

Heat shock protein 90 (HSP90), an essential component of several signal transduction systems, participates in the activation of endothelial nitric oxide synthase (eNOS) in cells. The objective of the current study was to determine if HSP90 and eNOS were functionally interdependent and colocalized in the cerebral circulation. The authors used isometric force recording, cyclic 3'5'-guanosine monophosphate (cGMP) radioimmunoassay (RIA), and immunogold electron microscopy (EM) to study canine basilar artery. They found that geldanamycin (0.1 to 10 microg/mL), a selective HSP90 inhibitor, caused concentration-dependent contractions in arterial rings (n = 6 dogs). Contractions to geldanamycin were unaffected by a cyclooxygenase inhibitor, indomethacin (10 micromol/L; P < 0.05, n = 6). Functional evidence for interaction between HSP90 and nitric oxide (NO)-mediated signaling included observations that the contractile effect of geldanamycin was the following: (1) endothelium-dependent, (2) abolished by Ng-nitro-L-arginine methylester (L-NAME; 0.3 mmol/L), and (3) non-additive with the contractile effect of this NOS inhibitor (P < 0.01, n = 6 for each). Furthermore, RIA showed significant reduction in cGMP levels in arteries treated with geldanamycin (3 microg/mL; P < 0.02, n = 8), whereas immunogold EM demonstrated areas of colocalization of HSP90 and eNOS selectively in the cytoplasm of endothelial cells. The current findings suggest that in cerebral arteries, endothelial HSP90 plays an important role in modulation of basal NO-mediated signaling. This interaction may be particularly important in stress-induced up-regulation of HSP90 with subsequent alteration of vasomotor function.

Value of the profundapopliteal collateral index for selecting between an in-flow and sequential arterial reconstruction in patients with multisegment arterial occlusive disease.

BACKGROUND: It remains difficult for surgeons to choose between an in-flow and sequential arterial reconstruction in patients with multisegment arterial occlusive disease. In addition, the exact criterion for the proper revascularization procedures of these patients also remains obscure. METHODS: The profundapopliteal collateral index (PPCI) was determined in all patients with occlusions of both the aortoiliac and superficial femoral arteries prior to undergoing an arterial bypass. The PPCI in the inflow bypass (IB) was also compared with the sequential bypass (SB). RESULTS: The symptoms of all patients undergoing either IB or SB improved. Preoperatively, the average PPCI in IB patients was significantly lower than that in SB patients. In addition, no significant difference was observed in the increased average rate of the ankle brachial index (ABI) between IB and SB. CONCLUSIONS: The PPCI is an accurate predictor of the hemodynamic potential of the geniculate collaterals. In cases with a low PPCI, especially in patients with multisegment arterial occlusive disease, in-flow procedures alone may often be sufficient for the successful treatment of such patients. The PPCI is thus considered to be useful for selecting the optimal revascularization procedures.

Enhancement of nitric oxide production after arterial reconstruction in patients with arteriosclerosis obliterans.

PURPOSE: Nitric oxide (NO) not only relaxes vascular smooth muscles, but it also reduces platelet adhesion and is itself a potent antiaggregatory substance. Experimental studies have shown that the release of NO is modulated by the blood flow. However, little clinical information is available about the effects of hemodynamic changes after arterial reconstruction on NO production. We therefore examined whether the plasma levels of nitrite (NO2-) and nitrate (NO3-) ions increased after arterial reconstruction in patients with arteriosclerosis obliterans (ASO). METHODS: Blood samples were obtained from the femoral artery in seven patients who underwent arterial reconstruction and seven healthy individuals (control). NO2- and NO3- levels were measured using high-performance liquid chromatography before the operation and 1 hour and 14 days after the operation. In addition, the mean femoral artery blood flow and ankle-brachial pressure index (ABI) were also measured using a duplex and Doppler velocimeter both before and after the operations. RESULTS: In the control subjects, the mean plasma NO2-, NO3-, and NOx (NO2- plus NO3-) levels in the femoral artery were 0.37 +/- 0.15 mumol/L, 45.6 +/- 10.8 mumol/L, and 46.0 +/- 10.9 mumol/L, respectively. Before the operation in the patients with ASO, the mean plasma NO3- (23.8 +/- 2.2 mumol/L) and NOx levels (24.0 +/- 2.3 mumol/L) were significantly lower than those in the control subjects, whereas the plasma NO2- levels (0.27 +/- 0.04 mumol/L) were comparable between the two groups. At 14 days after operation, the mean plasma NO3- and NOx levels in the femoral artery were significantly increased to 42.8 +/- 5.6 mumol/L and 43.4 +/- 5.6 mumol/L compared with those before the operation, whereas the mean plasma NO2- levels (0.50 +/- 0.05 mumol/L) changed significantly. The mean ABI and the mean flow rate before the operation were 0.32 +/- 0.07 and 344 +/- 145 ml/min, respectively. Both the ABI and the mean flow rate significantly increased to 1.04 +/- 0.06 and 627 +/- 141 ml/min after the operation. CONCLUSIONS: In patients who have ASO, the mean plasma level of NO is significantly lower than that of healthy individuals. In patients with ASO, the mean blood flow increased significantly after arterial reconstruction. This hemodynamic improvement may thus enhance NO production and may also help to maintain the patency of the bypass graft or native artery.

Down-regulation of endothelin B receptors in autogenous saphenous veins grafted into the arterial circulation.

OBJECTIVES: It has been postulated that endothelin (ET) might be involved in the development of atherosclerotic vascular lesions. The present study was done to characterize changes in the contractility and ET receptor subtypes in the autogenous saphenous vein graft (VG). METHODS: The rabbit saphenous vein (SV) was grafted into the ipsilateral femoral artery (FA), and at 4 weeks after the operation, VG was harvested. In the medial layer samples of SV, VG and FA, the cytosolic Ca2+ concentration ([Ca2+]i) and force were monitored using front-surface fluorometry of fura-PE3, and mRNA expression of ET receptors was evaluated using the reverse transcription polymerase chain reaction. RESULTS: ET-1 (10(-7) M) developed force in SV, VG and FA, to the same extent. Sarafotoxin (S6c; 10(-7) M) developed force in the SV to the same extent as ET-1. However, S6c did not develop force in FA, and slight force developed in VG. Contractions induced by ET-1 were associated with increases in [Ca2+]i. FA expressed ETA receptor mRNA predominantly, and SV expressed both ETA and ETB receptors mRNAs. In VG, the expression of ETB receptor mRNA was markedly reduced, but expression of ETA receptor mRNA remained unchanged. CONCLUSIONS: Functioning ETB receptors and their mRNA are down-regulated when veins are grafted into the arterial circulation. All these changes in gene expression and function are part of adaptive responses known as 'arterialization'.

The inhibition of canine vein graft intimal thickening using a newly developed antiplatelet agent.

OBJECTIVE: The purpose of this study was to evaluate the efficacy of a newly developed antiplatelet agent, 4-cyano-5, 5-bis[methoxyphenyl]-4-pentenoic acid (E5510) on intimal hyperplasia of experimental autologous vein grafts in a distal poor runoff canine model. METHOD: The femoral vein was implanted into the femoral artery preparing a distal poor runoff model. These animals were divided into three groups consisting of the E5510 group, the Aspirin group, and the Control group. The vein grafts were harvested at either 1 or 4 weeks after implantation. RESULTS: At 4 weeks, the degree of intimal hyperplasia of the graft of E5510 group was significantly less than that of the Aspirin group and the Control group (p < 0.05). No significant difference was observed between the Aspirin group and the Control group. At 1 week, the degree of intimal cell proliferation was determined by bromodeoxyuridine (BrdU) incorporation and was expressed as the BrdU labeling index. The BrdU labeling index of the E5510 group was also significantly lower than that of the Control group (p < 0.05). CONCLUSIONS: These data demonstrate the efficacy of E5510 in reducing intimal hyperplasia of vein grafts under distal poor runoff conditions by reducing the degree of smooth muscle cell proliferation.

Surgical strategy of abdominal aortic aneurysm with preoperative renal failure.

OBJECTIVES: To determine the effect of preoperative renal failure on the outcome of patients suffering from infrarenal abdominal aortic aneurysm (AAA). METHOD: During the period from January 1979 to August 1995, 364 patients with AAA were admitted to our hospital and 323 underwent elective repair. The patients were retrospectively analysed in three groups. Group I was composed of 273 patients with a normal renal function who underwent an aneurysm repair. Group II was composed of 50 patients who demonstrated a preoperative renal dysfunction (creatinine above 2.0 mg/dl or creatinine clearance below 40 ml/min) and underwent an operation, including three patients maintained on chronic haemodialysis. Group III was composed of 18 patients with a renal dysfunction who did not undergo repair, including one patients maintained on chronic haemodialysis. RESULTS: The operative mortality rate of groups I and II were 0.4% and 2.0%, respectively, although no significant difference was observed. The incidence of postoperative cardiac and pulmonary complications were also comparable in two groups. No patients required acute haemodialysis. The 5-year survival rate of group II (44%) was significantly higher than that of group III (20%), and seven of the 18 patients (39%) in group III ultimately died of a rupture of the AAA. CONCLUSIONS: Patients with chronic renal failure can undergo an abdominal aortic aneurysm repair based on the same indications as those without renal failure.

Mechanism of contraction induced by bradykinin in the rabbit saphenous vein.

1. By using fura-PE3 fluorometry and receptor-coupled permeabilization by alpha-toxin, the mechanism of the bradykinin (BK)-induced contraction was determined in the rabbit saphenous vein (RSV). The receptor subtype responsible for the BK-induced contraction of RSV was determined by means of a pharmacological blocker study and reverse transcription polymerase chain reaction (RT-PCR). 2. In the presence of extracellular Ca2+ (1.25 mM), BK (10(-11)-3 x 10(-7) M) induced increases in both the cytosolic Ca2+ concentration ([Ca2+]i) and force, in a concentration-dependent manner. Both the release of Ca2+ from the store site and the influx of extracellular Ca2+ contribute to an increase in [Ca2+]i induced by BK. 3. In the absence of extracellular Ca2+, the application of 10(-7) M BK induced transient elevations of [Ca2+]i and force, both of which thereafter declined to the levels observed before the application of BK. When extracellular Ca2+ was replenished (1.25 mM), [Ca2+]i and force increased to form a peak, followed by a sustained elevation in the presence of BK. When an RSV strip was pretreated with 10(-5) M thapsigargin for 20 min, the BK-induced transient increases in both [Ca2+]i and force were markedly inhibited. 4. These responses induced by BK were inhibited by Hoe 140 (D-Arg-[Hyp3, Thi5, D-Tic7, Oic8] bradykinin), a highly specific bradykinin B2 receptor antagonist, in a concentration-dependent manner. In RT-PCR, B2-receptor mRNA was expressed in the smooth muscle of RSV. 5. The [Ca2+]i-force relationships, which were determined by cumulative applications of extracellular Ca2+ (0-5 mM) during 118 mM K(+)-depolarization, shifted to the upper left in the presence of BK, thus indicating that BK induced a greater force than 118 mM K(+)-depolarization for a given level of [Ca2+]i. 6. In alpha-toxin-permeabilized preparations of RSV, application of 10(-7) M BK after a steady state contraction had been induced by a mixture of 5 x 10(-7) M Ca2+, 10(-6) M GTP and 10(-6) M captopril caused an additional force development at a constant [Ca2+]i. However, treatment with 1 mM guanosine-5'-O-(beta-thiodiphosphate) (GDP beta S) for 5 min before and during the application of BK (10(-7) M), abolished this BK-induced additional contraction. 7. These results indicated that in RSV: (1) BK elicits vasoconstriction by increasing the Ca2+ influx from the extracellular space, Ca2+ release from intracellular thapsigargin-sensitive storage sites and increasing the Ca2+ sensitivity of the contractile apparatus, (2) the BK-induced increase in Ca2+ sensitivity is mediated by G-protein, (3) the BK-induced contractions are mediated via B2-receptors and (4) the smooth muscle cells express B2-receptor mRNA.

The effect of probucol on intimal thickening of autologous vein grafts in hyperlipidemic rabbit.

Probucol is used to treat hypercholesterolemia and also has an anti-atherogenic effect. The effects of probucol on intimal thickening of autologous vein graft in hyperlipidemic rabbits with poor distal run-off were investigated. A poor distal run-off model was prepared in the right hindlimb of 18 rabbits allocated to four groups depending on diet: normolipidemic commercial diet, (NL group, n = 5); hyperlipidemic diet (HL group, n = 5); commercial diet with 1% probucol (NP group, n = 4); and hyperlipidemic diet with 1% probucol (HP group, n = 4). After 4 weeks the femoral vein grafts were implanted into normal (n = 18) or poor (n = 18) runoff limbs. Vein grafts were harvested 4 weeks after implantation. Intimal thickening of the graft was measured and macrophages therein examined immunohistochemically. The serum cholesterol level was not reduced by probucol treatment. The mean flow rate of the graft was significantly reduced in the poor run-off limb. On histological examination intimal thickening in the poor run-off limb was significantly greater than that of controls, while intimal thickening in the HL and HP groups was enhanced compared with that in the NL and NP groups, respectively. Mean intimal thickening in each limb in HP group rabbits was significantly lower than that in HL rabbits (microm): control (HL/HP): 99.4(7.4)/58.8(0.7) (P < 0.05); poor run-off (HL/HP): 155.3(9.6)/130.3(7.3) (P < 0.O5). There was no difference between NL and NP (microm): control (NL/NP): 44.6(24.7)/31.5(12.8); poor run-off (HL/HP): 115.3(13.8)/97.5(34.0). In addition, enhanced intimal thickening due to poor distal run-off was not suppressed. Immunohistochemical staining showed intimal macrophage infiltration in the HL and HP groups; however, macrophage infiltration in grafts in the HP group was less than in the HL group. In conclusion, under hyperlipidemic conditions, probucol decreased intimal thickening enhancement of the vein graft, and suppressed intimal macrophage infiltration. These findings were similar to the anti-atherogenic effect of probucol in the native artery. Hence, probucol administration after vascular reconstruction with vein grafts in patients with hyperlipidemia may be beneficial.

Acceleration of impairment of endothelium-dependent responses under poor runoff conditions in canine autogenous vein grafts.

OBJECTIVES: To assess the effects of changes in shear stress on endothelium-dependent responses. MATERIALS AND METHODS: Autologous vein grafts were implanted in poor or normal distal runoff limbs of 10 mongrel dogs. Six weeks after grafting the vein grafts were removed, cut into rings, and suspended in organ chambers for isometric tension recording. RESULTS: The average value of intimal thickening was 110.7 +/- 45.2 microns in poor runoff limbs and 65.5 +/- 27.9 microns in control limbs, respectively. There was a significant difference between the two groups. Acetylcholine caused comparable endothelium-independent contractions in both groups. In the control group, adenosine diphosphate, thrombin and A23187 caused endothelium-dependent relaxations. In the poor runoff group, the endothelium-dependent relaxations caused by adenosine diphosphate and thrombin were impaired, while A23187 caused comparable endothelium-dependent relaxations. Direct relaxations in response to sodium nitroprusside were comparable between the two groups. CONCLUSIONS: This dysfunction of the endothelium under conditions of abnormal flow may accelerate intimal thickening of the vein graft and result in late graft failure.

L-arginine inhibits smooth muscle cell proliferation of vein graft intimal thickness in hypercholesterolemic rabbits.

OBJECTIVE: The effect of the chronic administration of L-arginine on intimal thickness and the kinetics of smooth muscle cell proliferation in autovein grafts in hypercholesterolemic rabbits were examined. METHODS: Male rabbits were fed a 1% cholesterol diet (control group) and a 1% cholesterol diet supplemented by 2.25% L-arginine HCl in drinking water (arginine group). Each group underwent reversed autologous vein bypass grafting of the left common carotid artery using the left external jugular vein. At 2 or 4 weeks after operation, intimal cell proliferation was determined by 5-bromo-2'-deoxyuridine (BrdU) incorporation and intimal thickness of the graft was measured with an ocular cytometer. At 4 weeks after operation, endothelium-dependent responses were examined by isometric tension recording. RESULTS: At 4 weeks after operation, the level of plasma arginine and citrulline are significantly higher in the arginine group (n = 7), compared with the control (n = 7). Intimal thickness in the arginine group (n = 7) was significantly reduced, compared with that of the control (n = 7). At 2 weeks after operation, the BrdU labeling index of the control (n = 5) was significantly higher than that of the arginine group (n = 5). At 4 weeks after operation, ACh caused endothelium-dependent relaxation in the arginine group (n = 4), while in the control (n = 4), ACh did not relax. CONCLUSIONS: These results suggest that smooth muscle cell proliferation of the rabbit jugular vein grafts during hypercholesterolemia occurs at an early stage after graft implantation, prior to the development of intimal thickness. Intimal thickness of vein graft during hypercholesterolemia was reduced by chronic administration of dietary L-arginine, by inhibiting smooth muscle cell proliferation. The enhancement of NO production in the blood vessel wall may therefore be useful for preventing late graft failure.