In vivo electrical conductivity of hepatic tumours.

Knowledge of electrical tissue conductivity is necessary to determine deposition of electromagnetic energy and can further be used to diagnostically differentiate between normal and neoplastic tissue. We measured 17 rats with a total of 24 tumours of the K12/TRb rat colon cancer cell line. In each animal we measured in vivo hepatic tumour and normal tissue conductivity at seven frequencies from 10 Hz to 1 MHz, at different tumour stages between 6 and 12 weeks after induction. Conductivity of normal liver tissue was 1.26 +/- 0.15 mS cm(-1) at 10 Hz, and 4.61 +/- 0.42 mS cm(-1) at 1 MHz. Conductivity of tumour was 2.69 +/- 0.91 mS cm(-1) at 10 Hz, and 5.23 +/- 0.82 mS cm(-1) at 1 MHz. Conductivity was significantly different between normal and tumour tissue (p < 0.05). We determined the percentage of necrosis and fibrosis at the measurement site. We fitted the conductivity data to the Cole-Cole model. For the tumour data we determined Spearman's correlation coefficients between the Cole-Cole parameters and age, necrosis, fibrosis and tumour volume and found significant correlation between necrosis and the Cole-Cole parameters (p < 0.05). We conclude that necrosis within the tumour and the associated membrane breakdown is likely responsible for the observed change in conductivity.

Changes in electrical resistivity of swine liver after occlusion and postmortem.

The resistivity of swine liver tissue was measured in vivo, during induced ischaemia and post-mortem, so that associated changes in resistivity could be quantified. Plunge electrodes, the four-terminal method and a computer-automated measurement system were used to acquire resistivities between 10Hz and 1 MHz. Liver resistivity was measured in vivo in three animals at 11 locations. At 10 Hz, resistivity was 758 +/- 170 ohm x cm. At 1 MHz, the resistivity was 250 +/- 40 ohm x cm. The resistivity time course was measured during the first 10 min after the liver blood supply in one animal had been occluded. Resistivity increased steadily during occlusion. The change in resistivity of an excised tissue sample was measured during the first 12h after excision in one animal. Resistivity increased during the first 2h by 53% at 10 Hz and by 32% at 1 MHz. After 2h, resistivity decreased, probably owing to membrane breakdown. The resistivity data were fitted to a Cole-Cole circle, from which extracellular resistance Re, intracellular resistance Ri and cell membrane capacitance Cm were estimated. Re increased during the first 2h by 95% and then decreased, suggesting an increase in extracellular volume. Cm increased during the first 4 h by 40%, possibly owing to closure of membrane channels, and then decreased, suggesting membrane breakdown. Ri stayed constant during the initial 6h and then increased.

Hepatic bipolar radio-frequency ablation between separated multiprong electrodes.

Radio-frequency (RF) ablation has become an important means of treatment of nonresectable primary and metastatic liver tumors. Major limitations are small lesion size, which make multiple applications necessary, and incomplete killing of tumor cells, resulting in high recurrence rates. We examined a new bipolar RF ablation method incorporating two probes with hooked electrodes (RITA model 30). We performed monopolar and bipolar in vivo experiments on three pigs. The electrodes were 2.5 cm apart and rotated 45 degrees relative to each other. We used temperature-controlled mode at 95 degrees C. Lesion volumes were 3.9+/-1.8 cm3 (n=7) for the monopolar case and 12.2 +/- 3 cm3 (n=10) for the bipolar case. We generated finite-element models (FEMs) of monopolar and bipolar configurations. We analyzed the distribution of temperature and electric field of the finite element model. The lesion volumes for the FEM are 7.95 cm3 for the monopolar and 18.79 cm3 for the bipolar case. The new bipolar method creates larger lesions and is less dependent on local inhomogenities in liver tissue-such as blood perfusion-compared with monopolar RF ablation. A limitation of the new method is that the power dissipation of the two probes cannot be controlled independently in response to different conditions in the vicinity of each probe. This may result in nonuniform lesions and decreased lesion size.

Laparoscopic lumbar spinal fusion: the role of the general surgeon.

The refinement of minimally invasive surgical techniques has impacted all areas of surgical practice. Laparoscopic approaches to lumbar spine fusion via the transperitoneal and retroperitoneal routes have similarly evolved with the development of new techniques and instruments unique to this procedure. The benefits of laparoscopic fusion techniques include shorter hospital stay, improved postoperative relief of pain, and preservation of critical spinal musculature. A general surgical laparoscopist is a critical member of the operative team. Although the technical details of the procedure are becoming standardized, patient selection is critical to maximize benefit and minimize risk.

Initiation of mineralization in bioprosthetic heart valves: studies of alkaline phosphatase activity and its inhibition by AlCl3 or FeCl3 preincubations.

The principal cause of the clinical failure of bioprosthetic heart valves fabricated from glutaraldehyde-pretreated porcine aortic valves is calcification. Other prostheses composed of tissue-derived and polymeric biomaterials also are complicated by deposition of mineral. We have previously demonstrated that: (a) Failure due to calcification of clinical bioprosthetic valves can be simulated by either a large animal circulatory model or subdermal implants in rodents. (b) Calcification of bioprosthetic tissue has complex host, implant, and mechanical determinants. (c) The initial calcification event in the rat subdermal model is the mineral deposition in devitalized cells intrinsic to the bioprosthetic tissue within 48 to 72 h, followed later by collagen mineralization. (d) Initiation of bioprosthetic tissue mineralization, like that of physiological bone formation, has "matrix vesicles" as early nucleation sites. (e) Alkaline phosphatase (AP), an enzyme also associated with matrix vesicles involved in bone mineral nucleation, is present in both fresh and fixed bioprosthetic tissue at sites of initial mineralization. (f) Certain inhibitors of bioprosthetic tissue calcification (e.g., Al3+, Fe3+) are localized to the sites at which alkaline phosphatase is present. On the basis of these results, we hypothesize that alkaline phosphatase is a key element in the pathogenesis of mineralization of bioprosthetic tissue. In the present studies, we focused on the relationship of AP to early events in calcification, and the inhibition of both calcification and AP activity by FeCl3 and AlCl3 preincubations. Subdermal implants of glutaraldehyde pretreated bovine pericardium (GPBP) were done in 3-week-old rats. AP was characterized by enzymatic hydrolysis of paranitrophenyl phosphate (pnpp), and by histochemical studies. Calcification was evaluated chemically (by atomic adsorption spectroscopy) and morphologically (by light microscopy). The results of these studies are as follows: (a) Extractable AP activity is present in fresh but not glutaraldehyde-pretreated bovine pericardial tissue. However, histochemical studies reveal active AP within the intrinsic devitalized cells of GPBP, despite extended glutaraldehyde incubation. (b) Extrinsic AP is rapidly adsorbed following implantation, with peak activity at 72 h (424 +/- 67.2 nm pnpp/mg protein/min enzyme activity [units]), but markedly lesser amounts at 21 days (96.8 +/- 3.9 units). (c) Simultaneously to the AP activity maximum, bulk calcification is initiated, with GPBP calcium levels rising from 1.2 +/- 0.1 (unimplanted) to 2.4 +/- 0.2 micrograms/mg at 72 h, to 55.6 +/- 3.1 micrograms/mg at 21 days, despite a marked decline in AP activity at this later time.(ABSTRACT TRUNCATED AT 400 WORDS)