Changes In Tissue Impedance Research Articles

Three-dimensional hydrogel cultures for modeling changes in tissue impedance around microfabricated neural probes

One limitation to the use of neuroprosthestic devices for chronic application, in the treatment of disease, is the reactive cell responses that occur surrounding the device after insertion. These cell and tissue responses result in increases in device impedance and failure of the device to interact with target populations of neurons. However, few tools are available to assess which components of the reactive response contribute most to changes in tissue impedance. An in vitro culture system has been developed that is capable of assessing individual components of the reactive response. The system utilizes alginate cell encapsulation to construct three-dimensional architectures that approach the cell densities found in rat cortex. The system was constructed around neuroNexus acute probes with on-board circuitry capable of monitoring the electrical properties of the surrounding tissue. This study demonstrates the utility of the system by demonstrating that differences in cell density within the three-dimensional alginate constructs result in differences in resistance and capacitance as measured by electrochemical impedance spectroscopy. We propose that this system can be used to model components of the reactive responses in brain tissue, and that the measurements recorded in vitro are comparable to measurements recorded in vivo.

Bimodal electric tissue ablation (BETA) — in-vivo evaluation of the effect of applying direct current before and during radiofrequency ablation of porcine liver

To examine the effect of applying increasing amounts of direct current (DC) before and during alternating current radiofrequency ablation of porcine liver. Using a Radiotherapeutics RF3000 generator, a 9 V AC/DC transformer and a 16 G plain aluminium tube as an electrode, a control group of 24 porcine hepatic radiofrequency ablation zones was compared with 24 zones created using a bimodal electric tissue ablation (BETA) technique in three pigs. All ablations were terminated when tissue impedance rose to greater than 999 Omega or radiofrequency energy input fell below 5 W on three successive measurements taken at 1 min intervals. BETA ablations were performed in two phases: an initial phase of variable duration DC followed by a second phase during which standard radiofrequency ablation was applied simultaneously with DC. During this second phase, radiofrequency power input was regulated by the feedback circuitry of the RF3000 generator according to changes in tissue impedance. The diameters (mm) of each ablation zone were measured by two observers in two planes perpendicular to the plane of needle insertion. The mean short axis diameter of each ablation zone was subjected to statistical analysis. With increased duration of prior application of DC, there was a progressive increase in the diameter of the ablation zone (p<0.001). This effect increased sharply up to 300 s of pre-treatment after which a further increase in diameter occurred, but at a much lesser rate. A maximum ablation zone diameter of 32 mm was produced (control diameters 10-13 mm). Applying a 9 V DC to porcine liver in vivo, and continuing this DC application during subsequent radiofrequency ablation, results in larger ablation zone diameters compared with radiofrequency ablation alone.

Spatiotemporal pattern of the extracranial component of the rheoencephalographic signal

The use of rheoencephalography (REG) in the clinical practice to evaluate cerebral blood flow is conditional on the finding of a method for removing the extracranial interference caused by the scalp blood flow. To remove this undesirable influence, digital processing based on statistics could be an effective technique if the appropriate data model were applied. This paper focuses on the analysis of the spatiotemporal features of the extracranial REG component, by comparing its morphology and phase shift at several scalp sites. For this purpose, a numerical model of the scalp was employed to assess tissue impedance changes caused by the inflow of a stepwise blood pulse wave. These results were compared with the experimental impedance waveforms recorded on six pairs of adjacent electrodes. The correlation coefficients between each pair of impedance recordings of each subject were always greater than 0.942, showing a mean value of 0.986. This result suggests that the extracranial REG component can be considered as morphologically invariant. On the other hand, negligible phase shifts were observed when mean electrode distances, measured in the blood flow direction, were relatively small, although temporal corrections in the data model would be advisable for longer distances.

Combined Radiofrequency Ablation and Hot Saline Injection in Rabbit Liver

To determine whether combining hot saline injection (HSI) and radiofrequency ablation (RFA) can increase the extent of thermally mediated coagulation in in vivo rabbit liver tissue. In 66 rabbits, RF energy and/or hot saline-induced coagulations were produced using a 17-gauge cooled electrode or 21-gauge needle under ultrasound guidance. Rabbits were allocated into 1 of 5 groups: group A, RFA alone (n = 15); group B, HSI (1 mL hot saline infused, n = 10); group C, combined therapy for HSI followed by RFA (n = 21); group D, combined therapy for RFA immediately followed by HSI (n = 10); and group E, 1 mL room temperature saline infusion before RFA (n = 10). RF energy (30 W) was applied for 3 minutes. The changes in tissue impedance, current, power output, and temperature of the electrode tip were automatically measured. Before RFA, precontrast computed tomography was performed, and after RFA, pre- and postcontrast spiral computed tomographic scans were acquired. The maximum diameters of the thermal lesions on the gross specimens and complications of each group were compared. All procedures were technically successful. There were 9 of 61 procedure-related complications (14.8%) including 6 localized hematomas and 3 thermal injuries to the diaphragm and the stomach. In rabbits in groups C and E, a marked decrease of tissue impedance (43.4 omega, 44.1 omega) and an increase of current (709 mA, 722 mA) occurred with instillation of saline infusion compared with RFA only. Combined therapy for HSI followed by RFA produced a greater short-axis mean diameter of coagulation (14.6 +/- 4.3 mm) than that in rabbits of other groups, for RFA only (10.4 +/- 2.4 mm), HSI only (8.7 +/- 3.3 mm), and combined therapy for RFA immediately followed by HIS (12.0 +/- 1.4 mm; P < 0.05). Combined therapy for HSI followed by RFA can increase the volume of RFA-induced coagulation in the liver with a single application, and therefore may improve the results of RFA for the treatment of larger tumors.

Protection afforded by ischemic preconditioning is not mediated by effects on cell-to-cell electrical coupling during myocardial ischemia-reperfusion.

The end-effectors of ischemic preconditioning (IPC) are not well known. It has been recently shown that transgenic mice underexpressing the gap junction protein connexin43 (Cx43) cannot be preconditioned. Because gap junctions allow spreading of cell death during ischemia-reperfusion in different tissues, including myocardium, we hypothesized that the protection afforded by IPC is mediated by effects on gap junction-mediated intercellular communication. To test this hypothesis, we analyzed the effect of IPC (5 min ischemia-5 min reperfusion x 2) on the changes in electrical impedance (four electrode probe) and impulse propagation velocity (transmembrane action potential) induced by ischemia (60 min) and reperfusion (60 min) in isolated rat hearts. IPC (n = 8) reduced reperfusion-induced lactate dehydrogenase release by 65.8% with respect to control hearts (n = 9) (P = 0.04) but had no effect on the time of onset of rigor contracture (increase in diastolic tension), electrical uncoupling (sharp changes in tissue resistivity and phase angle in impedance recordings), or block of impulse propagation during ischemia. Normalization of electrical impedance during reperfusion was also unaffected by IPC. The lack of effect of IPC on ischemic rigor contracture and on changes in tissue impedance during ischemia-reperfusion were validated under in vivo conditions in pigs submitted to 48 min of coronary occlusion and 120 min of reperfusion. IPC (n = 12) reduced infarct size (triphenyltetrazolium) by 64.9% (P = 0.01) with respect to controls (n = 17). We conclude that the protection afforded by IPC is not mediated by effects on electrical coupling. This result is consistent with recent findings suggesting that Cx43 could have effects on cell survival independent on changes in cell-to-cell communication.

Effect of corticosteroid on lung parenchyma remodeling at an early phase of acute lung injury.

In vivo (lung resistive and viscoelastic pressures and static elastance) and in vitro (tissue resistance, elastance, and hysteresivity) respiratory mechanics were analyzed 1 and 30 days after saline (control) or paraquat (P [10 and 25 mg/kg intraperitoneally]) injection in rats. Additionally, P10 and P25 were treated with methylprednisolone (2 mg/kg intravenously) at 1 or 6 hours after acute lung injury (ALI) induction. Collagen and elastic fibers were quantified. Lung resistive and viscoelastic pressures and static elastance were higher in P10 and P25 than in the control. Tissue elastance and resistance augmented from control to P10 (1 and 30 days) and P25. Hysteresivity increased in only P25. Methylprednisolone at 1 or 6 hours attenuated in vivo and in vitro mechanical changes in P25, whereas P10 parameters were similar to the control. Collagen increment was dose and time dependent. Elastic fibers increased in P25 and at 30 days in P10. Corticosteroid prevented collagen increment and avoided elastogenesis. In conclusion, methylprednisolone led to a complete maintenance of in vivo and in vitro respiratory mechanics in mild lesion, whereas it minimized the changes in tissue impedance and extracellular matrix in severe ALI. The beneficial effects of the early use of steroids in ALI remained unaltered at Day 30.

The future of diagnostic ultrasound

You can predict the future at the airport: ARRIVALS show what’s in the air; physics predicts the descent. DEPARTURES tell you what’s under preparation. To predict further, visit the factory, development engineers, or airport planners. Pulse-echo ultrasound provides echo strength and phase, allowing conclusions about tissue impedance changes, velocities, motion, and strain. Comparing echoes from adjacent ultrasound scan lines reveals information about tissue layering. Periodic strain with the cardiac cycle reveals arteriolar dynamics and with the respiratory cycle reveals venular dynamics. Three-dimensional imaging adds anatomic relationships. Angle-dependent echogenicity and compound scanning, abandoned a quarter century ago, reveals tissue structure such as muscle myofibril alignment. Multi-frequency imaging can provide information on tissue periodicity, frequency-dependent echogenicity, and attenuation. Wide, segmented apertures allow automatic compounding and vector velocity measurements. Cross-modal methods such as opto-acoustics or acousto-optics, especially with selected optical frequencies hold promise of displaying optical spectral information on ultrasound images. Ultrasound can be used to interrogate implanted or natural biosensors. If the sensors are tiny bubbles, such as contrast agents, selection of contained gas and choice of surfactant for tissue-specific adsorptive properties and antigenic properties provide opportunities for identification of specific molecules on vascular walls. Static imaging rather than “real-time” scanning is preferred for many applications. Transmission ultrasound displaying attenuation, phase delay, or refraction can provide information on tissues. By combining the physical and physiological laws with diagnostic goals and financial and other resource constraints, the future of ultrasound can be predicted. Future ultrasonic diagnostic methods will not happen by themselves. They will only occur if there is a group of “advocates” who develop and validate the technology, convince the experts, train the users, demonstrate cost effectiveness, finance the production, and distribute the product. It is easier to shape the future than to predict the shape of the future.

Radio-frequency thermal ablation with hypertonic saline solution injection of the lung: ex vivo and in vivo feasibility studies.

The aim of this study was to assess the effects of simultaneous instillation of NaCl solutions during radio-frequency ablation (RFA) on the dimension of the ablated lesion in ex vivo bovine lung tissue and in vivo rabbit lung tissue. The RFA was induced in ex vivo bovine lung tissue which was inflated with room air and in vivo rabbit lung tissue by a 500-kHz RF generator and a 17-G cooled-tip electrode. In in vivo experiments, RFA was performed using CT guidance. The RF energy was applied for 5 min with or without instillation of 0.9 or 36% NaCl solutions. The changes in tissue impedance, current, power output, and temperature of the electrode tip were automatically measured. The maximum diameter of all thermal lesions was measured perpendicular to the electrode axis by two observers. In an ex vivo study, the mean lesion diameters using 36 and 0.9% NaCl solutions were larger than those of the control group: 51+/-8, 34+/-6, and 5+/-2 mm ( p<0. 05). In in vivo rabbit lung tissue, the mean lesion diameter with NaCl solution (15.3+/-3.1 mm) was larger than that of the lesion without NaCl solution (8.5+/-1.4 mm; p<0.05). With instillation of NaCl solutions, a marked decrease of tissue impedance (>100 Omega) and corresponding increase of current flow occurred in both ex vivo and in vivo studies. This experimental study demonstrates that RF ablation with simultaneous NaCl solution infusion of the lung is more effective in achieving coagulation necrosis than conventional RFA procedure.

Effects of Cortical Spreading Depression on Cortical Blood Flow, Impedance, DC Potential, and Infarct Size in a Rat Venous Infarct Model

A cortical venous infarction model has been evaluated as to the degree of regional flow reduction and by studying effects of cortical spreading depression (CSD). Two adjacent cortical veins were occluded photochemically with rose bengal and fiberoptic illumination. Seven rats served to demonstrate effects on regional cortical blood flow using laser Doppler scanning. In 36 rats local CBF, DC potential, and brain tissue impedance were measured continuously for 75 min after vein occlusion. No, 3, or 10 CSD waves were induced by potassium chloride injection during the initial 75 min. Rats were compared for spontaneous CSDs; baseline local CBF, CBF, and impedance response to CSD; and infarct volume. Seventy-five minutes after vein occlusion regional cortical flow in a 3.5 × 7-mm window was reduced to 34.3 ± 13.2%. At 45% of the 840 measured locations in 7 rats flow was <40% baseline and at 27.3% <30%, indicating a widespread penumbra territory. During the initial 75 min 2.1 ± 1.1 spontaneous CSDs were observed. There was a positive correlation between the number of spontaneous CSDs seen acutely and infarction volume after 5 days. Moreover, brain injury was significantly increased in the group with 10 KCl-induced CSDs. A reduced 1CBF response and an overshooting tissue impedance change during CSD were predictors of ischemic damage. This study demonstrates a CSD-related growth of the venous infarct. Second, the data indicate that flow after two-vein occlusion resembles that seen under penumbra conditions, allowing for studies of damage mechanisms responsible for infarct growth.

Changes in Myocardial Electrical Impedance Induced by Coronary Artery Occlusion in Pigs With and Without Preconditioning

Myocardial ischemia increases tissue electrical resistivity leading to cell-to-cell uncoupling, and this effect is delayed by ischemic preconditioning in isolated myocardium. Alterations in myocardial resistivity elicited by ischemia in vivo may influence arrhythmogenesis and local ST-segment changes, but this is not well known. Myocardial impedance (resistivity [omega x cm] and phase angle [degrees]), epicardial ST segment, and ventricular arrhythmias were analyzed during 4 hours of coronary artery occlusion in 11 anesthetized open-chest pigs; these were compared with 13 other pigs submitted to a similar coronary occlusion preceded by ischemic preconditioning. Myocardial resistivity rose slowly during the first 34+/-7 minutes of occlusion (237+/-41 to 359+/-59 omega x cm), increased rapidly to 488+/-100 omega x cm at 60 minutes, and reached a plateau value (718+/-266 omega x cm, ANOVA; P<.01) at 150+/-69 minutes. By contrast, phase-angle changes began after 17 minutes of ischemia (-3.0+/-1.6 degrees to -4.2+/-1.2 degrees at 29+/-8 minutes) and evolved faster thereafter (-12.5+/-5.3 degrees at 144+/-56 minutes). Marked changes in myocardial impedance were observed during the reversion of ST-segment elevation that occurred 1 to 4 hours after occlusion, but impedance changes were less apparent during the early ST-segment recovery seen at 15 to 35 minutes of ischemia. The second arrhythmia peak (30+/-5 minutes) coincided with the fast change in tissue impedance, and both were delayed (P<.05) by ischemic preconditioning. A rapid impairment of myocardial impedance occurs after 30 minutes of coronary occlusion, and its onset is better defined by shift in phase angle than by rise in tissue resistivity. Phase 1b arrhythmias are associated with marked impedance changes, and both are delayed by preconditioning. Reversion of ST-segment elevation is partially associated with impairment of myocardial impedance, but other factors play a role as well.

Initial in vivo experience with EIT as a thermal estimator during hyperthermia.

Thermal imaging experiments using electrical impedance tomography (EIT) have been conducted during hyperthermia treatments delivered to two human patients and one animal subject. Coplanar and circumferential arrays of 16 and 32 tin-plated copper electrodes etched on a 0.005" polyimide sheet were used to inject 12.5 KHz current patterns of increasing sinusoidal spatial frequencies and subsequent potential distributions were recorded at each electrode site. Image reconstruction was achieved with a finite element method and difference images of conductivity changes during the course of treatment were formed. An assumed linear relationship (2%/degree C increase) between tissue impedance change and temperature change was used to produce thermal images of the treatment field in patients whereas an empirically measured nonlinear relationship obtained from excised tissue samples was applied retrospectively in the animal subject case. Reconstructed conductivity changes are shown to be possible given electrical data measured in vivo during hyperthermia delivery with conventional equipment (spiral microstrip applicator at 433 MHz). These correlated well with direct temperature measurements and demonstrated quantitative levels of agreement to the extent that estimated temperature accuracies were approximately 1.5 degrees C; although large errors (> 5 degrees C) did exist. This work suggests that EIT is a potentially useful tool for hyperthermia treatment monitoring and assessment. The relationship between tissue impedance and temperature is complex and confounds the ability to make simple correlations between conductivity and temperature changes. Further, study is required to discern whether this will ultimately limit EIT as a thermal estimator or whether it will lead to more fundamental uses of impedance as an indicator of thermal effect.

Radiofrequency tissue ablation in the rabbit lung: Efficacy and complications

We assessed the feasibility and safety of performing percutaneous radiofrequency ablation of pulmonary tissue in rabbits. Using an aseptic technique and computed tomography (CT) guidance, insulated 19-gauge aspiration biopsy needles were inserted into the right lower lobe of eight New Zealand White rabbits. Radiofrequency was applied via a coaxial electrode for 6 min at 90 degrees C. Probe-tip temperature, tissue impedance, and wattage were recorded at baseline and at 60-sec intervals throughout the procedure. CT scanning was used to assess tissue destruction and the presence or absence of pneumothorax immediately after the procedure and at 24 hr, 3 days, 10 days, 21 days, and 28 days. Three rabbits were sacrificed immediately, and the remaining rabbits were euthanized at 24 hr and at 3 days. 10 days, and 28 days (two rabbits). Gross and microscopic pathology were obtained and correlated with CT findings. The mean initial tissue impedance was 509 +/- 197 omega, marked changes in tissue impedance were found during the procedure (240-1380 omega). Rigid temperature control required continuous manual fine-tuning of generator output. Increased respiratory rate was noted in one rabbit during the first 30 sec of radiofrequency application. Homogeneous, ovoid opacities 8.4 +/- 2.4 mm in diameter and 1.4 +/- 0.1 cm in length were found by CT scanning immediately after the procedure. These opacities showed maximal consolidation at 3 days, corresponding to coagulative necrosis and a peripheral acute inflammatory reaction. At 10 days, peripheral hyperattenuation with central hypoattenuation (early fibrosis surrounding degenerating blood products) was seen. Minimal residual fibrosis, pleural scarring, or both were noted by 28 days, suggesting a rapid, near-total recovery from the procedure. Lesion sizes were within 2 mm of gross pathologic findings. Pneumothoraces were noted in three of the eight rabbits (37.5%). Radiofrequency tissue ablation was safely performed in pulmonary parenchyma via a percutaneous, transthoracic approach using a coaxial needle technique. Tissue response to thermal injury was predictable and easily monitored by CT scanning with excellent radiologic-pathologic correlation.

A quasi-power theorem for bulk conductors: comments on rheoencephalography

A special case of Tellegen's theorem, the quasi-power theorem, can be readily developed for bulk conductors, and a bulk conductor analog of Cohn's theorem follows which allows prediction of sensitivity of impedance plethysmographic measurements to tissue impedance changes in a system of bulk conductors. An example addressing the effects of scalp and cranium on the inference of regional blood flow in brain tissue begs additional questions about the origins of the rheoencephalogram.

Effects of tetrodotoxin on impedance in normal and asphyxiated cerebral tissue

The effect of tetrodotoxin (TTX) on cerebral tissue impedance was studied in the cat, as was the effect of TTX on impedance changes induced by calcium and asphyxiation. Impedance measurements were made at 1.0 kHz, in focal volumes of approximately 1.0 mm 3, using a Wheatstone bridge technique. In cats with chronically implanted electrodes, introduction of 1–250 ng of TTX in 0.5 μl CSF into the lateral geniculate body caused no change in cerebral tissue impedance. In acute experiments, topical applications of 0.05–50 μg of TTX in 0.1 ml CSF markedly reduced the amplitude of the cortical EEG without altering cortical tissue impedance. When asphyxiation was preceded by treatment of cortex with TTX, postasphyxial increases in both resistive and reactive impedance were delayed by 4–6 min. A similar delay, together with a marked reduction in the postasphyxial resistance increase, has been shown previously to occur following treatment of the cortex with CaCl 2. The application of CaCl 2 to the cortex prior to asphyxiation did not interfere with the postasphyxial reactance rise. When TTX treatment of the cortex was followed by applications of CaCl 2, the resulting cortical impedance increases were indistinguishable from those following application of CaCl 2 without prior TTX treatment. Postasphyxial resistance changes in calcium treated cortices were inversely related to the resistance changes induced by the calcium prior to asphyxiation. However, when the cortex was treated with TTX followed by CaCl 2 prior to asphyxiation, this inverse relation was lost. The postasphyxial impedance change following cortical pretreatment with TTX and calcium were delayed as with TTX alone. In terms of models of cerebral tissue impedance the results suggest that conductivity changes in hydrated extracellular macromolecules may play an important role in cerebral tissue impedance changes.