Biomedical subjects

Peyman Mirtaheri

Publications and source records attributed to Peyman Mirtaheri.

6 recordsLinked to original sources

PubMed2005

Electrode polarization impedance in weak NaCl aqueous solutions.

In this paper, we characterize the polarization impedance behavior of several common metals in diluted NaCl solution operated at low current densities. The objective was to provide a useful reference for those wishing to calculate the electrode polarization impedance in diluted NaCl solutions. Serial equivalent resistance (R) and capacitance (C) for silver, aluminum, gold, platinum, and medical stainless-steel were measured as a function of frequency (10(-2)-10(3) Hz) and NaCl concentration (2.4-77.0 mmol/L). The ratio of electrode polarization impedance with respect to the bulk resistance was calculated and plotted against concentration for each metal. Such a ratio shows the effect of the electrode polarization contribution as a function of electrolyte concentration when the bulk resistance of the solution changes. All metals showed a decrease of serial resistance Rp and capacitance Cp as a function of frequency. The medical stainless-steel electrode showed largest impedance values at lower frequencies compared to the other electrodes, and was concentration independent at all frequencies. Aluminum had smallest polarization impedance at low frequencies. Pure gold and platinum behaved similar with the exception that the serial resistance for gold showed a lower value at higher frequencies.

Electric Impedance↗

PubMed2004

A new biomedical sensor for measuring PCO2.

Measuring PCO2 (partial pressure of carbon dioxide) in an organ can enable early detection of ischemia. However, there are few clinical applicable solutions for measuring PCO2. Based upon the requirement for clinical applications, a conductivity based PCO2 sensor is proposed. A conductivity based PCO2 sensor measures conductance in an aqueous solution separated from the measured object by a gas-permeable membrane. A bridge design with two cavities is favored for such a sensor. A planar and a cylindrical macro prototype based upon the bridge design were studied. The design criteria were based on the contribution from the electrode polarization, stray capacitances, contact area with the sample and design ability to miniaturize the sensor. The cylindrical sensor is favored because of its large contact area and advantages for miniaturization. Further investigation has to be done to confirm the functionality of such a design in a miniaturized form and its clinical performance.

Biomedical Technology↗

PubMed2004

Miniaturization of a biomedical gas sensor.

In a previous study, we concluded that a conductivity based PCO2 sensor is an attractive solution for early detection of ischemia and presented two design geometries. For organ surface measurements, the planar design was suitable but it was difficult to insert the sensor into the tissue. A cylindrical design solution was favored for insertion due to the large membrane contact area and easy placement in a medical catheter. Since the previous cylindrical prototype was large and could damage the tissue, a more miniaturized sensor was needed. In the current paper, we present a miniaturized sensor with an outer diameter of 1 mm. The applied technology for manufacturing the sensor was a combination of mechanical turning, excimer laser drilling and conventional molding technique. The materials applied were PEEK (polyetherether ketone), PI (polyimide) with gold layers and polysiloxane. The membrane had to be gas permeable while acting as a barrier for ion transport, and was made of polysiloxane and had a thickness of 100-150 microm. The miniaturized sensor was tested for calibration, response time, drifting and pressure sensitivity. The results show that the miniaturized PCO2 sensor is capable of rapid and stable measurements both in vitro and ex vivo. The result from this study will be applied for the industrial manufacturing of such a biomedical sensor as a clinical product.

Biosensing Techniques↗

PubMed2004

Detection of ischemia by PCO2 before adenosine triphosphate declines in skeletal muscle.

OBJECTIVE: Ischemia is a serious problem in clinical medicine, and effective methods are needed to detect ischemia before the injury becomes irreversible. In experimental studies on several organs, PCO2 was found to increase rapidly after the onset of supply-dependent anaerobic metabolism. A shortcoming of these studies was that PCO2 was not correlated with tissue concentrations of lactate and the energy status in the cell. Thus, in this study we have measured tissue concentrations of lactate, phosphocreatine, and adenosine triphosphate. We hypothesized that during ischemic conditions, PCO2 reflects lactate generation in the cell and not exhausted energy stores per se. If this is the case, PCO2 can be used to detect ischemia before the energy stores are depleted. Consequently, therapy can be instituted at a time when the organ is salvageable. DESIGN: Prospective laboratory study. SETTING: University research laboratory. SUBJECTS: Seven pigs. INTERVENTIONS: In a porcine model, gluteal skeletal muscles with no-flow ischemia were examined. PCO2 was measured both in situ and in vitro at increasing periods of time. Concomitantly, tissue lactate, adenosine triphosphate, and phosphocreatine were analyzed. MEASUREMENTS AND MAIN RESULTS: Tissue surface CO2 tension (PtCO2) increased rapidly after onset of ischemia. From a baseline of 63 +/- 3 torr (8.4 +/- 1.2 kPa) under aerobic conditions, it increased to 157 +/- 6 torr (21 +/- 2.2 kPa) after 30 mins of ischemia and 386 +/- 9 torr (51.5 +/- 3 kPa) at 120 mins. The rapid increase of PtCO2 correlated well with increasing values of lactate (r2 >.9) in the tissue. Adenosine triphosphate was essentially unchanged for 45 mins after onset of ischemia, after which it declined. Phosphocreatine decreased earlier than adenosine triphosphate in accordance with the notion that high-energy phosphate groups are transferred from phosphocreatine to adenosine triphosphate. CONCLUSION: In this porcine model of skeletal muscle ischemia, PtCO2 correlates well with tissue lactate and increases long before the energy stores of phosphocreatine and most notably adenosine triphosphate are severely reduced. Thus, PtCO2 could be monitored to detect and treat earlier stages of ischemia.

Adenosine Triphosphate↗

PubMed2003

Tissue carbon dioxide tension: a putative specific indicator of ischemia in porcine latissimus dorsi flaps.

Free flap surgical procedures are technically challenging, and anastomosis failure may lead to arterial or venous occlusion and flap necrosis. To improve myocutaneous flap survival rates, more reliable methods to detect ischemia are needed. On the basis of theoretical considerations, carbon dioxide tension, reflecting intracellular acidosis, may be suitable indicators of early ischemia. It was hypothesized that tissue carbon dioxide tension increased rapidly when metabolism became anaerobic and would be correlated with acute venoarterial differences in lactate levels, potassium levels, and acid-base parameters. Because metabolic disturbances have been observed to be less pronounced in flaps with venous occlusion, it was hypothesized that tissue carbon dioxide tension and venoarterial differences in lactate and potassium levels and acid-base parameters would increase less during venous occlusion than during arterial occlusion. In 14 pigs, latissimus dorsi myocutaneous flaps were surgically isolated, exposed to acute ischemia for 150 minutes with complete arterial occlusion (seven subjects) or venous occlusion (seven subjects), and reperfused for 30 minutes. After arterial occlusion, pedicle blood flow decreased immediately to less than 10 percent of baseline flow. Blood flow decreased more slowly after venous occlusion but within 3 minutes reached almost the same low levels as observed during arterial occlusion. Venous oxygen saturation decreased from approximately 70 percent to approximately 20 percent, whereas oxygen uptake was almost arrested. Tissue carbon dioxide tension increased to two times baseline values in both groups (p < 0.01). The venoarterial differences in carbon dioxide tension, pH, base excess, glucose levels, lactate levels, and potassium levels increased significantly (p < 0.01). Tissue carbon dioxide tension measured during the occlusion period were closely correlated with venoarterial differences in pH, base excess, glucose levels, lactate levels, and potassium levels (median r2, 0.67 to 0.92). After termination of arterial or venous occlusion, more pronounced hyperemia was observed in the arterial occlusion group than in the venous occlusion group (p < 0.05). Oxygen uptake (p < 0.05) and venoarterial differences in lactate and potassium levels (p < 0.05) were significantly more pronounced in the arterial occlusion group. In the venous occlusion group, with less pronounced hyperemia, venoarterial differences in acid-base parameters remained significantly different from baseline values before occlusion (p < 0.01). The data indicate that tissue carbon dioxide tension can be used to detect anaerobic metabolism, caused by arterial or venous occlusion, in myocutaneous flaps. The correlations between carbon dioxide tension and venoarterial differences in acid-base parameters were excellent. Because carbon dioxide tension can be measured continuously in real time, such measurements are more likely to represent a clinically useful parameter than are venoarterial differences.

Animals↗

PubMed2002

PCO(2) in the large intestine of mice, rats, guinea pigs, and dogs and effects of the dietary substrate.

PCO(2) in the lumen and serosa of cecum and colon was measured in rats, guinea pigs, and dogs to examine the relationship between serosal PCO(2) and the incidence of intestinal necrotic lesions after administration of gas-carrier contrast agents in rodents. The effects of the dietary substrate were tested in a group of mice maintained on a diet based on glucose as the only carbohydrate source. The anesthetic used was a fentanyl-fluanison-midazolam mixture (rodents) and pentobarbital (dogs). PCO(2) was measured in vivo and postmortem, and the kinetics of the postmortem serosal PCO(2) [transmural CO(2) flux (J(CO(2)))] was calculated. PCO(2) in the cecal serosa and lumen, respectively, was 64 +/- 4 and 392 +/- 18 Torr in rats, 67 +/- 3 and 276 +/- 17 Torr in guinea pigs, and 73 +/- 6 and 137 +/- 7 Torr in mice on glucose-based diet. In the colon serosa and lumen of dogs, PCO(2) was 30 +/- 6 and 523 +/- 67 Torr, respectively. Serosal PCO(2) increased rapidly after death in rats and slower in guinea pigs and mice, and the slowest change was observed in dogs. Compared with dogs, serosal PCO(2) and J(CO(2)) of rats and guinea pigs were significantly higher. Serosal PCO(2) of guinea pigs was similar to that of rats, whereas the J(CO(2)) of guinea pigs was significantly lower. These data suggest a causal relationship between the ability of the cecal and colonic wall to act as a barrier to CO(2) diffusion and the presence of characteristic gas-carrier contrast agent-induced intestinal lesions in mice and rats and their absence in guinea pigs, dogs, and other species.

Animals↗