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Biomedical subjects

Tor Inge Tønnessen

Publications and source records attributed to Tor Inge Tønnessen.

9 recordsLinked to original sources

Detection of ischemia and new insight into left ventricular physiology by strain Doppler and tissue velocity imaging: assessment during coronary bypass operation of the beating heart.

BACKGROUND AND OBJECTIVES: Detection of myocardial ischemia in humans by strain Doppler and tissue velocity imaging was validated in a novel, experimentally designed study model during coronary bypass operation of the beating heart. METHODS: Assessment of ischemia was made with an opened chest and pericardium inherent in the operative procedure. Longitudinal strain and tissue velocity of interventricular septal regions were measured by transesophageal echocardiography during occlusion of the left anterior descending coronary artery (LAD). RESULTS: Unexpectedly, baseline velocities demonstrated that the apical and basal septum moved toward each other during systole. This occurred when the apex was dislodged from the pericardial sac to obtain access to the LAD, without any change in strain. The preceding motion of all septal regions toward the apex was reestablished after the heart was repositioned within the pericardium. In 16 patients with antegrade LAD flow, strain Doppler detected ischemia during LAD occlusion by disclosing systolic lengthening of the apical septum ( P <.01) and reduced shortening of the mid septum ( P <.05). The location and degree of ischemic changes coincided with the concomitant deterioration of wall motion. Tissue velocity changed in the basal and mid septum ( P <.05) but not in the apical region, explained by tethering effects and the distinctive motion pattern at baseline. There was no evidence of ischemia by invasive hemodynamic measures. In 7 patients with retrograde LAD flow, there were no significant changes in strain or tissue velocity measurements during LAD occlusion. CONCLUSIONS: Strain by Doppler is a sensitive means for detecting myocardial ischemia, also capable of correctly localizing the ischemia, as opposed to tissue velocity assessment. However, velocity measurements provided new physiological information by disclosing the normal longitudinal motion of the heart to be dependent on the pericardial sac enveloping the apex, irrespective of the structural integrity of the pericardium.

Aged↗

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↗

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↗

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↗

[Transcatheter closure of atrial septal defects in the oval fossa].

BACKGROUND: We report five years' experience with transcatheter closure of defects in the oval fossa at Rikshospitalet University Hospital in Oslo, Norway. MATERIAL AND METHODS: We reviewed the results in 69 patients between 1.3 and 74 years of age (median 5.3), weighing median 20 kg (7.8-109), with pulmonary blood flow 2.40.74 (1.3-4.8) times systemic flow, and median diameter of the defect 18 mm (9-34). The patients were followed clinically for one year. RESULTS: In 69/77 (90%) the defect could be closed. None had a significant residual shunt. One patient showed a very small residual leak after one year. Two children, not yet seen after one year, had a small shunt after one month. The complication rate has been low, and we have not been able to demonstrate any sequelae. The hospital stay is two nights without any convalescence period. The results compare favourably to surgery. INTERPRETATION: The method was efficient and safe in all age and weight groups. The very limited total volume of such procedures indicates they should be centralised and only carried out by a small number of physicians.

Adolescent↗

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↗

Transcatheter closure of atrial septal defects in the oval fossa: is the method applicable in small children?

We report our experience from 1996 through 1999, representing our initial experience with use of the Amplatzer device to close atrial septal defects. Of 46 patients taken to the catheter laboratory with the intention to close the defect, the device was permanently implanted in 40 (87%). They were aged between 1.4 and 71.8 years, with weights ranging from 7.8 to 90 kg. Both age and weight distributed into two peaks, demonstrating two different populations. The size of the devices, taking the biggest device if two were inserted, was between 9 and 30 mm. We underwent a short learning curve, but the time required for fluoroscopy, or the number of difficulties experienced, showed no connection with the size or age of the patient, nor the size of the defect itself. A suspicion that young age and small size would increase the risk and difficulties, and result in more interrupted procedures, could not be substantiated. In children no interruption was procedural. Our early experience, therefore, demonstrates that an experienced interventional team can use the Amplatzer occluder successfully to close atrial septal defects in patients of all ages and sizes, at least from 7.8 kg and up.

Adolescent↗

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↗