Biomedical subjects

W Tao

Publications and source records attributed to W Tao.

112 records · Page 7Linked to original sources

PubMedDate not supplied

High flow/low resistance cannulas for percutaneous arteriovenous carbon dioxide removal.

Percutaneous cannulas with low resistance are necessary for arteriovenous carbon dioxide removal (AVCO2R) to allow highest flow at lowest pressure to maximize CO2 removal. Commercially available arterial (A) and venous (V) percutaneous cannulas (8-18 Fr) were tested for pressure/flow characteristics under conditions that simulated percutaneous AVCO2R at clinically pertinent flow rates between 200-1000 ml/min to obtain the M number previously described by Delius, et al. The Bio-Medicus (Bio-Medicus, Grand Rapids, MI) 17F A, Research Medical, Inc (RMI) (Model FEM II, Research Medical, Inc., Midvale, UT) 16F A, and RMI 18F V cannulas exhibited the lowest M numbers that correlated with low resistance to flow. The four most clinically favorable arterial cannulas (8, 10, 12, and 14 Fr), coupled with a venous cannula four French sizes larger, were used in an AVCO2R circuit in adult sheep (n = 3) at varying mean arterial pressures (MAP) between 65-105 mmHg. The 8, 10, 12, and 14 Fr arterial cannulas allowed an arteriovenous flow of 208 +/- 72, 530 +/- 37, 848 +/- 66, and 944 +/- 96 ml/min, respectively, at a MAP of 65 mmHg. An increase in MAP to 105 mmHg was associated with approximately a 41, 30, 32, and 27% increment in blood flow, respectively. In summary, an arterial percutaneous cannula of 10 Fr or larger will allow AVCO2R blood flow greater than 500 ml/min, as previously shown by Brunston et al. to achieve total CO2 removal without incurring hypercapnia.

Adult↗

PubMedDate not supplied

Organ blood flow during arteriovenous carbon dioxide removal.

Animal models of arteriovenous carbon dioxide removal (AVCO2R) have achieved lung rest during treatment of severe respiratory failure, with total CO2 removal at arteriovenous shunt flow rates of 10% to 25% of cardiac output (CO). Previously, no statistically significant changes were reported in heart rate, cardiac output, mean arterial pressure, or pulmonary arterial pressure during prolonged (7 days) AVCO2R with shunt flows to 25% of CO. In this study, to determine the effect of various shunt levels on organ blood flow, colored microspheres were used in a conscious ovine model of AVCO2R. A low resistance 2.5 m2 oxygenator was placed in a simple carotid-to-jugular arteriovenous circuit. The AVCO2R flow (Qb) was incrementally increased to 5%, 10%, 15%, 20%, and 25% of baseline CO. After equilibration, colored microspheres were injected into a left atrial catheter while reference blood was withdrawn from an arterial line at a constant rate. Organ blood flow obtained by measuring microspheres in the tissues, showed approximately a 10-20% decrease at a 5% shunt, but remained relatively unchanged thereafter at up to a 25% shunt, and was well tolerated without hemodynamic sequelae or evidence of end organ ischemia. It was concluded that AVCO2R can achieve lung rest during respiratory failure at flow rates of 10-25% CO, with a resultant mild decrease in critical organ blood flow that appears well tolerated.

Adult↗

PubMedDate not supplied

Efficacy of a heparin removal device in comparison with protamine after hypothermic cardiopulmonary bypass.

To reduce the risks of protamine reactions after cardiopulmonary bypass (CPB), a heparin removal device (HRD) with plasma separation and poly-L-lysine (PLL) affinity adsorption was developed. To compare the efficacy of HRD with that of protamine, blood coagulation variables were evaluated in a swine model of CPB. Female Yorkshire swine were randomly divided into the HRD group (n = 6, weight 79.7 +/- 7.0 kg) and the protamine group (n = 6, weight 79.3 +/- 6.8 kg), and subjected to 60 min of right atrium-to-aortic, hypothermic (28 degrees C) CPB. After weaning from CPB, the right atrium was recannulated with a two-stage, dual lumen cannula in the HRD group. Blood flow was drained from the inferior vena cava, through the plasma separation chamber of the HRD where heparin was bound to PLL, and re-infused into the right atrium. The HRD run time was determined by an established mathematical model of first-order exponential depletion targeted to 90% heparin removal. In the protamine group, protamine was given in a 100 U heparin to 1 mg protamine ratio after CPB in a slow intravenous infusion. Hemodynamics, activated clotting time (ACT), activated partial thromboplastin time (APTT), and heparin concentration were obtained before, every 5 min during, and after the use of the HRD or before and after protamine administration, and 1 and 3 hours after HRD or protamine. Heparin concentration immediately after CPB was 4.90 +/- 0.19 U/ml in the HRD group and 3.94 +/- 0.63 U/ml in the protamine group, respectively (p > 0.05 between groups). The ACT was 994 +/- 7 sec in the HRD group and 768 +/- 55 sec in the protamine group, and APTT was greater than 150 sec in both groups (p > 0.05 between groups). In the HRD group, the HRD run time was determined to be 31.5 +/- 2.4 min for the targeted 90% heparin removal, and the plasma heparin concentration followed first-order depletion kinetics. In the protamine group, the full dose of protamine was administered over 15 min. Immediately after the HRD run or protamine administration, plasma heparin concentration decreased to 0.48 +/- 0.09 U/ml in the HRD group and 0.13 +/- 0.02 U/ml in the protamine group (p < 0.01 between groups); likewise, ACT decreased to 188 +/- 25 sec in the HRD group and 101 +/- 5 in the protamine group (p < 0.01 between groups). The APTT was not significantly different between the groups at any time during the experiment. Plasma heparin concentration and ACT were not significantly different three hours after the HRD run or protamine administration. The authors conclude that the HRD is capable of predictable reversal of systemic heparinization after CPB, and is an alternative to achieve heparin clearance in subjects who may develop adverse reactions to protamine.

Animals↗

PubMedDate not supplied

Adeno-associated viral vectors: background and technical aspects.

There are several obstacles that prevent the successful clinical application of gene therapy. Some of these challenges are unique to the particular disease and organ that is being targeted. Desirable characteristics of approaches aimed at delivery of a therapeutic gene to the kidney ideally will require a vector that is safe, that efficiently transduces nondividing cells, and that can lead to long-term gene expression. Viral vectors that are derived from the small replication-deficient parvovirus, adeno-associated virus, offer many potential advantages. The wild-type virus is nonpathogenic and can site specifically integrate at a single location on chromosome 19, a process that offers the hope that this characteristic could be engineered into recombinant vectors as well. Recombinant adeno-associated virus can also efficiently integrate into the host genome, can transduce nondividing cells, and does not induce an immune response which destroys the transduced cells. Efforts focused both on gaining a more complete understanding of the virus life cycle as well on the efficient production of high-titer virus should bring this vector closer to clinical application.

DNA, Recombinant↗