ascorbic-acid and Embolism

Topics: Anesthesia, Local; Animals; Ascorbic Acid; Bandages; Blood Circulation; Embolism; Hernia, Inguinal; Humans; Leg; Length of Stay; Male; Physical Exertion; Postoperative Care; Postoperative Complications; Rats; Rest; Surgical Wound Dehiscence; Thrombophlebitis; Wound Healing

Besides low mortality and morbidity rates in cardiac surgery, the associated cognitive dysfunction is the focus of interest. One possible reason is microembolisation.. The authors analysed the crystallogenesis in the calcium-containing prime, inspired by their observation that the fluid sometimes becomes turbid during the priming process. Lactated Ringer-based prime solutions were tested, adding mannitol, NaHCO(3), and heparin. The oxygenator was ventilated with compressed medical air. Samples were taken for dynamic light scattering particulate level analysis. The priming was furthermore modelled in the laboratory by mixing the components and then ventilating the mixture through with compressed air. Turbid solutions from the operating room contained 100-6500 nm crystals, while clear solutions contained 20-473 nm particles. In the model, continuous pH measurement showed pH 6.4-7.4 after blending the solutions, which then elevated the pH to 7.5-8.0 after ventilation with concomitant turbidity. The pH of the prime can be stabilized by the addition of ascorbic acid (1-2 mg/ml) and, also, the turbidity may be prevented.. Ventilating the lactated Ringer-based calcium-containing primes after blending is not advisible because of alkalization and crystallogenesis. Ascorbic acid stabilizes the pH and prevents crystallogenesis in the prime. Pre-bypass filtration is recommended.

Topics: Alkalies; Ascorbic Acid; Calcium; Cardiac Surgical Procedures; Cardiopulmonary Bypass; Cognition Disorders; Crystallization; Embolism; Humans; Hydrogen-Ion Concentration; Isotonic Solutions; Microcirculation; Nephelometry and Turbidimetry; Particle Size; Ringer's Lactate

We addressed a potential mechanism of myocardial dysfunction following coronary microembolization at the level of myofibrillar proteins.. Anaesthetized pigs underwent intracoronary infusion of microspheres. After 6 h, the microembolized areas (MEA) had decreased systolic wall thickening to 38 +/- 7% of baseline and a 2.62 +/- 0.40-fold increase in the formation of disulphide cross-bridges (DCB) in tropomyosin relative to that in remote areas. The impairment in contractile function correlated inversely with DCB formation (r = -0.68; P = 0.015) and was associated with increased TNF-alpha content. DCB formation was reflected by increased tropomyosin immunoreactivity and abolished in vitro by dithiothreitol. Ascorbic acid prevented contractile dysfunction as well as increased DCB and TNF-alpha. In anaesthetized dogs, 8 h after intracoronary microspheres infusion, contractile function was reduced to 8+/-10% of baseline and DCB in MEA was 1.48+/-0.12 higher than that in remote areas. In conscious dogs, 6 days after intracoronary microspheres infusion, myocardial function had returned to baseline and DCB was no longer different between remote and MEA. Again contractile function correlated inversely with DCB formation (r = -0.83; P = 0.005).. Myofibrillar protein oxidation may represent a mechanistic link between inflammation and contractile dysfunction following coronary microembolization.

Topics: Analysis of Variance; Animals; Antioxidants; Ascorbic Acid; Blotting, Western; Cardiomyopathies; Coronary Vessels; Dithiothreitol; Dogs; Embolism; Immunohistochemistry; Microcirculation; Microspheres; Myocardial Contraction; Oxidation-Reduction; Reactive Oxygen Species; Swine; Swine, Miniature; Tropomyosin; Tumor Necrosis Factor-alpha

Oxygen-derived free radicals are thought to injure the ischemic heart during coronary microvascular embolization.. To test this idea, microspheres (15 microns in diameter) were repetitively administered into the left anterior descending coronary artery to cause microvascular embolization in dogs. Myocardial contractile and metabolic dysfunctions were significantly attenuated after treatments with recombinant human superoxide dismutase, an acyl derivative of ascorbic acid (CV3611, 2-O-octadecylascorbic acid), and xanthine oxidase inhibitor (allopurinol). The free radical scavengers and inhibitor enhanced the coronary hyperemic flow response during embolization, and the total number of microspheres causing maximal embolization was increased by these drugs. When 8-phenyltheophylline was additionally administered with superoxide dismutase, these beneficial effects were abolished, indicating that coronary effects of these drugs may be due to increased release of adenosine during coronary microvascular embolization.. We conclude that oxygen radicals worsen the ischemic injury in coronary microembolization.

Topics: Allopurinol; Animals; Ascorbic Acid; Body Water; Cardiomyopathies; Coronary Disease; Dogs; Edema; Embolism; Free Radical Scavengers; Free Radicals; Microcirculation; Microspheres; Oxygen; Superoxide Dismutase; Theophylline