Hemorheological changes in cerebral circulation of rabbits with acute carbon monoxide poisoning

Abstract

Carbon monoxide (CO) poisoning is a leading cause of poison-related morbidity and mortality. The severe complication of delayed neuropsychiatric sequelae seriously affects patient's living quality, but its mechanism remains controversial. In this study, we established an animal model by intraperitoneal injection of CO in rabbits at regular interval and kept the carboxyhemoglobin (HbCO) level in blood above 50% for at least 24 h. We investigated the dynamic changes in the hemorheological and coagulative properties of blood taken from venae jugularis interna before CO injection and at 30 min, 1-5 days after the last CO exposure. We found that RBC count, hemoglobin (Hb) concentration, and hematocrit (Hct) increased on 1 day and remained high level till 5 day. Whole blood viscosities at different shear rates decreased significantly at 30 min and then increased 1 day later until day 4. RBC deformation index (DI) and aggregation index decreased at 30 min and recovered to normal on day 3. Plasma viscosity and fibrinogen augmented from 30 min until day 5. Prothrombin time (PT) and active partial thromboplastin time (APTT) prolonged remarkably at 30 min and went back to normal on 3 day, plasma [Ca 2+ ] decreased at 30 min and approached to normal level on 3 day. The level of malondialdehyde (MDA) in RBCs at 30 min was significantly higher than that of control and recovered to normal on day 3. Our results suggest that the changes in hemorheology participate in the development of acute CO poisoning, which may play a role in delayed encephalopathy after acute CO poisoning.

Salvianolic Acids Attenuate Rat Hippocampal Injury after Acute CO Poisoning by Improving Blood Flow Properties

“…The widely accepted view is that the increase in blood flow may be able to supply enough oxygen so that there is no change in the oxygen consumption. Another interpretation is that the increase in blood flow may cause vasodilation independently based upon oxygen level with dilatory agent (such as NO) and maintain adequate tissue oxygen level with the increased oxygen extraction [ 40 ]. But the change in whole blood viscosity at low shear rate occurring on day 1 after CO exposure could have disturbed the microcirculation in brain, especially in the regions with poor vasculatures, such as white matter, globus pallidus, basal ganglia, and hippocampus.…”

Protective effect of sodium aescinate on lung injury induced by methyl parathion

“…[4][5][6] It is reported that lung injury, including thickening of the alveolar-capillary membrane, degeneration in alveoli, alveolar congestion, hamorrhage, neutrophil infiltration or aggregations and so on, does occur in AOPP. 7 Recent studies indicated that mechanisms other than AChE inhibition may be involved in the progression of AOPP, including oxidative stress, mitochondrial energy metabolism impairment, 8,9 microcirculation disturbance, [10][11][12] and acute inflammation. [13][14][15] Escin is one of the main bioactive constituents of Aesculus hippocastanum, which is a plant distributed all over the world because of its excellent resistance to environmental conditions.…”