Biomedical subjects

M H Koets

Publications and source records attributed to M H Koets.

3 recordsLinked to original sources

PubMed1995

Mechanism of induction of asthmatic attacks initiated by the inhalation of particles generated by airbag system deployment.

OBJECTIVE: We have previously demonstrated that inhalation of the dust produced by dual frontal airbag deployment can result in significant bronchospasm in approximately 40% of mild to moderate asthmatics. This study was performed to determine the cause of the asthmatic response. DESIGN: Controlled laboratory study. MATERIALS AND METHODS: Asthmatics who were previously tested for their response to airbag effluents were exposed for twenty minutes to either 1) airbag effluents from airbag systems in which the airbag was insulated from the hot deployment module; 2) non-sulfur containing airbag effluents; 3) sodium chloride aerosol; or 4) sodium carbonate-bicarbonate aerosol (pH 10). Pre-exposure, post-exposure, and 2 hour post exposure pulmonary spirometry and mechanics were measured. Subject's filled out symptoms questionnaires before exposure, 2, 4, 8, 12, and 19 minutes into the exposure, immediately post-exposure, and 2 hours post-exposure. MEASUREMENTS AND MAIN RESULTS: Prevention of the pyrolysis of the passenger-side bag as it rested on the hot module after deployment did not diminish the asthmatic response. Removal of sulfur-containing oxidants from the airbag pyrotechnic chemistry, which may have led to sulfite production, similarly did not alleviate the asthmatic response to the airbag effluents. Lastly, when asthmatics were exposed to sodium chloride and sodium carbonate-bicarbonate aerosols at approximately the same concentration (approximately 220 mg/m3) as the airbag aerosol concentration that occurred in the in-car tests, they had responses similar to those produced by the airbag exposures. CONCLUSIONS: We conclude that the amount of soluble particulate contained in the aerosol discharged into the passenger compartment by dual frontal airbag deployment is largely the cause of the observed evoked asthmatic attacks. The alkaline pH of the airbag and carbonate aerosols may have added an additional degree of provocation.

Adolescent↗

PubMed1985

Hemostasis changes during cardiopulmonary bypass surgery.

A number of hemostasis parameters were studied in a total of 63 patients undergoing cardiopulmonary bypass (CPB) for open heart surgery. In 33 patients fibrinogen, Factors II, V, VIII:C, X, XI, antithrombin, plasminogen, alpha 2-antiplasmin, and platelet counts were assayed before surgery, during maximal hypothermia, at the end of the bypass procedure, before and after protamine sulfate infusion, in the intensive care unit, and 48 hours postoperatively. All factors assayed decreased markedly when the patients were placed on the bypass machine, the drop fairly well paralleling the decrease in hematocrit. During bypass the factors remained low, although a slight tendency toward an increase was noted. Only platelet counts remained low with a decreasing trend until the end of bypass. In the intensive care unit a second decrease in fibrinogen, Factors II and V and antithrombin was noted. This drop was unrelated to four patients who experienced a greater blood loss during this time than the others. Forty-eight hours postoperatively, a marked increase could be found in all clotting factors and near normal levels were measured. Platelet counts remained low, however. The decrease in factors rarely dropped into a range where one would expect a compromised hemostasis (less than 30%). Although antithrombin levels decreased below 60%, no difficulties with heparinization were encountered. Several factors were assayed manually and by automated analyzer (Multistat III), and excellent correlations were found between both procedures. Also a good correlation was found between the activated whole blood clotting times and quantitative heparin assays. In 30 additional patients platelet function was studied before surgery, after thoracotomy, after heparin administration, after initiation of bypass, at maximal hypothermia, before and after protamine sulfate infusion, and 24 hours postoperatively. Platelet counts once again decreased as patients were placed on the CPB machine and remained low throughout the procedure. Mean platelet volumes were unchanged until protamine was given. At that time, a significant drop in mean platelet volume was recorded. Twenty-four hours postoperatively the volumes were normal again. Platelet aggregation studies were performed on a whole blood aggregometer using two concentrations of ADP, collagen, and ristocetin as aggregation inducers. A significant decrease in aggregability was seen when the patients were connected to the CPB apparatus.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗

PubMed1984

Early events in the formation of a venous thrombus following local trauma and stasis.

A jugular vein was exposed in 20 cats divided into four groups of five cats each. In group 1 the vein was removed immediately after exposure. In group 2 the vein was removed after three 5-minute periods of stasis and reflow. Groups 3 and 4 had the jugular vein occluded for 24 and 72 hours, respectively. In all groups, veins were perfused under physiologic pressure by heparinized saline to remove blood and immersed in 2.5% glutaraldehyde for fixation. All vessels were prepared for scanning and transmission electron microscopy. Group 1 cats had a normal-appearing luminal surface. Group 2 cats had deposition of leukocytes with few erythrocytes or platelets. Groups 3 and 4 had deposition of leukocytes, platelets, and erythrocytes. Leukocytes were found in all areas and associated with all cell types. Platelets and erythrocytes were seldom found in the absence of leukocytes. Thrombi were found on normal-appearing and damaged endothelium. The majority of thrombi were found at side branches and valve pockets. Our results suggest that leukocytes play a primary role in the initiation of deep vein thrombosis. Platelets may have only a secondary role.

Animals↗