Cardiopulmonary Dysfunctions Caused by ADP-Induced Platelet Aggregation
| Autor: | Itsuro Kobayashi, Paul Didisheim, Hiroh Yamazaki |
|---|---|
| Rok vydání: | 1975 |
| Předmět: |
Male
medicine.medical_specialty Mean arterial pressure Time Factors Platelet Aggregation Physiology Sinus bradycardia Blood Pressure Platelet Adhesiveness Heart Rate Internal medicine Heart rate Respiration Bradycardia medicine Animals Platelet Respiratory system Busulfan business.industry Central venous pressure Apnea Blood Cell Count Rats Adenosine Diphosphate Oxygen Endocrinology Injections Intra-Arterial Cardiovascular Diseases Anesthesia Injections Intravenous Sinoatrial Block Splenectomy medicine.symptom Respiratory Insufficiency Cardiology and Cardiovascular Medicine business Spleen |
| Zdroj: | Japanese Circulation Journal. 39:675-682 |
| ISSN: | 1347-4839 0047-1828 |
| DOI: | 10.1253/jcj.39.675 |
| Popis: | Intravenous (i.v.) injection of 0.1 mg/kg of ADP within one second in 13 rats caused a prompt drop in platelet count to 55.1 plus or minus 3.2% of the preinjection value with a statistical significance (p less than 0.01) at 30 seconds after the injection. At that time, mean arterial pressure and arterial PO2 decreased, while central venous pressure increased. Heart rate decreased with an appearance of sinus bradycardia and variable A-V block. Various respiratory effects such as shallow or slow respiration or apnea appeared. Such changes showed a tendency to recovery within 3 minutes. Splenectomy did not prevent these changes in 6 rats. In 6 thrombocytopenic and leukopenic rats treated with busulfan, these changes did not appear. Intra-arterial injection of the same amount of ADP induced almost no response. When ADP was injected twice 20 seconds apart in 10 rats, the second injection resulted in no effects or slight responses. In contrast, when 10 rats were injected twice 180 seconds apart, both the first and second injections showed the same effects on platelets and cardiopulmonary functions. The results suggests that the effects observed following I.V. ADP are probably due to transient obstruction of coronary and pulmonary microvessels by platelet aggregates. Reduced response following two successive injections may be due either to the reduced platelet count or to a refractory state induced by the first injection. ADP is probably rapidly metabolized in systemic microvascular beds. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|