BACKGROUND: Etomidate is short-acting non-barbiturate intravenous anesthetic with minimal cardiovascular depression. As a small change in venous capacitance significantly alters venous return and thus cardiac output, it is important to know the effects of intravenous anesthetics on venous capacitance. The purpose of this study was to examine the effect of etomidate or pentobarbital (control agent) on venous capacitance. METHOD: All twenty rats (etomidate group: 10, pentobarbital group: 10), weighing 350-450 gram, were anesthetized with pentobarbital 50 mg/kg given intraperitoneally for surgical preparation. Mean arterial pressure (MAP), heart rate (HR), and mean circulatory filling pressure (MCFP) were measured in the awake state(recovered from pentobarbital anesthesia for surgical preparation) as well as during anesthesia with etomidate or pentobarbital. Venous capacitance was assessed before and during anesthesia with etomidate or pentobarbital by measuring MCFP. MCFP was measured during a brief period of circulatory arrest produced by inflating a balloon inserted in right atrium. RESULTS: As compared with MCFP in the corresponding awake state, MCFP was not significantly altered by etomidate but significantly decreased by pentobarbital. As compared with MAP in the corresponding awake state, MAP was not significantly altered by etomidate but significantly decreased by pentobarbital. CONCLUSION: The results suggest that unaltered venous capacitance by etomidate may contribute to a maintained MAP but increased venous capacitance by pentobarbital decrease in MAP of the normovolemic rat.
Anesthesia ; Anesthetics, Intravenous ; Animals ; Arterial Pressure ; Cardiac Output ; Depression ; Etomidate* ; Heart Atria ; Heart Rate ; Pentobarbital ; Rats*

It is now well established that acute subarachnoid hemorrhage secondary to rupture of a cerebral aneurysm can precipitate life-threatening cardiac arrhythmia. We experienced a 60 year old patient with a subarachnoid hemorrhage (neurologic grade III) due to rupture of anterior communicating artery aneurysm who presented with such intraoperative electrocardiographic changes as ST segment elevation and T wave inversion which are hallmark of acute myocardial infarction. The operation was uneventfully ended. On the postoperative laboratory examination about suspected acute myocardial infarction, the patient was found to have normal triple enzyme study and echocardiographic finding. The electrocardiogram three days after subarachnoid hemorrhage due to cerebral aneurysm returned to normal sinus rhythm. This case suggests that this patient's electrocardiographic change simulating acute myocardial infarction is transient change due to subarachnoid hemorrhage.
Arrhythmias, Cardiac ; Echocardiography ; Electrocardiography* ; Humans ; Intracranial Aneurysm ; Middle Aged ; Myocardial Infarction* ; Rupture ; Subarachnoid Hemorrhage*

Silica exposure results in acute inflammatory response followed by chronic fibrotic change. The mechanism for the maintenance of silica-induced inflammation has not been understood yet. Apoptosis is a morphologically distinct form of programed cell death that plays major role during homeostasis and in many diseases including cancer, acquired immune deficiency syndrome and neurodegenerative disorders. Apoptosis is characterized by cell shrinkage, membrane blebbing and nuclear condensation. To demonstrate the involvement of apoptosis in underlying mechanism for the development of silica-induced pathological changes, this study was designed in vitro and in vivo models. In in vitro study, alveolar epithelial cell line (A549) was stimulated with silica and performed flow cytometry and DNA electrophoresis. In in vivo study, bronchoalveolar lavage (BAL) was done to count the total and apoptotic cells from silica-instilled rats. The results were as follows: 1. Apoptotic cell fraction of silica-treated groups (10 and 50 microgram/cm2) was significantly higher than that of control group. 2. Genomic DNA from silica-treated groups (10 and 50 microgram/cm2 ) showed DNA ladder in agarose gel electrophoresis, while group of 1 microgram/cm2 didn't. 3. Total cell number and apoptotic cell number of BAL fluid from silica-instilled rats (10, 20 and 40 mg/kg) were significantly higher than those of control. 4. Silica induced apoptosis of cells in BAL fluid was confirmed by microscopic observation with nuclear fragmentation. These results suggest that apoptosis may contribute to development of silica-induced pathological changes.
Acquired Immunodeficiency Syndrome ; Animals ; Apoptosis* ; Blister ; Bronchoalveolar Lavage ; Cell Count ; Cell Death ; DNA ; Electrophoresis ; Electrophoresis, Agar Gel ; Epithelial Cells ; Flow Cytometry ; Homeostasis ; Inflammation ; Membranes ; Microscopy ; Neurodegenerative Diseases ; Rats ; Silicon Dioxide* ; Silicosis