thiopental and Myocardial-Infarction

The performance of the cardiovascular system depends on the interaction of the left ventricle and arterial system. An appropriate coupling of these two components is important to quantify the efficiency of myocardium, determined by Ea/Ees. The end-systolic elastance of the left ventricle (Ees) is an index of contractility which is independent of loading conditions, while the arterial end-systolic elastance (Ea) represents the properties of the arterial system. The aim of our study is to investigate the effects of a bolus of remifentanil (R) on myocardial efficiency.. In a period of 3 months we examined prospectively the effects of R in a group of 12 patients, ASA IV, 49-75 years old, submitted intraoperatively to cardiac anesthesia for revascularization of myocardium. After induction of anesthesia and before the beginning of surgery, a bolus of R (1 mg/kg/min) was administered and with the use of trans-esophageal echocardiography we determined both the left ventricle end-systolic volume and end-diastolic volume to assess, with different end-systolic arterial pressures, the ventricle elastance (Ees) and arterial elastance (Ea) before and after administration of R.. The present findings indicate that R decreases the ventricular elastance from 6.07 mmHg/ml/m2 to 4.8, with a less decrease of arterial elastance from 3.69 mmHg/ml/m2 to 3.07.. The results suggest that R preserves a good left ventricular-arterial coupling and mechanical efficiency, despite a little increase of coupling, probably because ventricular and arterial properties are so matched as to minimize the systolic work of the left ventricle.

Topics: Aged; Anesthetics, Intravenous; Aorta; Cardiovascular Agents; Combined Modality Therapy; Coronary Artery Bypass; Coronary Disease; Echocardiography, Transesophageal; Electric Impedance; Female; Heart Failure; Heart Rate; Hemorheology; Humans; Injections, Intravenous; Male; Middle Aged; Myocardial Contraction; Myocardial Infarction; Oxygen Consumption; Piperidines; Propofol; Prospective Studies; Remifentanil; Stroke Volume; Thiopental; Vascular Resistance; Vecuronium Bromide; Ventricular Function, Left

The effects of laryngeal mask airway (LMA) insertion and tracheal intubation on circulatory responses were studied in normotensive (n = 24) and hypertensive (n = 22) patients. In a randomized, double-blind manner, LMA insertion or tracheal intubation was performed after induction of anaesthesia with thiopentone and muscle relaxation with succinylcholine. In both normotensive and hypertensive patients, heart rate (HR), mean arterial pressure (MAP) and rate-pressure product increased after tracheal intubation or LMA insertion compared with baseline (P < 0.05). The haemodynamic changes were greater after intubation than after LMA insertion (P < 0.05). Following intubation of the trachea or insertion of the LMA, HR increased more markedly in hypertensive patients than in normotensive patients (P < 0.05). Plasma adrenaline and noradrenaline concentrations after tracheal intubation or LMA insertion increased compared with baseline values (P < 0.05) in normotensive and hypertensive patients. The increase in noradrenaline concentration after tracheal intubation was greater than that after LMA insertion (P < 0.05). No patient revealed ECG evidence of myocardial ischaemia. We conclude that insertion of LMA is associated with less circulatory responses than tracheal intubation in both normotensive and hypertensive patients.

Topics: Adult; Aged; Anesthesia, Intravenous; Blood Pressure; Cardiac Complexes, Premature; Double-Blind Method; Epinephrine; Female; Heart Rate; Humans; Hypertension; Intubation, Intratracheal; Laryngeal Masks; Male; Middle Aged; Myocardial Infarction; Neuromuscular Junction; Norepinephrine; Succinylcholine; Thiopental; Ventricular Dysfunction

To investigate the effects of propofol, midazolam and thiopental sodium on outcomes and amino acid accumulation in focal cerebral ischemia-reperfusion in rats.. Male Sprague Dawley (SD) rats were scheduled to undergo 3-hour middle cerebral artery occlusion by intraluminal suture and 24-hour reperfusion. Neurologic outcomes were scored on a 0-5 grading scale. Infarct volume was shown with triphenyltetrazolium chloride staining and measured by an image analysis system. Concentrations of various amino acids (aspartate, glutamate, glycine, taurine, and gama-aminobutyric acid) were measured after 3 hours of reperfusion using high performance liquid chromatography. Propofol, midazolam and thiopental sodium were given intraperitoneally at the beginning of reperfusion.. Both propofol and midazolam attenuated neurological deficits and reduced infarct and edema volumes. Propofol showed better neurological protection than midazolam while thiopental sodium did not exhibit any protective effect. Both propofol and midazolam decreased excitatory amino acids accumulation, while propofol increased gama-aminobutyric acid accumulation in ischemic areas in reperfusion.. Propofol and midazolam, but not thiopental sodium, may provide protective effects against reperfusion induced injury in rats subjected to focal cerebral ischemia. This neurological protection may be due to the acceleration of excitatory amino acids elimination in reperfusion.

Topics: Adenosine Triphosphate; Animals; Brain; Brain Edema; Brain Ischemia; Excitatory Amino Acids; Male; Midazolam; Myocardial Infarction; Neuroprotective Agents; Propofol; Rats; Rats, Sprague-Dawley; Reperfusion Injury; Thiopental

Many anesthetic agents are known to have cardiac effects. The effects of pentobarbital, thiopental and isoflurane on dogs with electrical remodeling are lacking.. We studied 12 dogs that underwent two anesthesias. First, anesthesia was induced (N=12) with intravenous thiopental (17 mg/kg) induction followed by isoflurane inhalation (1.5%-3% via endotracheal tube). For electrical remodeling, we created complete atrioventricular block (CAVB) and myocardial infarction (MI). In 6 of the 12 dogs we also infused nerve growth factor (NGF) to the right stellate ganglion. All dogs had an implantable cardioverter-defibrillator (ICD) implanted. A second anesthesia was done 66 +/- 20 days later. In 8 of the 12 dogs (6 without NGF), pentobarbital was used as the only anesthetic. In the remaining 4 dogs (all with NGF), 3 received thiopental and 1 received isoflurane.. During the first anesthesia, none of 12 dogs had cardiac arrhythmia. During the second anesthesia, none of the 8 dogs that received pentobarbital developed ventricular fibrillation (VF). In contrast, all the dogs receiving either thiopental or isoflurane died of VF within 2 to 3 minutes. QT and P-P intervals before VF were 440 +/- 36 milliseconds and 298 +/- 28 milliseconds, longer and shorter (respectively) than those obtained the day prior to surgery (315 +/- 25 milliseconds, P < 0.001; 330 +/- 22 milliseconds, P < 0.01, respectively).. Thiopental and isoflurane are not arrhythmogenic in normal dogs and dogs with acute MI and CAVB, but are extremely proarrhythmic in dogs with chronic MI and CAVB. Consistent with the results of in vitro studies, pentobarbital did not induce ventricular arrhythmia in dogs with cardiac electrical remodeling.

Topics: Anesthetics, Inhalation; Anesthetics, Intravenous; Animals; Death, Sudden, Cardiac; Disease Models, Animal; Dog Diseases; Dogs; Heart Block; Isoflurane; Myocardial Infarction; Thiopental; Torsades de Pointes

Several investigators have demonstrated that the opioid pathway is involved in tissue preservation during hypoxia or ischemia and that this protection is mediated via the delta (delta)-opioid receptor. Subsequently, we have shown that opioid receptors are involved in ischemic preconditioning (PC) in the rat heart and that morphine produces a cardioprotective effect; however, the class of opioid receptors involved in mediating these effects is still unknown. Therefore, the purpose of the present study was to test the hypothesis that ischemia- and morphine-induced cardioprotection are mediated via stimulation of the delta-opioid receptor in the rat heart. Anesthetized, open-chest Wistar rats were subjected to one of six protocols. The control group was subjected to 30 min of occlusion and 2 h of reperfusion. Ischemic PC was elicited by three 5 min occlusion periods interspersed with 5 min of reperfusion. Morphine-induced cardioprotection was produced by three 5 min morphine infusions (100 microg/kg/infusion, i.v.) interspersed with a 5-min drug-free period. To determine if the delta-opioid receptor has a role in ischemic PC and morphine-induced cardioprotection, naltrindole (NTI), a selective delta-opioid receptor antagonist, was utilized. NTI (5 mg/kg, i.v.) was given 10 min prior to ischemic PC (NTI+PC) or morphine infusion (NTI+MOR). Also, NTI (5 mg/kg, i.v.) was given 10 min before the 30 min occlusion period in untreated rats. Infarct size (IS) as a percent of the area at risk (AAR) was determined by 2,3,5-triphenyltetrazolium chloride staining. Ischemic PC and morphine infusions resulted in similar reductions in IS/AAR from 51+/-4 to 11+/-3 and 15+/-4% (*P<0.05), respectively. NTI completely abolished the cardioprotective effect induced by ischemia and morphine. The results of the present study suggests a role of delta;-opioid receptors in ischemic PC or morphine-induced myocardial protection in the rat.

Topics: Animals; Cardiovascular Agents; Heart; Ischemic Preconditioning, Myocardial; Male; Morphine; Myocardial Infarction; Myocardium; Naltrexone; Narcotic Antagonists; Rats; Rats, Wistar; Receptors, Opioid, delta; Thiopental

We examined the effects of intravenous anesthetics (thiopental, fentanyl and morphine) on the ventricular activation in a canine myocardial infarction model. Thiopental at 5 and 10 mg/kg delayed or abolished the delayed activation in the infarcted zones with slight delay of activation of the normal zones. Fentanyl at 30 micrograms/kg slightly but significantly prolonged the activation time in both normal and infarcted zones. Morphine at 1 mg/kg did not produce any significant effect. Thiopental, but neither fentanyl nor morphine, inhibited ventricular stimulation-induced arrhythmias. Thus, thiopental, but not fentanyl nor morphine, markedly depressed the delayed activation in myocardial infarction, which may affect and probably inhibits the ventricular arrhythmias in myocardial infarction. It also should be kept in mind that thiopental may have arrhythmogenic effects in myocardial infarction.

Topics: Action Potentials; Animals; Blood Pressure; Disease Models, Animal; Dogs; Electrocardiography; Fentanyl; Heart Rate; Heart Ventricles; Infusions, Intravenous; Morphine; Myocardial Infarction; Thiopental

The effect of a single dose (10 mg/kg) of intravenous thiopental (TP), during acute myocardial infarction, on infarct size was studied in conscious dogs randomized 10 minutes after left circumflex coronary artery occlusion to either the TP group (n = 10) or a control group given 0.9% saline solution (n = 10). During the first hour following therapy, myocardial blood flow (microspheres), arterial pressure, left atrial pressure, and arterial blood gases were similar in the two groups, but the heart rate (140 +/- 3 vs 110 +/- 3 bpm; p less than 0.001) and rate-pressure product (15,090 vs 12,210 bpm X mm Hg; p less than 0.025) were greater in the TP group. Infarct size (planimetry) and occluded bed size (postmortem coronary arteriography) measured 2 days later revealed that: the slope of the relation between infarct and occluded bed mass, as a percentage of the left ventricle (% LV) was greater with TP than with saline solution (1.10 vs 0.61; p less than 0.001); excluding hearts (four TP and three saline solution) with small occluded beds (less than 22% LV), infarcts were also larger with TP (n = 6) than with saline solution (n = 7), both as a percentage of the left ventricle (26.4 vs 12.2%; p less than 0.02) or occluded bed (61.5 vs 28.9%; p less than 0.005); and transmural and endocardial extents of the infarcts on topographic maps were greater with TP than with saline solution. In 12 other conscious dogs, increasing the heart rate between 10 and 70 minutes after left circumflex coronary artery occlusion to the average rate of the TP group (140 bpm) by atrial pacing resulted in infarcts larger than those in control dogs but similar to those in the TP group. Thus, TP therapy after left circumflex occlusion increased infarct size in dogs. This effect appeared to be due mainly to the increased heart rate, probably via increased myocardial oxygen demands.

Topics: Animals; Dogs; Heart; Hemodynamics; Myocardial Infarction; Myocardium; Thiopental

Myocardial infarction was produced in dogs and cats by occlusion of the left anterior descending coronary artery. Arrhythmia was present in dogs but not in cats 6 to 48 h after occlusion. The absence of arrhythmia in cats was not due to persistent myocardial depressant effects of anaesthesia administered during surgery. Studies in cats with surgically-induced heart block revealed multiple ventricular pacemakers but no change in average ventricular rate following coronary occlusion. These results suggest that sinus overdrive, although not elevated compared with the dog, is sufficient to suppress arrhythmia in the cat. Further, since small dogs developed significantly less arrhythmia than large dogs, heart size may be an additional factor in explaining the absence of arrhythmia in the cat.

Topics: Animals; Arrhythmias, Cardiac; Atrioventricular Node; Body Weight; Cats; Disease Models, Animal; Dogs; Female; Heart; Heart Conduction System; Heart Ventricles; Male; Myocardial Infarction; Organ Size; Thiopental; Vagus Nerve

Topics: Anesthesia; Animals; Blood Pressure; Calcium; Cardiac Output; Dogs; Electrocardiography; Heart; Heart Rate; Heart Ventricles; Myocardial Infarction; Myocardium; Sarcoplasmic Reticulum; Thiopental

Topics: Adult; Anesthesia, General; Craniotomy; Diagnosis, Differential; Electrocardiography; Humans; Male; Myocardial Infarction; Subarachnoid Hemorrhage; Thiopental; Wolff-Parkinson-White Syndrome

Topics: Anesthesia, General; Angina Pectoris; Humans; Myocardial Infarction; Thiopental

Topics: Analgesia; Anesthesia; Anesthesia, General; Blood Pressure; Dihydroergotoxine; Electrocardiography; Ergot Alkaloids; Fever; Geriatrics; Heparin; Humans; Myocardial Infarction; Sodium; Theophylline; Thiopental