Milrinone improves lung compliance in patients receiving mechanical ventilation for cardiogenic pulmonary edema

BACKGROUND: Cardiogenic pulmonary edema is a frequent cause of respiratory failure. We investigated whether milrinone improved lung compliance. METHODS: We selected 10 patients with respiratory failure due to severe cardiogenic pulmonary edema to receive mechanical ventilation. Patients were administered a bolus injection of milrinone (50 microg kg-1) over 10 min, followed by continuous intravenous infusion (0.5 microg kg-1 min-1). Lung compliance, blood gas values, hemodynamic parameters, and sample plasma milrinone levels were assessed over 120 min after the onset of the continuous infusion of milrinone. RESULTS: Ten min following milrinone infusion, dynamic compliance (Cdyn) and static compliance (Cst) increased from 37 +/- 12 to 42 +/- 12 ml cmH2O-1 and from 40 +/- 13 to 45 +/- 12 ml cmH2O-1, respectively (P < 0.01). Plasma milrinone levels reached a therapeutic level for vasodilator and positive inotropic effect at 10 min after milrinone infusion. A significant decrease in mean pulmonary artery pressure and pulmonary artery wedge pressure occurred simultaneously with an increase in respiratory system compliance. However, an increase in cardiac index was observed later than these changes. There were significant correlations between the mean pulmonary artery pressure and Cdyn (r = -0.39, P < 0.01) and Cst (r = -0.38, P < 0.01). CONCLUSIONS: Milrinone-induced improvement in lung compliance along with an improvement of hemodynamics was found together with an inverse relationship between compliance and mean pulmonary artery pressure.     

Rebreathing and ventilatory response to different fresh gas flows in the Bain and Lack systems. A clinical study

Thirty-four adults were studied during halothane anaesthesia with spontaneous breathing, while undergoing orthopaedic surgery. They were randomly divided into two groups according to whether the Bain (n = 18) or the Lack (n = 16) system was used. Respiratory flows were recorded and arterial blood gases drawn at different fresh gas flows (VF). The values obtained were compared with those recorded under non-rebreathing conditions (NRC). In the Bain system the proportion of rebreathers was 0.22, 0.25, 0.55 and 0.83 when the VF was 175, 150, 125 and 100 ml X min-1 X kg-1 body weight (b.w.), respectively. In the Lack system these proportions were 0.43, 0.55 and 0.92 at VF of 85, 70 and 55 ml X min-1 kg-1 b.w., respectively. The ventilatory response to rebreathing was an increase in minute ventilation (VE), keeping the partial pressure of arterial carbon dioxide (PACO2) almost unaltered. In the Bain system the VE X kg-1 X b.w. thus increased by 18% and 38% at VF of 125 and 100 ml X min-1 X kg-1 b.w., respectively, when compared to NRC (P less than 0.05). The corresponding increases in the Lack system were 15% and 37% at VF of 70 and 55 ml X min-1 X kg-1 b.w., respectively (P less than 0.01). In the Lack group also the PACO2 increased by 6% when a VF of 55 ml X min-1 X kg-1 b.w. was used compared to the value obtained under NRC (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Extracorporeal membrane oxygenation for newborn respiratory failure

Respiratory failure is the leading cause of death in the newborn. Conventional therapy is very successful with 80% of infants weaned from ventilatory support. For neonates with severe respiratory failure, unresponsive to maximal medical therapy, extracorporeal membrane oxygenation (ECMO) offers an alternative means of management. Venoarterial bypass is achieved by cannulating the right atrium via the internal jugular vein and the aortic arch via the right common carotid artery. A 5-inch roller pump is used to circulate the blood through a 0.4 or 0.8 m2 silicone membrane lung. Management includes heparinization, intravenous alimentation, antibiotic coverage, and reduction of FiO2 and airway pressure. Thirty infants aged 12 to 186 hours were placed on ECMO. Each met strict criteria designed to predict greater than 90% mortality. Time on bypass ranged from 37 to 250 hours. Success, defined by weaning from ECMO and ventilatory support, was achieved in 23. Twenty-one remain alive; 18 have excellent outcome with normal growth and development although follow-up is short (1 to 19 mos). These results corroborate reports from the pioneers of the technique and further support the use of ECMO for neonates with respiratory failure unresponsive to conventional therapy.     

A case of hyperperfusion syndrome treated successfully by propofol

Carotid endoarterectomy was performed for a 67-year-old male with severe stenosis in the right carotid artery under propofol-fentanyl anesthesia. After the surgery, blood pressure was controlled by sodium nitroprusside to maintain at the preoperative level. On the first postoperative day, he was alert and without neurological deficit, but he became restless with the left hemiparesis appearing on the next day. ECD-SPECT revealed hyperperfusion of the right hemisphere. Propofol was administered at the dose of 3-5 mg.kg-1.h-1 to normalize the perfusion. It appears that the cerebral blood flow was normalized. Hyperperfusion after carotid endoarterectomy can be controlled by propofol.     

A case report of anesthesia for concomitant right pneumonectomy and coronary artery bypass operations

A 61-year-old man with previous myocardial infarction, was diagnosed as having lung cancer. Coronary arteriogram revealed stenoses of left anterior descending artery. We did the concomitant pulmonary and cardiac operations. Anesthesia was induced with fentanyl 1.5 mg and pancuronium 6 mg. A 37 Fr double-lumen endotracheal tube was inserted. Then a pulmonary artery catheter was inserted. The patient was given nitroglycerin for prevention of myocardial ischemia. The tumor had invaded pulmonary artery and therefore right pneumonectomy was necessary. After resection of right lung, coronary artery bypass operation was performed. On weaning from cardio-pulmonary bypass, pulmonary artery pressure increased to 48/20mmHg. Therefore he required dopamine and dobutamine each 4 micrograms.kg-1.min-1 for weaning. But we experienced no serious complications such as hypoxemia or perioperative myocardial infarction.     

Comparison of methohexital and isoflurane on neurologic outcome and histopathology following incomplete ischemia in rats

Using a rat model of incomplete cerebral ischemia the effects of isoflurane (iso) and methohexital (metho) were compared with those of 70% nitrous oxide controls (N2O). Two levels of incomplete cerebral ischemia were produced by right carotid occlusion plus hypotension for 30 min: moderate = 30 mmHg, FIO2 = 0.30; severe = 25 mmHg, FIO2 = 0.20. The iso doses (1 and 2 MAC) and metho doses (0.01 and 0.1 mg.kg-1.min-1) were tested at each ischemic level. These iso and metho doses were selected because without ischemia they produced similar decreases in cerebral oxygen consumption (CMRO2) compared with that produced in N2O controls. In the absence of ischemia, the electroencephalogram (EEG) was suppressed by 0.01 mg.kg-1.min-1 metho and 1 MAC iso and showed burst-suppression with 0.1 mg.kg-1.min-1 metho and 2 MAC iso. The EEG was further depressed by ischemia under all anesthetic conditions. Neurologic outcome was evaluated for 3 days following incomplete cerebral ischemia by using a graded deficit score (0 = normal, 5 = death associated with stroke). Following moderate ischemia all four anesthetic treatments improved outcome compared with N2O controls, but after severe ischemia only 2 MAC iso significantly improved outcome. Neurohistopathology was evaluated on a scale of 0 to 40, 24 h after ischemia. The neurohistopathology score was significantly improved by all four anesthetic treatments compared with N2O following moderate ischemia and was better with 2 MAC iso compared with 0.1 mg.kg-1.min-1 metho after both moderate and severe ischemia. These results show that both iso and metho improve outcome from cerebral ischemia compared with that associated with N2O, but only 2 MAC iso resulted in an improved outcome following severe ischemia. This difference in outcome between the two anesthetics may be related to greater neuronal depression with iso, which may occur with little difference in cerebral metabolic depression.     

Myocardial ischemia during vasodilator therapy in a canine model of pulmonary hypertension and coronary insufficiency.

Pulmonary vasodilator therapy during increased right ventricular (RV) afterload and insufficient RV myocardial perfusion might further impair RV performance by lowering systemic and, thus, coronary perfusion pressure. This hypothesis was tested by initially inducing pulmonary hypertension (80% increase in resting pulmonary artery pressure by injection of autologous muscle) and subsequent right coronary artery stenosis (40% decrease in flow by external cuff occlusion) in eight open-chest dogs. Then the effects of nitroglycerin (5 micrograms.kg-1.min-1), prostaglandin E1 (0.2 microgram.kg-1.min-1), and hydralazine (mean 0.14 mg/kg) on global and regional (ultrasonic dimension technique) RV performance and coronary hemodynamics (electromagnetic flow probes) were determined. Following all three drugs, right coronary artery flow decreased by 40-65% (mean values) accompanied by severe regional myocardial dysfunction suggestive of ischemia (akinesis, systolic lengthening, and postsystolic shortening). Heart rates increased by 20-40%; aortic pressure decreased by 15-25%; and RV end-diastolic pressure remained unchanged. Despite similarly adverse effects on regional RV performance and comparable effects on heart rate, perfusion and filling pressures with all three drugs, RV systolic pressure, RV dP/dt, and pulmonary artery pressure during nitroglycerin and prostaglandin E1 remained unchanged, and stroke volume and pulmonary artery flow decreased, but they all increased or were maintained (stroke volume) during hydralazine. Gas exchange was not affected by any of the vasodilators. Thus, in this model of combined acute pulmonary hypertension and right coronary artery insufficiency, nitroglycerin, prostaglandin E1, and hydralazine elicited severe regional dysfunction suggestive of ischemia, probably related to concomitant increases in heart rate and decreases in coronary perfusion pressure. Despite such evidence of severe regional RV ischemia, hydralazine maintained global RV pump function. These results indicate 1) that in the presence of increased RV afterload and coronary insufficiency, reduction in coronary perfusion pressure during pulmonary vasodilator therapy may be deleterious, and 2) that even severe regional myocardial ischemia may not necessarily be accompanied by respective changes in global hemodynamics and thus may go undetected.     

Experimental Results Using Nafamostat Mesilate as Anticoagulant During Extracorporeal Lung Assist for 24 Hours in Dogs

Abstract: We report on the experimental application of nafamostat mesilate (NM, 6-amidino-2-naphthyl p -guanidinobenzoate dimethanesulfonate, FUT®), a new anticoagulant, to extracorporeal lung assist (ECLA) with an artificial membrane lung. Venovenous ECLA, from the jugular vein to the femoral vein, was performed with a hollow-fiber membrane lung at a blood flow rate of approximate 82 ml kg^-1 min^-1 for 24 h in 7 dogs under anesthesia and hypoventilation. Heparin (10 U ml^-1 in a priming lactated Ringer solution of 140 ml, and 200 U kg^-1) was administered before blood access cannulation. After start of ECLA, however, no heparin was used, and nafamostat mesilate was continuously infused into the drainage line of the bypass circuit to control activated coagulation time (ACT) at about 150 to 200s. To maintain the prolonged ACT, 8:0 ± 1.7 mg kg^-1 h^-1 of NM was required. Arterial blood pressure and pulse rate decreased significantly. Though fibrin monomer test revealed hypercoagulability after 6 h of ECLA, platelet counts did not significantly decrease. Total blood loss remained less than 40 g. The artificial membrane lung sustained a good gas exchange and low flow resistance throughout ECLA. Macroscopic examination revealed small spotty thrombi in the artificial lung but no major pathologic changes of the visceral organs in the all dogs at autopsy. High-dose NM administration could control blood coagulation and decrease blood loss during ECLA for 24 h without deterioration of the artificial lung and systemic complication other than mild hypotension and bradycardia.     

Trachea-innominate artery fistula: successful management of 3 consecutive patients.

Trachea-innominate artery fistula is an uncommon but frequently fatal complication of tracheostomy. Three successive patients who developed this complication while receiving ventilatory assistance through a tracheostomy tube were successfully managed, with long-term survival. Bleeding was controlled by direct digital pressure on the innominate artery or by hyperinflation of the balloon cuff of the tracheostomy tube. In 2 patients, replacement of the tracheostomy tube with an orotracheal tube improved direct access to the innominate artery for digital compression. Late follow-up examination of the right carotid circulation revealed complete reversal of flow in the right internal and common carotid arteries in the 2 patients studied.     

Coronary artery spasm during vascular surgery

A 56-year-old male with arteriosclerosis obliterans was scheduled for aorto-biiliac artery bypass graft surgery. He had episodes of chest pain lasting for several minutes. Preoperative electrocardiogram (ECG) and myocardiac scintigram showed no abnormal findings. Anesthesia was induced with thiopental 225 mg, fentanyl 100 micrograms and tracheal intubation was facilitated with vecuronium 10 mg. Anesthesia was maintained with O2 2 l.min-1, N2O 4 l.min-1, sevoflurane 0.5-1% and epidural injection of 1% mepivacaine 6-10 ml.hr-1. Nitroglycerin was infused at a rate of 0.125 microgram.kg-1.min-1. During surgery, a transient elevation of the ST segment occurred three times in lead II of the ECG. For the first episode with decrease in blood pressure at declamping the external iliac artery, administration of phenyrephrine 100 micrograms improved ST segment elevation in ECG. For the second event with a slight decrease in blood pressure, an increased dose of nitroglycerin decreased ST segment elevation. The third incident with increased blood pressure and heart rate was alleviated by decreasing the dose of dopamine. Postoperative ECG and serum creatine kinase level were within normal limits. These three episodes of ST segment elevation might be due to coronary spasms induced by decreased blood pressure or increased blood pressure and heart rate.     

Treatment of Pulmonary Hypertension and Hypoxia Due to Oleic Acid Induced Lung Injury with Intratracheal Prostaglandin E1 during Partial Liquid Ventilation

Background: Partial liquid ventilation using perfluorocarbon liquids may be of therapeutic benefit in patients with acute respiratory failure. This study investigated the effects of prostaglandin E1 (PGE1) delivered intratracheally during partial liquid ventilation on lung function and pulmonary circulation in rabbits with acute respiratory distress syndrome.

Methods: Lung injury was induced by intravenous oleic acid in adult Japanese white rabbits, 1 h after which they were divided into four groups of 10 animals. Group 1 received mechanical ventilation alone, group 2 received aerosolized PGE1 (5 [micro sign]g followed by 0.1 [micro sign]g [middle dot] kg-1 [middle dot] min-1) under mechanical ventilation combined with 5 cm H2 O positive end-expiratory pressure, and groups 3 and 4 received partial liquid ventilation with 15 ml/kg perflubron. Group 4 received a 5-[micro sign]g bolus followed by 0.1 [micro sign]g [middle dot] kg-1 [middle dot] min-1 PGE1 instilled intratracheally (not by aerosol) in combination with partial liquid ventilation. Measurements were performed at 30-min intervals for 120 min after lung injury.

Results: After lung injury, hypoxemia, hypercapnia, acidosis, and pulmonary hypertension developed in all animals and were sustained in groups 1 and 2 throughout the experiment. The partial pressure of oxygen in arterial blood of animals in group 3 improved with initiation of treatment, with statistical significance achieved at the 30 and 60 min time points as compared with controls. Group 4 animals had immediate and sustained increases in the partial pressure of oxygen in arterial blood that were significant compared with all other groups during the experiment. Statistically significant reductions in mean pulmonary artery pressure were seen only in group 4 animals compared with all other groups.     

Traumatic infarction of the right ventricle caused by coronary dissection

A case is reported of a 47 year-old man who suffered from a right ventricular myocardial infarct which occurred as a result of right coronary arterial dissection after non-penetrating anteroposterior chest compression. The patient was admitted with right heart failure and a central venous pressure of 17 cm H2O. The ST segment in leads V1 to V3 (V2: 7mm) was significantly elevated. Echocardiography showed dilatation of both right atrium and ventricle, with a deviated septum. Emergency cardiac angiography confirmed a hypokinetic right ventricle, with no other abnormal finding. Coronary angiography, performed 24 h after admission, revealed a dissection of the second part of the right coronary artery, with a normal left coronary system which reperfused that part of the right coronary arterial territory located beyond the dissection. The ST segment elevation stopped at the 10th hour. Initially, the patient's condition worsened. Thereafter, he slowly improved under treatment (5.5 micrograms.kg-1.min-1 dobutamine, and fluids so as to maintain a pulmonary wedged pressure of about 15 mmHg). As post-traumatic myocardial infarction is rare, the diagnostic and therapeutic strategies are discussed.     

Effects of dopamine on the portal circulation after therapeutic hepatic artery ligation

The effects of exogenous dopamine (2, 4 and 6 micrograms.kg-1.min-1 i.v.) on the portal circulation were studied in six patients following therapeutic hepatic artery ligation. Portal blood flow (PBF) was measured by the continuous thermodilution technique. Portal venous pressure (PVP, n = 3) was monitored through the thermodilution catheter to allow derivation of preportal vascular resistance (PVR). Blood samples were taken through the portal venous catheter for measurement of dopamine. A significant increase in PBF and a decrease in PVR were observed during graded i.v. dopamine infusion. Thus, PBF was 961 +/- 119 ml.min-1 during control conditions and increased to 1446 +/- 221 ml.min-1 during the dopamine infusion at 6 micrograms.kg-1.min-1. No significant changes in mean arterial pressure or PVP were observed during dopamine administration. The pharmacokinetics of dopamine did not differ from that previously reported in patients with an intact arterial supply. In conclusion, our data indicate that exogenous dopamine consistently increases PBF by preportal vasodilation, also in patients with a surgically restricted hepatic arterial blood supply.     

Prostaglandin F2 alpha improves oxygen tension and reduces venous admixture during one-lung ventilation in anesthetized paralyzed dogs

The authors investigated the effect of prostaglandin F2 alpha infused into the pulmonary artery of an acutely atelectatic lung in dogs. Seven dogs were anesthetized with piritramid and pentobarbital and intubated with a Kottmeier canine endobronchial tube. Cardiac output, pulmonary arterial, capillary wedge, and systemic arterial pressure were measured via indwelling catheters. Ventilating both lungs with 66% O2, PaO2 was 327 +/- 15 mmHg (mean +/- SD) and venous admixture (Qsp/Qt) was 11 +/- 3%. One-lung atelectasis reduced PaO2 to 91 +/- 12 mmHg and increased Qsp/Qt to 40 +/- 4%. Prostaglandin F2 alpha in doses of 0.4, 0.6, 1.2, and 1.8 micrograms X kg-1 X min-1 was infused into the pulmonary artery of the atelectatic lung through a second pulmonary artery catheter. Up to a dose of 1.2 micrograms X kg-1 X min-1 there was a dose-dependent reduction in Qsp/Qt to a minimum of 25 +/- 4% and an increase in PaO2 to 168 +/- 25 mmHg, which could be explained by enhanced pulmonary vasoconstriction in the atelectatic lung with increased blood flow diversion toward the ventilated lung. Infusion of 1.8 micrograms X kg-1 X min-1 decreased PaO2 to 156 +/- 32 mmHg and increased Qsp/Qt to 32 +/- 9%. Increased systemic effects of prostaglandin F2 alpha were observed and presumably were related to saturation of prostaglandin-dehydrogenase leading to vasoconstriction in both lungs and thus reduced blood flow diversion toward the ventilated lung.     

Changes in platelets and blood coagulation during prolonged ECLA with a heparin bonded hollow fiber membrane lung

Effects of the heparin bonded artificial membrane lung and circuit on blood coagulation were investigated during prolonged extracorporeal lung assist on goats. A veno-venous bypass ECLA was performed on 18 goats up to 10 days. Twelve of them (Group I) were with a heparin bonded device and the other six (Group II) were with the usual device. In Group I, heparin was continuously infused at a rate of 15.2 units.kg-1.hr-1 to maintain the activated coagulation time, ACT, at around 130 sec., while in Group II, 25.5 units.kg-1.hr-1 of heparin was necessary to maintain ACT at about 200 sec. to prevent blood coagulation in the bypass circuit. Platelets decreased significantly in Group I (by 50% of pre ECLA value) as well as in Group II, but aggregation activity in Group I was higher than in Group II. Fibrinopeptide A and antithrombin III showed no significant difference between the two groups. Autopsy showed no significant pathological findings. ECLA, with a heparin bonded surface, showed excellent blood compatibility and required only a little systemic administration of heparin. The heparin bonded bypass circuit will enable safer ECLA even in patients with some bleeding sites.     

Improvement of ischemic symptoms and cerebral blood flow after percutaneous transluminal angioplasty for renovascular hypertension. Report of a case with multiple cerebrovascular occlusive disease]

A 53-year-old male complained of frequent left motor-sensory transient ischemic attack for 4 months. On admission, he demonstrated mild right hemiparesis, dysarthria, and right hemisensory disturbance of all modalities. Cerebral angiography demonstrated complete occlusion of the left internal carotid artery just above the origin of the ophthalmic artery and a stenotic lesion at the horizontal segment of the right middle cerebral artery. Renal angiography showed severe stenosis of the right renal artery. Systolic blood pressure was over 200 mmHg and marked circadian variation of blood pressure was noted. Serum renin was 4.0 ng/ml/hr. Four months after superficial temporal artery-middle cerebral artery anastomosis, left carotid angiography showed good patency of the bypass and the ischemic symptoms completely disappeared. Single photon emission computed tomography (SPECT) showed increased cerebral blood flow (CBF), especially in the left hemisphere after surgery. Six months after the bypass surgery, he complained of mild right hemiparesis again. Shortly after percutaneous transluminal angioplasty (PTA) for renal arterial stenosis, his hemiparesis was improved and the systolic blood pressure stabilized to 150-170 mmHg. SPECT showed the CBF had also recovered in both hemispheres. The improvement in ischemic symptoms and increased CBF after PTA were probably related to stabilization of the systemic blood pressure or inhibition of serum renin-angiotensin.     

Arterial air embolism of venous origin in dogs: effect of nitrous oxide in combination with halothane and pentobarbitone

The effects of using nitrous oxide (N2O) with halothane or pentobarbitone anaesthesia on the filtration of venous air emboli (VAE) by the pulmonary circulation were studied in dogs. Dogs anaesthetized with either pentobarbitone, pentobarbitone/N2O, halothane, or halothane/N2O were embolized with venous air into the right atrium at 0.25 to 0.35 ml.kg-1.min-1 for 30 min. The animals were in a supine, head down position. A Doppler ultrasonic probe located over the suprarenal aorta detected arterial bubbles that escaped filtration by the lungs. No bubbles were detected at 0.25 ml.kg-1.min-1, but at 0.30 ml.kg-1.min-1 the incidence was 11 per cent (pentobarbitone), 0 per cent (pentobarbitone/N2O), 33 per cent (halothane), and 63 per cent (halothane/N2O) and at 0.35 ml.kg-1.min-1, 44 per cent (pentobarbitone), 14 per cent (pentobarbitone/N2O), and 56 per cent (halothane). Half of the dogs receiving VAE with halothane/N2O at 0.30 ml.kg-1.min-1 died within the first 10 min of the air infusion. Thus, no animals were studied at the next higher dose (0.35 ml.kg-1.min-1). The results suggest that the occurrence of VAE with nitrous oxide anaesthesia may result in greater haemodynamic consequence and increased likelihood for spillover of the venous bubbles into the arteries if used with halothane as compared to pentobarbitone.     

Ventilatory response to CO2 following intravenous ketamine in children

The effects of intravenous ketamine (bolus of 2 mg.kg-1 followed by a continuous infusion at a rate of 40 micrograms.kg-1.min-1) on ventilatory response to carbon dioxide were studied in nine children ranging in age from 6 to 10 yr and in weight from 20 to 48 kg. Ketamine did not affect resting respiratory rate, tidal volume, end-tidal CO2 tension (PETCO2), or minute ventilation. Five minutes after the ketamine bolus, the slope VE/PETCO2 decreased significantly (P less than 0.05) from 1.71 +/- 0.47 to 1.05 +/- 0.23 1.min-1.mmHg-1 (mean +/- SD). After 30 min of continuous iv ketamine infusion, the slope returned to 1.65 +/- 0.44 1.min-1.mmHg-1, a significantly higher value (P less than 0.05) compared with the nadir and not significantly different from control. The minute ventilation at a PETCO2 of 60 mmHg decreased from 824 +/- 98 to 626 +/- 26 ml.kg-1.min-1 5 min after iv ketamine, and remained depressed (640 +/- 125 ml.kg-1.min-1 P less than 0.05) throughout the 30-min ketamine infusion. In addition, the slope VT/PETCO2 and the VT 60 did not change during the study; nonetheless, the slope f/PETCO2 and the f 60 decreased significantly following iv bolus ketamine, and the f 60 remained significantly decreased following ketamine infusion. The authors conclude that clinically useful doses of iv ketamine significantly alter ventilatory control in children.     

The effect of etomidate pretreatment on cerebral high energy metabolites, lactate, and glucose during severe hypoxia in the rat

Etomidate was compared with thiopental with respect to preventing loss of brain high energy metabolites and accumulation of lactate during 20 min of hypoxemia (Pa2 of 16-19 mmHg) in rats with unilateral carotid artery ligation. Male Sprague-Dawley rats, anesthetized with halothane and nitrous oxide (N2O) in oxygen were randomly assigned to one of six groups. A normoxic control group which received 70% N2O in oxygen, a hypoxia group received no iv drug treatment (hypoxia-N2O), and four iv drug treatment groups (N2O was replaced by 70% nitrogen at the start of drug administration). The iv drug groups were treated as follows: hypoxia-etomidate low dose (1 mg.kg-1 iv followed by an infusion at 0.35 mg.kg-1.min-1); hypoxia-etomidate high dose (1 mg.kg-1 then 1.3 mg.kg-1.min-1); hypoxia-thiopental low dose (15 mg.kg-1, then 1.5 mg.kg-1.min-1); and hypoxia-thiopental high dose (15 mg.kg-1, then 5 mg.kg-1.min-1). After hypoxia or a corresponding period in the normoxic group, the brains were frozen in situ for later biochemical analysis. Blood was obtained prior to and at the end of hypoxia and analyzed for glucose. Brain metabolite concentrations on the side ipsilateral to the ligated carotid artery in the normoxia-N2O group were adenosine triphosphate (ATP), 2.76 +/- 0.1, phosphocreatione (PCr) 3.88 +/- 0.12, lactate 2.34 +/- 0.16, and glucose 3.56 +/- 0.28 (mumole.g-1 wet weight, mean +/- SE). There was no significant decrease in ATP in any of the hypoxia groups. PCr decreased by 45% (compared to normoxia-N2O) in the hypoxia-N2O group.(ABSTRACT TRUNCATED AT 250 WORDS)     

Sufentanil does not block sympathetic responses to surgical stimuli in patients having coronary artery revascularization surgery

The effects of a moderate dose of sufentanil (1 microgram.kg-1 + 0.015 micrograms.kg-1.min-1) plus nitrous oxide (30% O2/70% N2O) anesthesia (group I; n = 8) and of high-dose sufentanil/O2 anesthesia (10 micrograms.kg-1 + 0.15 micrograms.kg-1.min-1) without N2O (group II; n = 8) on cardiovascular dynamics, myocardial blood flow, myocardial oxygen consumption, myocardial lactate balance, and hypoxanthine release were studied in two groups of male patients scheduled for elective coronary artery bypass surgery. All patients were on maintenance doses of calcium channel blockers and nitrates with the last doses of medications given the morning of operation. All patients were premedicated with flunitrazepam (2 mg orally), piritramide (7.5 mg IM) and promethazine (25 mg IM). Measurements were performed before the induction of anesthesia with the patients premedicated but awake; 20 min after induction of anesthesia with sufentanil plus pancuronium 0.1 mg.kg-1 for muscle relaxation before surgery; and during sternotomy and sternal spread. Sufentanil at either dose decreased mean arterial pressure, as well as cardiac and stroke volume index while heart rate remained unchanged. Following the induction myocardial blood flow and myocardial oxygen consumption decreased 23% (79 ml.min-1.100 g-1 to 61 ml.min-1.100 g-1 and 28% (9.2 ml O2.min-1.100 g-1 to 6.6 ml O2.min-1.100 g-1) in group I and 14% (78 ml.min-1.100 g-1 to 67 ml.min-1.100 g-1 and 18% (8.7 ml O2.min-1.100 g-1 to 7.1 ml O2.min-1.100 g-1) in group II. Myocardial ischemia was seen in one patient of group II (patient No. 4), as indicated by a hypoxanthine release into the coronary sinus, when after the induction MAP decreased from 93 to 67 mm Hg and heart rate increased from 56 to 71 min-1. During sternotomy 8 of 16 patients (50%) developed hypertension and 9 of 16 patients (56%) showed signs of myocardial ischemia, i.e., a lactate and hypoxanthine release.(ABSTRACT TRUNCATED AT 250 WORDS)