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S E Ricksten

Publications and source records attributed to S E Ricksten.

At least 55 records · Page 3Linked to original sources
PubMed1993

Six-hour preservation of the isolated working rat heart improved with University of Wisconsin solution.

University of Wisconsin (UW) solution was compared with modified St. Thomas cardioplegic solution for 6-hour preservation of isolated working rat hearts. The hearts (9 in each group) were arrested with the respective solution and stored, still cannulated, for 6 hours at 4 degrees C. After retrograde reperfusion for 30 minutes, antegrade perfusion was begun at constant left atrial and aortic pressures. Following 25 minutes of antegrade perfusion the hemodynamic recovery of the UW-preserved hearts was superior to that of the other hearts (cardiac output 46.0 +/- 4.8% of the preischemic control values in the UW group and 10.0 +/- 6.0% in the St. Thomas group, p < 0.01). The adenosine triphosphate content was significantly higher in the UW-preserved hearts (18.8 +/- 0.9 vs. 14.7 +/- 1.6 mumol/g dry weight, p < 0.05). No significant intergroup difference was found in aspartate aminotransferase leak or tissue glycogen. The study demonstrated both better function and enhancement of high-energy phosphates with UW solution vs. modified St. Thomas solution in isolated rat hearts, although without difference in enzyme leakage or tissue glycogen, after 6-hour preservation.

Adenosine↗
PubMed1993

Effects of adenosine on renal function and central hemodynamics after coronary artery bypass surgery.

In the early postoperative period after coronary artery bypass surgery, arterial hypertension commonly occurs which requires intravenous vasodilator therapy. Purine adenosine is a potent vasodilator and when exogenously administered it decreases systemic arterial blood pressure effectively. We evaluated the effects of adenosine on central hemodynamics and renal function when used to control postoperative hypertension after coronary artery bypass grafting (CABG). Two separate series of experiments were performed postoperatively in the Intensive Care Unit (ICU). In the first study (n = 10), postoperative hypertension was controlled in the rewarming phase, with sodium nitroprusside (SNP, 1.7 +/- 0.4 micrograms.kg-1 x min-1) or adenosine (147.2 +/- 38.9 micrograms.kg-1 x min-1) to keep mean arterial systolic pressure at approximately 80 mm Hg. In the second study on a separate group of patients (n = 9), low doses of adenosine (0, 30, 60, 90, and 0 micrograms.kg-1 x min-1) were infused when the patients were normotensive and rewarmed. Central hemodynamics, urine flow (UF), renal blood flow (RBF), glomerular filtration rate (GFR), and ECG were evaluated during periods of 30 min for each drug in the first study and during each dose of adenosine in the second study. RBF and GFR were determined using standard urinary clearance methods for 51Cr-ethylenediaminetetraacetic acid and p-aminohippuric acid. In the first study, adenosine infusion, compared to SNP, decreased (A - V)O2, increased central filling pressures and heart rate, and caused a more pronounced ST segment depression. During adenosine administration RBF (-44%), GFR (-52%), and UF (-76%) decreased, while renal vascular resistance and filtration fraction (FF) were unaltered compared to data obtained during SNP infusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed1993

Vasodilation with adenosine or sodium nitroprusside after coronary artery bypass surgery: a comparative study on myocardial blood flow and metabolism.

The effects of adenosine and sodium nitroprusside (SNP) on central hemodynamics and myocardial blood flow and metabolism were investigated postoperatively after elective coronary artery bypass (CABG) surgery in ten sedated and mechanically ventilated patients in the intensive care unit. During three consecutive 15-min periods, SNP (0.8 +/- 0.1 micrograms.kg-1 x min-1), adenosine (88.9 +/- 13.3 micrograms.kg-1 x min-1), and then again SNP (0.7 +/- 0.1 micrograms.kg-1 x min-1) were infused to control postoperative hypertension at a mean arterial pressure of approximately 80 mm Hg. Systemic and pulmonary hemodynamics and global (coronary sinus flow, CSF) as well as regional (great cardiac vein flow, GCVF) myocardial blood flow and metabolic variables were measured. During adenosine infusion, in comparison to SNP, heart rate was unchanged, stroke volume index and cardiac index increased (24% and 32%, respectively), and the systemic vascular resistance index decreased (-26%). Mean pulmonary arterial pressure (24%) as well as pulmonary capillary wedge pressure (27%) and central venous pressure (18%) were higher with adenosine compared to SNP. Adenosine also increased CSF and GCVF (108% and 103%, respectively) without altering the CSF/GCVF flow ratio compared to SNP. Furthermore, adenosine increased the coronary oxygen content (51%) and decreased the arterio-great cardiac vein oxygen content difference (-48%) without changing regional myocardial oxygen consumption, indicating a more pronounced hyperkinetic myocardial circulation compared to SNP. In addition, adenosine infusion decreased arterial PO2 (-11%) and increased the intrapulmonary shunt fraction (57%). The PR interval time of the electrocardiogram was prolonged (12%) and the ST segment was more depressed during adenosine infusion compared to SNP.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed1992

Myocardial circulatory and metabolic effects of halothane when used to control intraoperative hypertension in patients with coronary artery disease.

The effect of halothane on regional myocardial metabolism and blood flow, when used as an adjunct to fentanyl-nitrous oxide anaesthesia, to treat intraoperative hypertension was investigated. Fifteen patients with two- or three-vessel coronary artery disease with an ejection-fraction greater than 0.5 and on beta-blockers up to the morning of surgery were studied during elective coronary artery by-pass grafting. Systemic and pulmonary haemodynamics, global (coronary sinus, CSF) and regional (great cardiac vein, GCVF) myocardial blood flow were measured. Measurements were made: 1) after induction of anaesthesia but prior to skin incision, 2) during sternotomy, and 3) during halothane administration after its use to reduce arterial pressure to the pre-sternotomy level. The increase in systemic arterial pressure during sternotomy was due to an increase in systemic vascular resistance index (SVRI), and was accompanied by an increase in pulmonary capillary wedge pressure (PCWP), regional myocardial oxygen consumption and extraction, GCFV and CSF. Halothane reduced arterial blood pressure to pre-sternotomy levels within 7.1 +/- 0.6 min at an end-tidal concentration of 0.96 +/- 0.11%. Halothane caused a decrease in SVRI, total coronary vascular resistance, regional myocardial oxygen consumption and extraction, while cardiac index, heart rate and GCVF/CSF ratio remained unchanged. Mean regional myocardial lactate extraction was not affected by sternotomy or halothane. During halothane administration one patient developed regional myocardial lactate production which was not present during sternotomy. However, another two patients, who had regional myocardial lactate production during sternotomy, did not produce lactate or had less negative value of regional myocardial lactate extraction during halothane administration.

Aged↗
PubMed1992

Effects of surgical stress and volatile anesthetics on left ventricular global and regional function in patients with coronary artery disease. Evaluation by computer-assisted two-dimensional quantitative transesophageal echocardiography.

We investigated the effects of halothane, enflurane, and isoflurane on central hemodynamics and left ventricular global and regional function when used to control intraoperative hypertension in 39 patients with coronary artery disease. Left ventricular short-axis, midpapillary images were obtained by transesophageal echocardiography. Using a centerline algorithm, we analyzed left ventricular images for global area ejection fraction (GAEF) and segmental area ejection fraction (SAEF). The SAEF/GAEF ratio was calculated for each of eight segments. Measurements were performed after induction of anesthesia but before skin incision; 1 min after sternotomy; and during administration of the inhaled anesthetic. The increase in arterial blood pressure during sternotomy was due to an increase in vascular resistance accompanied by increases in heart rate and filling pressures while GAEF decreased. No changes in the SAEF/GAEF ratio appeared during sternotomy. The inhaled anesthetics restored arterial blood pressure by a similar decrease in vascular resistance. Isoflurane caused an increase in cardiac index that was not seen with halothane or enflurane (halothane vs isoflurane, P < 0.05). The GAEF was decreased by halothane but unaffected by isoflurane and enflurane (halothane vs enflurane; P < 0.05). Isoflurane induced a decrease in the SAEF/GAEF ratios of two segments corresponding to the inferolateral wall of the left ventricle that was, in one of these segments, significantly more pronounced compared with both halothane and enflurane. Halothane or enflurane did not cause any change in regional wall motion. We conclude that isoflurane is more likely to cause regional wall motion changes than halothane or enflurane in patients with coronary artery disease.

Adult↗
PubMed1991

Effects of adenosine on myocardial blood flow and metabolism after coronary artery bypass surgery.

The effects of adenosine on myocardial blood flow and metabolism, central hemodynamics, and the intrapulmonary shunt fraction were investigated. Fourteen patients with two- or three-vessel coronary artery disease and with an ejection fraction greater than 0.5 were studied in the operating room following sternal closure after elective coronary artery bypass grafting. Systemic and pulmonary hemodynamics and global (coronary sinus), as well as regional myocardial blood flow (great cardiac vein flow), and metabolic variables were measured. Adenosine was given in infusion rates of 15, 30, 60, and 120 micrograms.kg-1.min-1. Infusion rates of 60 and 120 micrograms.kg-1.min-1 decreased mean arterial blood pressure (11% and 16%, respectively), systemic vascular resistance index (30% and 43%), and pulmonary vascular resistance index (24% and 31%), increased cardiac index (25% and 45%), heart rate (14% and 15%), and stroke volume index (9% and 25%), and had no effect on central filling pressures. These infusion rates doubled the intrapulmonary shunt fraction and decreased arterial O2 tension by 26%. Great cardiac vein flow and coronary sinus flow increased 60% with adenosine infusion of 30-60 micrograms.kg-1.min-1 and 120% with 120 micrograms.kg-1.min-1. The ratio of great cardiac vein flow to coronary sinus flow, regional myocardial oxygen consumption, and mean regional lactate extraction and uptake were not significantly altered by adenosine. Adenosine caused a significant depression of the ST segment at infusion rates of 60 and 120 micrograms.kg-1.min-1.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed1990

Effects of thoracic epidural anesthesia on coronary arteries and arterioles in patients with coronary artery disease.

The effect of cardiac sympathetic blockade by high thoracic epidural anesthesia (TEA) (T1-T6, bupivacaine) on the luminal diameter of normal and diseased portions of epicardial coronary arteries was determined by quantitative coronary angiography in patients (n = 27) with severe coronary artery disease (CAD). In a separate group of patients (n = 9) with severe CAD, the effects of TEA on coronary arterioles (resistance vessels) were studied, by measuring total and regional myocardial blood flow and metabolism with the retrograde coronary sinus thermodilution technique. At the stenotic segments, TEA induced an increase in luminal diameter from 1.34 +/- 0.11 to 1.56 +/- 0.13 mm (P less than 0.002), but did not change the diameter of the nonstenotic segments (3.07 +/- 0.13 to 2.99 +/- 0.13 mm). In the second group of patients, TEA induced no changes in coronary perfusion pressure, total or regional myocardial blood flow, coronary venous oxygen content, coronary blood flow distribution, regional myocardial oxygen consumption, or lactate extraction or uptake. Two patients had chest pain in the control situation and had regional myocardial lactate production that was attenuated by TEA. We conclude that TEA may increase the diameter of stenotic epicardial coronary artery segments in patients with CAD without causing a dilation of coronary arterioles. These effects may be beneficial when high TEA is used to treat severe ischemic chest pain in patients at rest.

Aged↗
PubMed1990

Effects of thoracic epidural anaesthesia on central haemodynamics compared to cardiac beta adrenoceptor blockade in conscious rats with acute myocardial infarction.

The study aimed to compare the effects of thoracic epidural anaesthesia (TEA) with those of the beta-adrenoceptor blocker, metoprolol, on central haemodynamics in conscious rats with acute myocardial infarction. During methohexital anaesthesia, appropriate vascular catheters were inserted, a thoracic epidural catheter was implanted and the left coronary artery was ligated. A recovery period of 1-2 h elapsed after termination of surgery and anaesthesia. Experiments were performed on four separate groups of animals (A-D). In Group A (n = 10) mean arterial pressure (MAP), heart rate (HR), and cardiac output (CO) were measured, and stroke volume (SV) and systemic vascular resistance (SVR) were calculated before and 10-15 min after the induction of TEA (bupivacaine 5 mg.ml-1). In Group B (n = 6) left ventricular end-diastolic pressure (LVEDP) and maximal dP/dt were recorded as in Group A. In Group C (n = 10) central haemodynamics were measured 10 min after i.v. metoprolol (0.5 mg.kg-1) and again 10-15 min after the addition of TEA. In Group D (n = 6) LVEDP and max dP/dt were measured as in Group C. The reduction in CO, SV, HR and max dP/dt was of the same magnitude with TEA and metoprolol. TEA lowered MAP by 17%, while metoprolol did not change MAP. Metoprolol caused an increase in LVEDP from 20.8 +/- 1.8 to 27.5 +/- 2.7 mmHg (2.8 +/- 0.2 to 3.7 +/- 0.4 kPa) (P less than 0.01), while TEA induced a decrease in LVEDP from 24.2 +/- 1.4 to 17.8 +/- 1.6 mmHg (3.2 +/- 0.2 to 2.4 +/- 0.2 kPa) (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Epidural↗
PubMed1990

Thoracic epidural anesthesia improves global and regional left ventricular function during stress-induced myocardial ischemia in patients with coronary artery disease.

The aim of the present investigation was to study the effects of high thoracic epidural anesthesia (TEA), including the cardiac sympathetic segments, on ischemic ST-segment changes and left ventricular global and regional wall motion abnormalities. Ten patients with a two- or three-vessel coronary artery disease, all treated with the beta-adrenergic blocker metoprolol because of severe stable angina pectoris, performed two identical exercise stress tests, the first without TEA (control exercise) and the second with TEA (TEA exercise). Before each stress test, intravenous metoprolol was given to achieve maximal or near maximal beta-adrenoceptor blockade. Systolic and diastolic arterial pressures (radial artery cannula), heart rate, and rate-pressure product, as well as global and regional ejection fractions, using equilibrium radionuclide angiography in the left anterior oblique projection, were measured at rest and during maximal exercise. ST-segment analysis (V3 or V5) was performed, and the regional wall motion score was calculated at control exercise and TEA exercise. Intravenous metoprolol or intravenous metoprolol plus TEA at rest did not cause any significant changes of any of the variables. During TEA exercise, systolic arterial pressure, diastolic arterial pressure, and rate-pressure product, but not heart rate, were significantly lower compared to control exercise. The global and anterolateral ejection fractions were significantly higher (52.8% versus 46.5% and 53.2% versus 46.0%, respectively, P less than 0.05), and the regional wall motion score was significantly lower (8.8 versus 11.8, P less than 0.01) during TEA exercise than during control exercise. ST-segment depression was significantly lower during TEA exercise (-1.03 versus -1.84 mV, P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1990

Regional changes in sympathetic nerve activity and baroreceptor reflex function and arterial plasma levels of catecholamines, renin and vasopressin during naloxone-precipitated morphine withdrawal in rats.

The aim of the study was to examine regional changes in sympathetic nerve activity (SNA) and baroreceptor function and arterial plasma catecholamines, arginine vasopressin (AVP) and plasma renin activity during morphine withdrawal in chloralose-anesthetized rats. Dependence was induced by s.c. morphine base pellets. Adrenal, renal and splanchnic SNA and SNA from the lumbar sympathetic chain were recorded before and after i.v. injections of naloxone. Baroreceptor function was examined with phenylephrine-induced increases in mean arterial pressure. In separate experiments, arterial plasma norepinephrine, epinephrine, dopamine, plasma renin activity and AVP were measured before and after naloxone-precipitated withdrawal. Naloxone administration elicited an increase in mean arterial pressure and heart rate. Although renal SNA was inhibited by approximately 50%, adrenal SNA and lumbar SNA increased by approximately 400 and 80%, respectively. Splanchnic SNA did not change significantly. The baroreceptor-mediated inhibition of adrenal SNA was facilitated while that for renal SNA was attenuated. The arterial plasma level of norepinephrine was doubled and epinephrine increased almost 20-fold. AVP increased about 15-fold, whereas plasma renin activity showed only a minor increase after naloxone. This study shows that a marked differentiation of the SNA response occurs during morphine withdrawal in rats, which suggests an interaction between opioid receptors and the control of regional sympathetic output. Furthermore, large amounts of AVP and epinephrine are released, which probably contribute to the cardiovascular changes seen in the withdrawal phase.

Animals↗
PubMed1990

Controlled hypotension with adenosine or sodium nitroprusside during cerebral aneurysm surgery: effects on renal hemodynamics, excretory function, and renin release.

Adenosine, a potent vasodilator both in animals and in humans, has been used to produce controlled hypotension in patients, especially during cerebral aneurysm surgery. However, in animals adenosine by intrarenal infusion decreases renal blood flow (RBF), glomerular filtration rate (GFR), urine flow, and causes an inhibition of renin secretion. In this study we evaluated the effect of adenosine on RBF in patients (n = 15) scheduled for cerebral aneurysm surgery who had been anesthetized with a modified neurolept-anesthesia during controlled hyperventilation. Perioperative hypotension was achieved with infusion of adenosine (252.8 +/- 55.8 micrograms.kg-1.min-1) (n = 8) or sodium nitroprusside (2.5 +/- 0.8 micrograms.kg-1.min-1) (n = 7). Mean arterial pressure was lowered by 25%-30%, to approximately 60-70 mm Hg, in both groups. Glomerular filtration rate and RBF were measured using standard renal clearance methods for 51Cr-ethylenediaminetetraacetic acid and paraaminohippuric acid. Urine and blood samples were collected during normotension before and after a bolus dose of hypertonic mannitol, during hypotension, and during normotension after clipping of the aneurysm. Adenosine induced a marked decrease in GFR (-91%) and RBF (-92%), and a pronounced increase in renal vascular resistance. Sodium nitroprusside caused a significantly (P less than 0.01) less pronounced decrease in GFR (-24%) and RBF (-36%), but did not affect renal vascular resistance. After discontinuation of the hypotensive agents, GFR returned to baseline levels in both groups. Renal blood flow, however, increased above baseline after discontinuation of adenosine (+93%) but not after sodium nitroprusside. Sodium nitroprusside increased renin secretion, which was not seen with adenosine. Four patients in the adenosine group developed reversible atrioventricular conduction disturbances.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed1989

Thoracic epidural anaesthesia in patients with unstable angina pectoris.

The effect of high thoracic epidural anaesthesia with intermittent epidural bolus injections of bupivacaine (2.5 or 5 mg ml-1) was studied in 28 patients with unstable angina pectoris. The majority of the patients had a history of previous acute myocardial infarction(s) and/or angina pectoris and severe coronary artery disease. All patients were treated with nitroglycerin infusion for greater than 24 h and were included in the study if they had chest pain, not caused by acute myocardial infarction, at bed rest or recurrent anginal pain at rest greater than 2 days after infarction. 4.4 +/- 0.3 ml of bupivacaine induced a blockade of the upper seven sympathetic segments (Th1-7) for 98 +/- 9 min. Heart rate decreased significantly from 70 +/- 3 to 64 +/- 3 beats min-1 while blood pressure was unaffected by thoracic epidural anaesthesia. In 27 patients (96%) the anaesthesia induced complete analgesia. Nitroglycerin infusion was discontinued definitely within 3 h in 26 patients (93%) and pain was thereafter controlled by means of thoracic epidural anaesthesia as the sole treatment in 23 patients (82%) and as the major treatment in 25 patients (89%). Twenty-one patients (75%) were fully mobilized and stabilized. Treatment with thoracic epidural anaesthesia lasted for 6.0 +/- 1.1 days. The number of daily epidural injections decreased significantly with time from 2.7 +/- 0.3 the first day to 0.9 +/- 0.3 the fourth day (P less than 0.01, n = 19). Two patients developed acute myocardial infarction during the anaesthesia treatment period, and one of these patients died.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Changes in muscle sympathetic nerve activity, venous plasma catecholamines, and calf vascular resistance during mechanical ventilation with PEEP in humans.

The sympathetic reflex response to mechanical ventilation with PEEP was studied in conscious human volunteers (n = 8). Muscle sympathetic nerve activity (MSNA) was measured from the peroneal nerve, calf blood flow, forearm venous plasma catecholamines, blood pressure, heart rate, airway pressure, and end-tidal CO2 (%) during spontaneous breathing and during mechanical ventilation with 0-20 cmH2O PEEP. MSNA increased (P less than 0.01) during PEEP ventilation, from 22 bursts.min-1 at spontaneous breathing to 39 bursts.min-1 at 20 PEEP. This increase in MSNA was accompanied by an increase (P less than 0.01) in calf vascular resistance (CVR) from 35 PRU100 at spontaneous breathing to 48 PRU100 at 15 PEEP with no further increase at 20 PEEP. Venous plasma norepinephrine concentrations increased (P less than 0.01) during PEEP ventilation from 0.19 ng.ml-1 at spontaneous breathing to 0.31 ng.ml-1 at 20 PEEP, whereas plasma epinephrine and dopamine were less than 0.03 ng.ml-1 during the experiment. Blood pressure and heart rate were not affected by PEEP ventilation except at 20 PEEP, where blood pressure and heart rate increased (P less than 0.01). The results show that PEEP ventilation induces a considerable reflex increase of MSNA, reflected also by an increase in CVR and venous plasma norepinephrine. It is proposed that the main mechanism responsible for these reflex adjustments is caused by a decreased activity of the cardiopulmonary low-pressure baroreceptors, in turn resulting from a decrease in cardiac transmural pressures due to PEEP ventilation.

Adult↗
PubMed1989

The opiate antagonist naloxone counteracts the inhibition of sympathetic nerve activity caused by halothane anesthesia in rats.

The study was undertaken to examine if endogenous opioid systems mediate the response of the sympathetic nervous system to halothane anesthesia. Steady state values of renal sympathetic nerve activity (rSNA), mean arterial pressure (MAP), and heart rate (HR) were continuously recorded in the conscious state and at three depths of halothane anesthesia (0.6%, 1.2%, and 2.4%) in rats. Halothane caused an inhibition of rSNA and hypotension and a decrease in HR at the three halothane concentrations. Repeated bolus doses of the opiate antagonist (-)naloxone given iv during 1.2% halothane anesthesia did not significantly increase any of the variables. However, pretreatment with (-)naloxone (2 or 15 mg.kg-1) induced an increase in rSNA at 0.6% halothane, and subsequently the rSNA inhibition was less pronounced at the two higher halothane concentrations compared with control. HR showed a similar pattern, whereas the hypotension was essentially unaffected. Pretreatment with the pharmacologically inactive compound (+)naloxone had no effect on the halothane-induced depression of rSNA. The ED50 halothane concentration concerning nociceptive aversive behavior was not significantly changed with (-)naloxone pretreatment (2 mg.kg-1). In order to determine if sympathoinhibitory bulbospinal serotonin pathways are activated during halothane anesthesia, rSNA, MAP, and HR were recorded in rats pretreated with the serotonin synthesis inhibitor parachlorophenylalanine (PCPA). However, PCPA pretreatment did not affect the rSNA response to halothane compared with control. These findings indicate that the halothane-induced inhibition of rSNA might partially result from a stereospecific activation of opioid receptors, whereas halothane analgesia does not seem to be mediated by opioid mechanisms.

Anesthesia, Inhalation↗
PubMed1989

Control of intraoperative hypertension with isoflurane in patients with coronary artery disease: effects on regional myocardial blood flow and metabolism.

The effect of isoflurane on regional myocardial metabolism and blood flow, when used as an adjunct to fentanyl-nitrous oxide anesthesia, to control intraoperative hypertension was investigated. Twenty-two patients with two- or three-vessel coronary artery disease with an ejection fraction greater than 0.5 and on beta-blockers up to the morning of surgery were studied during elective coronary artery by-pass grafting. Systemic and pulmonary hemodynamics, and regional (great cardiac vein, GCVF) myocardial blood flow and myocardial metabolic parameters were measured. In 10 patients, both GCVF and global (coronary sinus, CSF) myocardial blood flows were recorded. Measurements were made 1) after induction of anesthesia but prior to skin incision, 2) during sternotomy, and 3) during isoflurane administration after its use to reduce arterial pressure to the presternotomy level. The increase in systemic arterial pressure during sternotomy was due to an increase in systemic vascular resistance accompanied by increases in heart rate, pulmonary capillary wedge pressure, (PCWP) regional myocardial oxygen consumption and extraction, GCVF and total coronary vascular resistance. Isoflurane reduced systemic arterial pressure but not PCWP, to presternotomy levels within 6.9 +/- 0.7 minutes at an end-tidal concentration of 1.5 +/- 0.2%. Isoflurane induced a pronounced systemic and coronary vasodilatation and increases in cardiac index, heart rate and regional myocardial oxygen extraction while the GCVF/CSF ratio remained unchanged. While mean regional--MLE% values were not effected by sternotomy, in two patients myocardial lactate production was seen during sternotomy but not during isoflurane. In another two patients, isoflurane induced lactate production.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗