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Although diazepam has been shown to reduce the stress response, the protective effect of midazolam, a newer benzodiazepine from a stressful event, tracheal intubation, has not been studied as yet by catecholamine assays in patients undergoing coronary artery bypass surgery, who also receive intravenous sufentanil as a component of the neuroleptanalgesic technique. Therefore, we evaluated the influence of midazolam in combination with sufentanil on the plasma free catecholamines before and after midazolam, after sufentanil and pancuronium and before and after intubation in 15 adult patients undergoing coronary artery surgery. After routine premedication, midazolam 0.14 +/- 0.01 mg.kg-1 i.v. was given over 1 min followed 5 min later by sufentanil in incremental i.v. doses of 1.5 micrograms.kg-1 to a total pre-intubation dose of 4.0-5.0 micrograms.kg-1 injected in 10 min. The incremental doses of sufentanil were given when a greater than 15 per cent increase in rate-pressure product occurred. One min after the initial dose of sufentanil, pancuronium 0.1 mg.kg-1 i.v. was given to provide muscle relaxation. Midazolam administration per se caused a significant decrease in systolic and diastolic blood pressures with a concomitant reduction in systemic vascular resistance. Sufentanil reduced the left ventricular stroke-work index. Tracheal intubation, a strong stressor during anesthesia, elicited no increase in catecholamines and/or adverse hemodynamic responses in contrast to a marked increase in plasma catecholamines routinely observed in patients anesthetized by the commonly used technique of intravenous barbiturates in combination with succinylcholine.
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PMID:Protection from stress of tracheal intubation with midazolam-sufentanil neuroleptanalgesia. 213 34

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)
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PMID:Sufentanil does not block sympathetic responses to surgical stimuli in patients having coronary artery revascularization surgery. 252 78

Sufentanil, a synthetic opioid that is 5-10 times as potent as fentanyl, has been suggested by some authors to prevent hypertensive responses to noxious stimuli in patients undergoing coronary artery bypass surgery much better than fentanyl, while in other studies it has failed to maintain cardiovascular stability during surgical stimulation. This study was designed to investigate the cardiovascular and electroencephalographic effects of high-dose sufentanil/O2/pancuronium anesthesia in patients undergoing coronary artery bypass surgery. METHODS. Two different doses of sufentanil were administered to two groups including a total of 20 male patients. Patients in group 1 (n = 10) received 10 micrograms.kg-1 sufentanil as an induction dose plus 0.15 microgram.kg-1.min-1 as a continuous infusion, while 10 micrograms.kg-1 plus 0.3 microgram.kg-1.min-1 were administered to the patients in group 2 (n = 10). Hemodynamic measurements were performed with the patients awake (I), 15 min following the induction of anesthesia with sufentanil and pancuronium at rest (II), and during sternotomy and sternal spreading (III). Patients were ventilated with oxygen in air (FiO2 = 0.5). Cerebral electrical activity was recorded by periodic analysis of the EEG, and plasma concentrations of sufentanil were measured throughout the entire study period. RESULTS AND DISCUSSION. The dosage scheme used in this study, which consisted of a sufentanil bolus followed by a continuous infusion, prevented plasma concentrations of sufentanil from declining in both groups during the entire study period. Following induction there was a significant decrease in systolic arterial pressure by 12% in group 1 and 20% in group 2 accompanied by a reduction in cardiac index by 25% and 21%, respectively, and in stroke volume index by 19% in group 1 and 24% in group 2, while systemic vascular resistance increased by 27% and 10%, respectively. Sternotomy led to a rise in systolic arterial pressure that did not exceed the awake values in both groups, while diastolic and mean arterial pressures (MAP) increased by 17% and 14% and by 15%, respectively, due to further increases in systemic vascular resistance by 57% and 41% above the control values. Cardiac and stroke volume indexes stayed significantly lower than the awake values, whereas heart rate remained essentially unchanged during the course of the study. There were no statistically significant differences between the groups during all measurements. In the EEG, sufentanil anesthesia was characterized by a decrease in the number of higher frequency waves and an increase in lower frequency (delta) waves, which did not change during sternotomy in 17 of the 20 patients.
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PMID:[The effect of sufentanil in high doses on hemodynamics and electroencephalography activity in coronary patients]. 253 57

Since the administration of both diazepam and midazolam are claimed to cause adverse haemodynamic effects following fentanyl or sufentanil intravenous injection, we evaluated the effectiveness and safety of the reverse sequence, (midazolam-sufentanil) on haemodynamic variables, adequacy of analgesia, amnesia and recovery in 15 adult patients undergoing coronary artery surgery (with a mean +/- SEM ejection fraction of 0.41 +/- 0.03). After routine premedication, midazolam 0.14 +/- 0.01 mg.kg-1 IV was given over one min followed 5 min later by sufentanil in incremental IV doses of 1.5 micrograms.kg-1 to a total pre-intubation dose of 4.0-5.0 micrograms.kg-1 injected in 10 min. One minute after the initial dose of sufentanil, pancuronium 0.1 mg.kg-1 IV was given in 30 seconds. The incremental doses of sufentanil were based on a greater than 15 per cent increase in rate-pressure product. The mean dose of sufentanil before cardiopulmonary bypass was 9.6 +/- 2.1 micrograms.kg-1 and 13.9 +/- 1.3 micrograms.kg-1 for the entire procedure. A significant decrease in systolic and diastolic blood pressures occurred after midazolam administration which was sustained until sternotomy. A significant reduction in systemic vascular resistance occurred following midazolam. Sufentanil reduced the left ventricular stroke-work index. Tracheal intubation, skin incision and sternotomy elicited no adverse haemodynamic responses. Adequate analgesia, complete amnesia and early recovery of wakefulness were observed.
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PMID:Haemodynamic stability with midazolam-sufentanil analgesia in cardiac surgical patients. 297 65

The hemodynamic effects of high doses of sufentanil, a newly synthetized highly potent analgesic, were investigated in dogs. This study compared the early (30 min) cardiovascular effects of sufentanil 0.01 mg . kg-1 and morphine 4 mg . kg-1. Sufentanil caused a moderate and insignificant decrease in mean arterial pressure (MAP). A 30% decrease in cardiac index (CI) was almost outbalanced by an increased systemic vascular resistance (SVRI). The lowering of CI was due to a more than 50% decrease in heart rate (HR) which was partly compensated for by a greater stroke volume index (SVI). In the first 5 min after morphine injection, MAP fell significantly to about 50 mmHg (below 50% of the control value). CI was reduced to about 50% of the control value because of significant decreases in both SVI and HR. The calculated SVRI was unchanged after morphine. Within 30 min some of the initially changed parameters had returned to control levels. Central venous pressure (CVP) and pulmonary capillary wedge pressure (PCWP) increased immediately after sufentanil, but decreased after morphine. With time, both parameters returned towards control values. Peak left ventricular dP/dt decreased by about 25-50% after both analgesics. The rate-pressure products (RPP) were significantly decreased to less than one half of the control values after both analgesics. Mixed venous oxygen tension (PVO2), oxygen transport and oxygen consumption were significantly lowered in the sufentanil group, whereas immediate decreases after morphine were followed by gradual increases towards control values. We conclude that the use of high doses of sufentanil in dogs is safe. Apart from initial, transient changes, a stable cardiovascular state characterizes the high-dose sufentanil anesthesia, while morphine causes fluctuations in several hemodynamic parameters. Compared to morphine anesthesia, sufentanil anesthesia appears to be an attractive alternative which deserves further evaluation in humans.
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PMID:Early response in central hemodynamics to high doses of sufentanil or morphine in dogs. 611 71

In propranolol-pretreated dogs (2 mg . kg -1) the immediate cardiovascular effects of sufentanil (0.01 mg . kg -1) or morphine (4 mg . kg -1) were compared. Besides a 40% decrease in cardiac index (CI), sufentanil and morphine initiated quite different hemodynamic changes. Sufentanil did not significantly change mean arterial pressure (MAP), central venous pressure (CVP) and mean pulmonary artery pressure (MPAP), while the pulmonary capillary wedge pressure (PCWP) increased by 50%. After morphine, MAP declined significantly by about 65%, and significant decreases in MPAP (14%) and PCWP (33%) were also observed. Propranolol reduced heart rate by 16%, and morphine caused no further reduction in HR. A significant decrease of about 30% was seen in HR after sufentanil. Sufentanil significantly raised systemic vascular resistance index (SVRI) by 15%, whereas morphine decreased it by 32%. Pulmonary vascular resistance index (PVRI) was unchanged after sufentanil, but significantly increased after morphine. Right ventricular stroke work index (RVSWI) was unaffected by both analgesics, and morphine decreased left ventricular work index (LVSWI) significantly by 80%. Oxygen transport index declined significantly after both analgesics. Sufentanil reduced oxygen consumption by 20%, while morphine left this parameter unaffected. We conclude that the administration of high-dose sufentanil leads to a stable circulation, even when a total beta-blockade exists.
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PMID:High-dose analgesic anesthesia with morphine or sufentanil in propranolol-treated dogs. 612 28