ISSN:0003-3022    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

Eighteen patients undergoing total hip replacement (n = 13) or knee arthroplasty (n = 5) due to osteoarthritis or osteoarthrosis were prospectively studied in an investigation of complement activation and anaphylatoxin release in association with reinfusion of aspirated wound blood. Twelve of the patients needed blood transfusions and received an average of 390 ± 75 ml (±SD) of autologous blood within 45 min. Plasma complement components, anaphylatoxins, and inhibitors were studied 1 min before and 15 min after the start of and 15 min after the completion of autologous transfusion. Samples also were taken from the collected blood, before and after passing it through a microporous filter. Blood gases and systemic complement samples were drawn simultaneously. There were no significant changes in systemic complement variables before, during, or after transfusion of autologous blood. However, in the aspirated blood, increased concentration of anaphylatoxins (C3a and C5a) and terminal complement complexes (TCC) were present (P< 0.001). There were no differences observed between samples drawn before and after filtration of the blood. The concentration of C5 was less in the collected blood than in the systemic blood (P< 0.05). No changes in blood gases were observed. This study demonstrated that post-operatively salvaged whole blood underwent anaphylatoxin formation and complement activation. However, after reinfusion of this blood, neither systemic complement activation nor clinical complications were observed.

ISSN:0003-3022    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

Eighty women receiving spinal anesthesia for postpartum tubal ligation were entered into a double-blind, randomized protocol studying the effects of epinephrine on intrathecal fentanyl-induced postoperative analgesia. All patients received 70 mg hyperbaric lidocaine with either 0.2 mg epinephrine (LE), 10 μg fentanyl (LF), epinephrine and fentanyl (LFE), or 0.4 ml saline (L). Onset and regression of anesthesia, degree of intraoperative comfort, incidence of pruritus, and extent of postoperative analgesia were evaluated. The simultaneous administration of epinephrine and fentanyl prolonged the duration of complete analgesia (137 ± 47 min (LFE); 76 ± 32 min (LE); 85 ± 44 min (LF); 65 ± 36 min (L)) and the duration of effective analgesia (562 ± 504 min (LFE); 227 ± 201 min (LE); 203 ±178 min (LF); 198 ± 342 min (L)). Administration of epinephrine decreased the incidence of pruritus associated with intrathecal fentanyl (1/18 (LFE); 1/21 (LE); 8/19 (LF); 2/19 (L)).

ISSN:0003-3022    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

The authors studied the optimal epinephrine content of an epidural test dose, and determined criteria to identify intravascular injections in subjects with or without β-adrenergic blockade. Nine healthy nonpregnant subjects 25–36 years of age were given intravenous infusions of saline or esmolol in random order. During each infusion, they received a series of five injections (3 ml each) of either saline, 1% Iidocaine or 1% lidocaine containing 5, 10, or 15 μg of epinephrine. Thirty minutes after completing these two infusions, propranolol was administered as a bolus injection, and the series of five injections repeated. All injections were double blind and randomized. During saline infusion, all injections containing epinephrine significantly increased heart rate (HR) by an average of 31–38 beats/min when compared with that following plain lidocaine (P< 0.05), and increased systolic blood pressure by an average of 17–26 mmHg (P< 0.05 for the 15-μg dose only). During esmolol infusion, epinephrine injections increased HR by an average of 23–31 beats/min (P< 0.05), and increased systolic blood pressure by an average of 18–30 mmHg (P< 0.05 for 10 and 15 μg). After propranolol injection, epinephrine injections caused a decrease in HR by an average of 21–28 beats/min (P< 0.05), whereas systolic blood pressure increased by an average of 22–35 mmHg (P< 0.05 for 10 and 15 μg only). Without β-adrenergic blockade, an increase in HR ≥ 20 beats/min was 100% sensitive and specific for intravascular injection of 10 or 15 μg of epinephrine. After selective and nonselective β-adrenergic blockade, HR changes were not reliable, but an increase in systolic blood pressure (SBP) of ≥ 15 mmHg was diagnostic of injection of 10 or 15 μg of epinephrine. Hemodynamic changes occurred within 2 min after intravascular (iv) injections, and lasted at least 35 s. Injection of 5 μg of epinephrine did not produce reliable hemodynamic changes in any group. The authors conclude that in young, nonpregnant, individuals: 1) a test dose containing at least 10 μg epinephrine is a reliable marker of intravascular injection; 2) intravascular injection can be reliably detected by an absolute variation in HR of ≥ 20 beats/min in non–β-blocked subjects, and by an increase in SBP of ≥ 15 mmHg in the presence of β-adrenergic blockade.

ISSN:0003-3022    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

The right ventricular responses to mild hypocarbia and hypercarbia were studied in 18 anesthetized and paralyzed patients following coronary artery bypass surgery. Maintaining constant tidal volume (8 ml · kg−1), FIo2(0.5), and PEEP (5 cm H2O), the ventilator rate was varied to sequentially produce: 1) normocarbia (Paco2, 38.3 ± 2.5 mmHg; mean ± SD), 2) hypocarbia (Paco2, 33.2 ± 2.8 mmHg), 3) hypercarbia (Paco2, 49.8 ± 2.9 mmHg) and 4) normocarbia (Paco2, 38.8 ± 3.6 mmHg). Pulmonary and right ventricular hemodynamics were assessed using a rapid-response pulmonary artery catheter after 10 min of stabilization at each Paco2. Pulmonary and right ventricular hemodynamics remained unaffected by slight hypocarbia. In contrast, hypercarbia increased pulmonary vascular resistance by 54% (P< 0.001) and mean pulmonary artery pressure by 34% (P< 0.001). This was accompanied by a 24% (P< 0.001) increase in right ventricular end-diastolic volume, a 38% (P< 0.001) increase in right ventricular end-systolic volume, and a 20% decrease (P< 0.001) in right ventricular ejection fraction. Despite an increase in right ventricular afterload, stroke volume was maintained unchanged because of a 45% (P< 0.001) increase in right ventricular stroke work index. Although the patients maintained pulmonary blood flow during hypercarbia using preload augmentation, compensatory reserve might be exceeded in patients with more compromised right ventricular function.

ISSN:0003-3022    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

Double-burst stimulation (DBS), a new technique to evaluate neuromuscular function, consists of two 50-Hz trains of 60-ms duration and 750 ms apart. DBS was compared with train-of-four (TOF) stimulation in 21 children aged 3–10 yr, during halothane anesthesia. On one arm the ulnar nerve was stimulated supramaximally with TOF stimulation every 12 s and the force of the evoked contraction of the adductor pollicis measured with an FTO3 force transducer and recorded on paper. Atracurium (0.4–0.5 mg · kg−1) was administered. During recovery from neuromuscular blockade, TOF stimulation was interrupted periodically and DBS substituted. The same stimulation patterns were applied to the ulnar nerve of the other arm simultaneously, and the clinical anesthesiologist was asked to estimate the degree of fade with both. There was good correlation between the measured TOF ratio (ratio of fourth to first response) and DBS ratio (ratio of second to first response). The TOF and DBS ratios above which fade could no longer be appreciated manually were (mean ± SEM) 0.44 ± 0.03 and 0.67 ± 0.04 (P= 0.0002). Corresponding ranges were 0.3–0.8 for TOF and 0.4–0.9 for DBS, but DBS fade was always apparent if TOF fade could be detected. Therefore, in children, DBS is more sensitive than is TOF stimulation for the clinical assessment of recovery from neuromuscular blockade.

ISSN:0003-3022    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

The authors determined the effect of propofol on cerebral blood flow, intracranial pressure, and cerebral arteriovenous oxygen content difference in severely brain-injured patients during orthopedic treatment of fractures of the extremities. The Glasgow Coma Scale score was 6 or 7 at the time of the study. Data were collected in the operating room before and during (5 and 15 min) administration of propofol (2 mg/kg iv bolus immediately followed by a 150 μg · kg−1· min−1infusion) before surgical stimulation. Propofol was infused during 41.4 ± 7.3 min. After operation, the last set of measurements was made 15 min after propofol was stopped. The study was performed on 10 adults (age range, 15–40 yr) whose lungs were mechanically ventilated (air/O2) and who were sedated (phenoperidine, 1 mg/h), and was conducted using a radial artery cannula; a 7.5-Fr, thermodilution, flow-directed, pulmonary artery catheter; an intraventricular catheter; and a catheter in the jugular venous bulb. The133xenon intra-internal carotid artery injection technique was used to determine regional cerebral blood flow (rCBF). Anesthetic blood concentration of propofol (3–5 μg/ml) was associated with decreases in cerebral perfusion pressure (CPP; from 82 ± 14 to 59 ± 7 mmHg;P< 0.001), rCBF (from 35 ± 6 to 26 ± 5 ml · 100 g−1· min−1;P< 0.01), and intracranial pressure (ICP; from 11.3 ± 2.6 to 9.2 ± 2.5 mmHg;P< 0.001). Cerebrovascular resistance and cerebral arteriovenous oxygen content difference were unchanged. After propofol was stopped (at a blood propofol concentration theoretically corresponding to recovery from anesthesia), rCBF and ICP returned to preinduction values without any rebound. It was concluded that propofol reduces ICP but may lower CPP because of its effects on mean arterial pressure. Propofol appears to exert no consistent effect on cerebral vascular resistance and does not alter cerebral arteriovenous oxygen content difference.

ISSN:0003-3022    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

The authors sought to determine whether neostigmine, given at a time when no response to peripheral nerve stimulation could be elicited, hastened recovery from a vecuronium-induced neuromuscular blockade (NMB). The effect of neostigmine (70 μg/kg) in antagonizing a profound (no-twitch) vecuronium-induced (0.1 mg/kg) NMB in 40 healthy patients was studied. Patients were randomly assigned to one of four groups specifying the sequence of neostigmine administration. Fifteen minutes after the administration of vecuronium, when there was no detectable twitch response, each patient received either neostigmine (70 μg/kg) with glycopyrrolate (15 μg/kg) or an equivalent volume of normal saline (placebo). When T1 (the first response in the train-of-four [TOF] sequence) recovered to 10% of control, patients again received either neostigmine with glycopyrrolate in the same doses as before or the placebo. The following variables were measured: times from vecuronium injection until T1 recovered to 10% (t [10]) and 90% (t [90]) of control, and time until the TOF ratio was equal to 75% (t [TOF75]). Mean values of t (90) and t (TOF75) were shorter (54.7–75.2 min and 60.4–79.5 min, respectively) for the three groups who received neostigmine as compared with patients who received two doses of placebo (104.3 and 122.6 min, respectively). There were no differences in the t (90) and t (TOF75) values among the three groups who received neostigmine. The authors concluded that the total time to achieve adequate recovery of neuromuscular function is the same whether neostigmine (70 μg/kg) is administered 15 min after vecuronium (0.1 mg/kg) or whether neostigmine is given when T1 has recovered to 10% of control. Furthermore, a second dose of neostigmine (70 μg/kg) neither hastens nor prolongs recovery. Thus, recovery time from a profound vecuronium-induced NMB can be shortened with the administration of neostigmine given before spontaneous recovery, and repeated administration of neostigmine does not alter the course of recovery.

ISSN:0003-3022    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

The effect of the rate of intravenous infusion of protamihe on the acute hemodynamic and pulmonary effects of heparin neutralization was investigated in six adult sheep surgically instrumented for chronic studies. Bovine lung heparin at a dose of 200 IU/kg was injected intravenously over 10 sec, 5 min before the start of protamine administration. On separate experimental days, each sheep received protamine at the same dose of 2 mg/kg, but it was infused over four different time periods: 3 s, 30 s, 300 s, or 30 min. At an additional session, protamine was administered over 3 s without prior heparinization to assess the effect of protamine alone. The sequence of the sessions was randomized and performed blindly. Injecting protamine in unheparinized sheep produced no change in any of the measured variables. In contrast, when protamine was injected over 3 s in heparinized sheep, it induced a transient and significant (P< 0.001) pulmonary hypertension (from 17.2 ± 1.5 to 45.6 ± 2.4 mmHg at 1 min) with an increased pulmonary (five-fold) and systemic (2.5-fold) vascular resistance; a decrease of cardiac output (from 3.85 ± 0.43 to 1.93 ± 0.291/min) without change in left atrial pressure (from 5.3 ± 1.3 to 6.0 ± 1.7 mmHg;P= NS); a significant (P< 0.001) increase of plasma thromboxane B2(TxB2) concentrations (from 349 ± 131 to 974 ± 218 pg/ml); leukopenia (76 ± 4% of baseline white blood cell counts); and hypoxemia (Pao2decreased from 81 ± 3 to 63 ± 4 mmHg at 2 min). Administering the same amount of protamine after heparin at a slower infusion rate significantly attenuated and delayed all components of the adverse response to protamine. This attenuation occurred in an infusion rate-dependent fashion, so that when protamine was infused over 30 min, no significant changes in any of the measured variables were noted. The time course of plasma heparin concentrations following protamine indicated that chemical heparin was completely neutralized over the time period of protamine infusion. These results demonstrate that therateof generation of heparin–protamine complexes (as detected by changes of plasma concentrations of chemical heparin) during iv protamine infusion started 5 min after heparin administration is a factor involved in the generation of sufficient mediators required to initiate a characteristic physiologic response in sheep, including systemic and pulmonary vasoconstriction, TxB2generation, and leukopenia. Infusing a neutralizing dose of protamine over 30 min avoids these adverse reactions in sheep.

ISSN:0003-3022    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

Modulatory effects of spinal opioid, α-adrenergic, and benzodiazepine receptors on the somato-sympathoadrenal reflex response, evoked by supramaximal bilateral sciatic nerve stimulation (50 times minimal motor threshold) were evaluated in halothane-anesthetized cats. Group 1 (n = 8) served as a control; group 2 (n = 7) received intrathecally (it) the opioid receptor agonist morphine (500 μg); group 3 (n = 7), the α2-adrenergic agonist clonidine (200 μg it); and group 4 (n = 7), the benzodiazepine receptor agonist midazolam (1 mg it). Plasma samples were collected from the adrenal vein at baseline, after it drug administration, and during sciatic nerve stimulation for the measurement of norepinephrine, epinephrine, and dopamine. In control cats (group 1), sciatic nerve stimulation evoked significant increases in adrenal vein catecholamine plasma levels, blood pressure, and heart rate. Morphine (group 2) did not have any effect on spontaneous hemodynamics and adrenal secretion. During stimulation (group 2), there were no significant increases in adrenal norepinephrine and epinephrine concentrations, whereas dopamine concentrations, blood pressure, and heart rate rose significantly. Clonidine (group 3) led to a decrease in heart rate and adrenal vein norepinephrine and epinephrine concentrations at baseline. During sciatic nerve stimulation in this group (3), significantly lower concentrations were observed in adrenal vein catecholamines compared with control, whereas the hemodynamic response was not suppressed. Midazolam suppressed baseline and stimulation-evoked adrenal vein catecholamine concentrations, but hemodynamics were not significantly affected. Although the study was conducted in a halothane-anesthetized cat model, employing single doses of agonists, the data clearly indicate a complex modulation of the somato-sympathoadrenal reflex response that is differentially inhibited by spinal opioid, benzodiazepine, and α-adrenergic receptor systems.

ISSN:0003-3022    

出版商:OVID    

年代:1990

数据来源: OVID