Showing papers in "Anesthesiology in 1984"

An analysis of major errors and equipment failures in anesthesia management: considerations for prevention and detection.

Abstract: Adaptations of the critical-incident technique were used to gather reports of anesthesia-related human error and equipment failure. A total of 139 anesthesiologists, residents, and nurse-anesthetists from four hospitals participated as subjects in directed or open-ended interviews, and 48 of them functioned as "trained observers." A total of 1,089 descriptions of preventable "critical incidents" were collected. Of these, 70 represented errors or failures that had contributed in some way to a "substantive negative outcome." From these incidents, ten potential strategies were developed for prevention or detection of incidents. Overall patterns observed in this wider study were similar to those of our earlier report. The incidents most frequently reported included breathing circuit disconnections, drug-syringe swaps, gas-flow control errors and losses of gas supply. Only 4% of the incidents with substantive negative outcomes involved equipment failure, confirming the previous impression that human error is the dominant issue in anesthesia mishaps. Among the broad categories of key strategies for mishap prevention were additional technical training, improved supervision, improved organization, equipment human-factors improvements, and use of additional monitoring instrumentation. The data also suggest that less healthy patients are more likely to be affected adversely by errors. It is suggested that, in future studies of anesthesia mortality and morbidity, untoward events should be classified according to preventive strategy rather than outcome alone as an aid to those who wish to apply the experience of others to lessen the risk in their individual practice.

Effect of Age, Gender, and Obesity on Midazolam Kinetics

Abstract: The effects of age, sex, and obesity on the kinetics of single intravenous (iv) and oral doses of midazolam were evaluated in healthy volunteers who received 2.5-5 mg of iv midazolam on one occasion and 5-10 mg orally on another. Kinetics were determined from multiple plasma midazolam concentrations measured during 24 h after dosage. Midazolam elimination half-life (t1/2) after iv dosage was significantly prolonged in elderly (aged 60-74 yr) versus young (24-33 yr) males (5.6 vs. 2.1 hours, P less than 0.01) and total clearance was significantly reduced (4.4 vs. 7.8 ml X min-1 X kg-1, P less than 0.01), leading to increased systemic availability of the oral dose (50% vs. 41%, P less than 0.05). However total volume of distribution calculated by the area method (Vd) (1.6 vs. 1.3 1/kg) and protein binding (3.5 vs. 3.4% unbound) did not differ between groups. Among women there were no significant differences between elderly (64-79 yr) and young (23-37 yr) volunteers in t1/2 (4.0 vs. 2.6 h), clearance (7.5 vs. 9.4 ml X min-1 X kg-1), Vd (2.1 vs. 2.0 1/kg), protein binding (3.7% vs. 3.7% unbound), or oral bioavailability (38% vs. 36%). In obese volunteers (mean weight 117 kg; 173% of ideal weight) versus control subjects of normal weight (66 kg, 95% of ideal weight) matched for age, sex, and smoking habits, midazolam Vd was increased significantly (311 vs. 114 1, P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

A Review of Pulmonary Artery Catheterization in 6,245 Patients

Abstract: From July 1977 to December 1982, 6,245 patients requiring cardiac and noncardiac operations had pulmonary artery (PA) catheterizations for perioperative monitoring. Their ages ranged from 4 to 94 years. PA catheters were inserted through the external or internal jugular vein in 6,146 patients, while arm veins were used in 99 patients. Complications included persistent PVCs requiring therapy in 193 (3.1%), right bundle branch blocks in three (0.048%), left bundle branch and complete heart block each in one patient (0.016%), intrapulmonary hemorrhage in four (0.064%), minor pulmonary infarcts in four (0.064%), perforation of right ventricle in one (0.016%), and death from uncontrollable pulmonary hemorrhage in one patient (0.016%). This investigation reveals a low incidence of morbidity associated with PA catheterization.

Postthoracotomy pain and pulmonary function following epidural and systemic morphine.

Abstract: Thirty patients undergoing thoracotomy for lung resection were entered in a randomized, double-blind trial comparing the effects of epidural (E) versus intravenous (iv) morphine on postoperative pain and pulmonary function. Postoperatively the patients were given repeated doses of either 5.0 mg of morphine epidurally or 0.05-0.07 mg/kg morphine intravenously until there were no further spontaneous complaints of pain. Two, 8, and 24 h postoperatively, the following indices were measured: linear analogue pain score, somnolence score, vital signs, arterial PaO2, PaCO2, and pH, forced vital capacity (FVC), forced expiratory volume in the first second (FEV1), and peak expiratory flow rate (PEFR). Patients receiving epidural morphine had significantly less pain at 2 h (P less than 0.01) and 8 h (P less than 0.004) postoperatively. There was no difference in vital signs except for significantly slower respiratory rates at 2 h (P less than 0.04), 8 h (P less than 0.02) and 24 h (P less than 0.01) in the epidural group. No significant differences occurred in the somnolence scores or blood-gas measurements, which were within normal limits.(ABSTRACT TRUNCATED AT 250 WORDS)

Opioid analgesics in anesthesia: with special reference to their use in cardiovascular anesthesia.

Abstract: In this article, an attempt has been made to review the use of receptor stimulating pure agonist opioids in anesthesia, especially in patients with cardiovascular disease. Particular emphasis has been placed on the use of opioids in high doses to produce anesthesia, techniques that recently have become popular in cardiovascular anesthesia. A major benefit of opioid anesthesia is the cardiovascular stability obtained during induction and throughout operation, even in patients with severely impaired cardiac function. There is a considerable body of evidence to support this claim when fentanyl is used. Anesthetic doses of morphine are associated with a higher incidence of cardiovascular disturbances and other problems, and, therefore, more attention to detail is required in order to achieve adequate anesthesia and hemodynamic stability. Although other opioids have been used as sole or principal agents in anesthesia for cardiovascular surgery, none have gained widespread acceptance. Meperidine, for example, which is widely used in lower (nonanesthetic) doses as a supplement to nitrous oxide in cardiac and noncardiac surgery, has proved unsuitable because of severe hemodynamic disturbances when high doses are given. However, initial reports concerning two of the newer agonist opioids, sufentanil and alfentanil, suggest that they may prove to be suitable alternatives and perhaps provide advantages over morphine and fentanyl in patients with or without cardiovascular disease. Although cardiovascular stability usually can be assured in the chronically sick cardiac patient with opioid anesthesia, this is not always so with the healthier patient, particularly those presenting for coronary artery surgery. A frequently occurring problem in these patients is hypertension during or after sternotomy, which can result in myocardial ischemia and infarction. The incidence of severe hypertension (increases in systolic blood pressure greater than 20% of control values) can be reduced drastically by increasing the dose of opioid, e.g., up to 140 micrograms/kg of fentanyl. However, despite such large doses, some patients will continue to need treatment with vasodilators, inhalation anesthetics, or other supplements at certain periods during cardiovascular operations. The use of very large doses of opioids also will prolong postoperative respiratory depression. High doses of opioids can reduce or prevent the hormonal and metabolic responses to the stress of surgery. However, even very large doses of fentanyl or its newer analogues do not prevent marked increases in plasma catecholamine concentrations in response to cardiopulmonary bypass.(ABSTRACT TRUNCATED AT 400 WORDS)

The Pharmacokinetics of Sufentanil in Surgical Patients

Abstract: The pharmacokinetics of sufentanil, a new thienyl analogue of fentanyl, were studied in 10 surgical patients. Sufentanil, 5 micrograms/kg, was given intravenously as a bolus injection and plasma concentrations measured at intervals up to 8 h. Plasma sufentanil concentrations decreased rapidly after injection--98% of the administered dose having left the plasma within 30 min. In 9 of the 10 patients, a tri-exponential equation optimally described the sufentanil concentration decay curve, with average (+/-SEM) half-lives for the rapid (pi) and slow (alpha) distribution phases of 1.4 +/- 0.3 min and 17.7 +/- 2.6 min, respectively. The average terminal elimination (beta) half-life was 164 +/- 22 min. The average value for Vd beta was 2.9 +/- 0.2 1/kg, Vdss 1.7 +/- 0.2 1/kg and total plasma clearance 12.7 +/- 0.8 ml X kg-1 X min-1 (935 +/- 50 ml/min). In one patient, a bi-exponential equation was sufficient to describe the concentration-time data, yielding a distribution half-life of 4.7 min and an elimination half-life of 117 min.

Preoperative Cessation of Smoking and Pulmonary Complications in Coronary Artery Bypass Patients

Abstract: La reduction des complications pulmonaires apres au moins 2 mois d'interruption de fumer est en rapport avec l'amelioration de la fonction ciliaire et des voies aeriennes et une diminution de la production d'expectoration

A Comparison of the Cerebrovascular and Metabolic Effects of Halothane and Isolflurane in the Cat

Abstract: Halothane is a well known cerebral vasodilator that can produce dangerous increases in intracranial pressure (ICP) in certain neurosurgical patients. It has been suggested that isoflurane may be a less potent cerebral vasodilator. The authors therefore undertook a direct comparison of the effects of halothane and isoflurane on cerebral blood flow (CBF), cerebral vascular resistance (CVR), intracranial pressure, and cerebral metabolic rate for oxygen (CMRO2). Studies were carried out in normocarbic mechanically ventilated cats, using the intracarotid 133Xe injection technique to measure CBF. The effects of three doses were examined: 0.5, 1.0, and 1.5 MAC, studied in the continued presence of 75% N2O. Autoregulation also was tested at 1.0 MAC (plus 75% N2O) by recording CBF and CVR before and after elevation of blood pressure with angiotensin. Both agents had similar effects on blood pressure and ICP. However, while halothane produced significant increases in CBF at all doses, with values of 61 +/- 5 ml X 100 g-1 X min-1 (123 +/- 8% of control, mean +/- SE) at 1.0 MAC, isoflurane anesthesia caused no significant changes in CBF at any level, (e.g., 48 +/- 8 ml X 100 g-1 X min-1 or 94 +/- 12% of control at 1.0 MAC). Both drugs produced dose-related decreases in CVR, but the changes were greater with halothane, e.g., CVR at 1.0 MAC halothane = 1.46 +/- 0.20 mmHg X ml-1 X 100 g X min (47 +/- 7% of control) compared with 2.23 +/- 0.40 mmHg X ml-1 X 100 g X min (72 +/- 9% of control).(ABSTRACT TRUNCATED AT 250 WORDS)

Etomidate Inhibits Adrenocortical Function in Surgical Patients

Abstract: Postoperative adrenocortical function was compared in 23 outpatients receiving either thiopental, 4 mg/kg, for induction and a thiopental infusion, 0.26 mg·kg−1 min−1 in combination with nitrous oxide 70% for maintenance of anesthesia (control); etomidate, 0.4 mg/kg, for induction followed by an eto

Volume Expansion versus Norepinephrine in Treatment of a Low Cardiac Output Complicating an Acute Increase in Right Ventricular Afterload in Dogs

Abstract: The authors investigated the effects of treatment on ventricular performance when cardiac output (CO) was reduced significantly because of an acute increase in pulmonary vascular resistance (PVR). In eight anesthetized, ventilated dogs, the effects of volume expansion (100 ml 6% dextran) on ventricular performance were determined before and after PVR was elevated. Resistance was increased by microembolization of the pulmonary vascular bed with glass beads (80-100 microns). When PVR was normal, volume expansion increased (P less than 0.05) stroke volume (SV) and mean blood pressure (BP). Alternatively, when RV afterload was increased, volume resulted in RV failure, i.e., decrease in SV (P less than 0.01) from 9.1 to 6.3 ml and a decrease (P less than 0.05) in mean BP from 97 to 65 mmHg, despite increased right ventricular end diastolic pressure (RVEDP) (P less than 0.05). Right ventricular dysfunction occurred with volume expansion, despite constant PVR and a decrease (P less than 0.01) in mean pulmonary artery pressure (PAP). In contrast to volume, norepinephrine infusion decreased biventricular filling pressures (P less than 0.01) and increased (P less than 0.01) SV from 6.2 to 11.3 ml. Accordingly, when RV afterload is increased significantly, even a relatively small increase in blood volume may result in RV dysfunction. Alternatively, inotropic agents with pressor effects may be the treatment of choice to increase CO when RV afterload is increased.

Liver Circulation and Function during Isoflurane and Halothane Anesthesia

Abstract: Hepatic arterial blood flow (HABF) and portal blood flow (PBF) were measured in 18 dogs while awake and during isoflurane and halothane anesthesia. Surgical preparation 1 week before the measurements consisted of a left thoracotomy, placement of a left atrial catheter, and insertion of another catheter into the distal aorta via the left femoral artery. Cardiac output and liver blood flow were determined using microspheres at three stages: stage 1-awake state; stage 2-after 45 min of 1 MAC of isoflurane (eight dogs) or halothane (10 dogs) anesthesia; and stage 3-after 45 min of 2 MAC of inhalation anesthesia. Half-life and fractional clearance for indocyanine green (ICG) were determined 1 day before the experiment (awake state), and at the end of stages 2 and 3. Mean arterial pressure (MAP) and cardiac index (CI), as well as PBF, decreased during isoflurane and halothane anesthesia. HABF increased significantly during isoflurane anesthesia, remained unchanged during 1 MAC of halothane anesthesia, and significantly decreased during 2 MAC of halothane anesthesia. Apparently, hepatic oxygen supply was maintained much better during isoflurane than during halothane anesthesia. PBF correlated with CI during halothane (r = 0.97) and, to a certain extent, with MAP during isoflurane (r = 0.66). HABF correlated with CI and MAP during halothane (r = 0.74 and 0.71, respectively) but did not correlate with systemic hemodynamic variables during isoflurane. ICG half-life significantly increased during 1 and 2 MAC of halothane anesthesia. The degree of increase did not correlate with the level of anesthesia or the decrease in total hepatic blood flow.(ABSTRACT TRUNCATED AT 250 WORDS)

Vecuronium-induced neuromuscular blockade during enflurane, isoflurane, and halothane anesthesia in humans.

Abstract: To determine the effect of the commonly used volatile anesthetics on a vecuronium-induced neuromuscular blockade, the authors studied 54 patients anesthetized with 1.2 MAC or 2.2 MAC enflurane, isoflurane, or halothane (MAC value includes contribution from 60% nitrous oxide). During 1.2 MAC enflurane, isoflurane, and halothane, the ED50S (the doses depressing twitch tension 50%) for vecuronium were 12.8, 14.7, and 16.9 micrograms/kg, respectively. During 2.2 MAC enflurane, isoflurane, and halothane, the ED50S for vecuronium were 6.3, 9.8, and 13.8 micrograms/kg, respectively (P less than 0.05). Time from injection to peak effect was the same for each anesthetic group (6.5 +/- 0.5 min, mean +/- SD), except for the group given 2.2 MAC enflurane (9.7 +/- 0.6 min) (P less than 0.05). The duration of a 50% block from injection to 90% recovery was the same for each group (mean 20 +/- 4 min), except for the group given 2.2 MAC enflurane (46.5 min) (P less than 0.05). The authors conclude that enflurane is the most potent volatile anesthetic, followed by isoflurane and then halothane, in augmenting a vecuronium-induced neuromuscular blockade. Increasing the concentration of volatile anesthetic has less effect on a neuromuscular blockade produced by vecuronium than on one produced by other nondepolarizing relaxants (e.g., pancuronium and d-tubucurarine).

Effects of Etomidate on Hormonal Responses to Surgical Stress

Abstract: The hormonal responses to surgical stress were examined in 10 patients scheduled for elective gynecologic laparotomy. Anesthesia was induced with either thiopental, 4 mg/kg, or etomidate, 0.35 mg/kg, and maintained with nitrous oxide and enflurane. Plasma cortisol, aldosterone, ACTH, and catecholamines were measured during the 24 h after the induction of anesthesia. The catecholamine responses of the patients whose anesthesia was induced with either drug were similar. The plasma ACTH concentrations for the etomidate group were greater than baseline values and the concentrations in the thiopental group (P less than 0.05) in the fourth and fifth hours. In the patients receiving thiopental, both cortisol and aldosterone concentrations were greater than the baseline value (P less than 0.05) in the second to fourth hours after induction. In the etomidate group, the plasma concentrations of cortisol were less than baseline values (P less than 0.05) in the first and second hours after induction of anesthesia and both cortisol and aldosterone were lower than those in the thiopental group (P less than 0.05) in the half to fourth hours after induction. These results confirm an earlier report of the suppression of cortisol after etomidate administration and, because aldosterone also was suppressed, suggests that etomidate exerts its effect by inhibiting early stages of steroidogenesis in the adrenal cortex.

Recall of Surgery for Major Trauma

Abstract: Major traumatic injury frequently causes hemodynamic instability that necessitates reducing the usual dose of anesthetic given for surgery. Nevertheless, a lower dose may be sufficient to provide anesthesia because of conditions present in trauma victims that are known to reduce anesthetic requirement (hypotension, hypothermia, and acute alcohol intoxication). To determine the incidence and patient perception of recall of surgery, 51 patients were interviewed after surgery for major trauma. Patients were assigned to one of two groups. Thirty-seven patients were given an anesthetic for endotracheal intubation and had continuous or almost continuous anesthesia during surgery. Of the four who recalled surgery (11%), two considered this awareness their worst hospital experience. Fourteen other patients, who were more severely injured, were not given an anesthetic for endotracheal intubation and/or for 20 or more consecutive minutes during surgery. Of the six patients in this group who recalled surgery (43%), two considered this awareness their worst hospital experience. No condition known to reduce anesthetic requirement did so reliably enough that recall of surgery did not occur when the anesthetic dose had to be reduced because of major trauma. The authors conclude that the incidence of recall of surgery in victims of major trauma is considerable, and that reducing the dose of anesthetic increases this incidence, despite the presence of conditions known to reduce anesthetic requirement.

Controlled Hypotension with Adenosine in Cerebral Aneurysm Surgery

Abstract: The cardiovascular effects of adenosine-induced controlled hypotension were studied in 10 patients undergoing cerebral aneurysm surgery. Adenosine and its metabolites were measured in arterial plasma using high-pressure liquid chromatography. Whole body and cerebral arteriovenous oxygen content diff

Smoking and anesthesia: preoperative abstinence and perioperative morbidity.

Abstract: Much less is known of the effects of stopping smoking than of continuing to smoke, and many of the studies on smoking cessation are concerned with long-term effects rather than effects within 48 hr. Studies concerned with this period are required, especially in terms of postoperative respiratory morbidity, before an authoritative assessment can be made of the benefits and risks of stopping smoking in the short period before operation. Present studies are convincing that great benefit will accrue in the cardiovascular system, mainly from carbon monoxide and nicotine elimination, after 12-24 h. A few days may greatly improve ciliary beating and 1-2 weeks provide a significant reduction in sputum volume. However, a minimum period of 4-6 weeks would seem appropriate to greatly influence postoperative respiratory morbidity, although the statement that "one needs 4-6 weeks to influence postoperative respiratory morbidity" must not be misapplied and become "there is no point in giving up smoking unless it is 4-6 weeks prior to operation." There are no proven disadvantages to the respiratory system from stopping smoking in the short term, and it seems unwise to sacrifice proven advantages for a theoretic consideration that sputum may become "stickier" and more difficult to clear. Less is known with regard to the time course of offset of smoking effects on drug metabolism and the immune system, although 6-8 weeks would be expected to produce some benefit.(ABSTRACT TRUNCATED AT 250 WORDS)

Pulmonary and systemic hemodynamic responses to ketamine in infants with normal and elevated pulmonary vascular resistance

Abstract: Avoidance of ketamine has been recommended in children with pulmonary hypertension or with limited right ventricular reserve, despite absence of data about the effects of ketamine on pulmonary vascular resistance (PVR) in children. Ketamine has been associated with increased PVR in studies of adults; in these studies adults were spontaneously breathing through unprotected airways, despite ketamine's known effects of ventilatory depression and partial loss of airway. The authors measured pulmonary and systemic hemodynamic responses to ketamine during spontaneous ventilation in 14 intubated infants who were receiving minimal ventilatory support with an intermittent mandatory ventilation (IMV) of 4 at an FIO2 of 0.3-0.4. No significant changes were found in cardiac index (CI), pulmonary vascular resistance index (PVRI), or systemic vascular resistance index (SVRI) in a group of seven infants with normal PVRI or in another group of seven infants with preexisting increased PVRI. Results did not differ in infants receiving diazepam sedation. The authors conclude that ketamine has little effect on baseline hemodynamics in mildly sedated infants whose airway and ventilation are maintained; in particular, PVRI is little changed by ketamine administration in ventilated infants with either normal or increased baseline PVRI.

Pharmacokinetic aspects of intrathecal morphine analgesia.

Abstract: Fifteen patients undergoing thoracotomy were given 0.25 or 0.50 mg morphine intrathecally (L2-L3 or L3-L4) for an analgetic and pharmacokinetic study. Administration of morphine at the end of the operation resulted in a highly variable duration of analgesia ranging from 1-20.5 and 1-40 h for the 0.25 and 0.50 mg groups, respectively. Calculation of cumulative consumption pattern of additional analgesics given im indicated a dose-related analgesia lasting around 12 h. Morphine concentrations in the CSF were high and dose dependent. Thus, at 1 h, CSF concentrations (means +/- SEM) were 4,228 +/- 361 ng/ml and 10,447 +/- 1,538 ng/ml for the 0.25 and 0.50-mg groups, respectively. The plasma concentrations generally were very low, i.e., under 1 ng/ml. For the 0.50 and 0.25 mg groups, the terminal elimination half-life in CSF was 175 +/- 9 min and 196 +/- 13 min, respectively: the volume of CSF distribution was 0.88 +/- 0.16 ml X kg-1 and 1.06 +/- 0.17 ml X kg-1, respectively: and the clearance from CSF was 2.81 +/- 0.41 microliter X kg-1 X min-1 and 3.41 +/- 0.55 microliter X kg-1 X min-1, respectively (means +/- SEM). The study indicates that the significant pharmacokinetic parameter related to the long duration of analgesia after intrathecal morphine administration probably is the high CSF concentrations found, since the rate of elimination from CSF is similar to what is reported for morphine in plasma. Furthermore, modulation of nociceptive input in the thoracic region also may be achieved by lumbar administration, but a slower onset should be anticipated.

Rapid tracheal intubation with vecuronium: the priming principle.

Abstract: Following the administration of a single 0.1 mg/kg dose of vecuronium bromide, satisfactory conditions for tracheal intubation developed in 156 +/- 12 s (mean +/- SEM), and the clinical duration of the initial dose was 36 +/- 2 min. When the initial dose of vecuronium was administered in two increments, a 0.015 mg/kg "priming" dose, followed 6 min later by a 0.050 mg/kg "intubating" dose, intubation time decreased to 61 +/- 3 s and clinical duration to 21 +/- 1 min. The priming dose that had no unpleasant effect on premedicated, awake patients could be administered 3-4 min before, and the intubating dose 2 to 3 min after induction of anesthesia. With the described technique, comparable intubating conditions could be obtained just as rapidly with vecuronium as with succinylcholine chloride, without subjecting the patients to the side effects of and the complications occasionally encountered with succinylcholine. An added advantage of the use of a priming dose is that it will reveal undiagnosed, pathologic, or idiopathic increase of sensitivity to nondepolarizing muscle relaxants.

Lidocaine constricts or dilates rat arterioles in a dose-dependent manner.

Abstract: The microvascular effects of varying concentrations of lidocaine were evaluated with the use of videomicroscopy in an in vivo rat cremaster muscle preparation. Animals were anesthetized with chloralose and urethane and breathed room air spontaneously. Mean arterial pressure and heart rate were measured via a carotid artery cannula. The cremaster muscle was suffused with a balanced electrolyte solution and pH, temperature, PO2, PCO2, and osmolarity were controlled. Internal diameters of fourth-order arterioles in the cremaster muscle were measured with an electronic vernier system. In one group of animals (n = 7), arteriolar diameters were measured every 30 s during a 10-min control period, a 10-min period of topical application of lidocaine hydrochloride, and a 10-min recovery period. Lidocaine hydrochloride, 10(0), 10(1), 10(2), 10(3), or 10(4) micrograms X ml-1, produced changes in arteriolar diameters to 88.9 +/- 0.9, 79.0 +/- 1.3, 67.5 +/- 2.4, 60.1 +/- 3.4, and 127.1 +/- 7.2 per cent of control, respectively (P less than 0.001). In a second group of animals (n = 4), fourth-order arteriolar diameters were measured during administration of intravenous lidocaine, 1.2 mg X kg-1 bolus plus 0.3 mg X kg-1 X min-1. Vasoconstriction to 91.3 +/- 0.9% of control was observed (P less than 0.001). These results demonstrate a biphasic dose-dependent response to lidocaine. At lesser concentrations, including those that occur in the plasma of patients during intravenous infusion or nerve blocks, dose-related vasoconstriction occurred. Lidocaine, 10(4) micrograms X ml-1, a concentration similar to that which occurs at the site of injection during infiltration, nerve block, or epidural anesthesia, produced vasodilation.(ABSTRACT TRUNCATED AT 250 WORDS)

Photodegradation of sodium nitroprusside: biologic activity and cyanide release.

Abstract: Because the belief that cyanide is released from nitroprusside in vivo recently was challenged, the authors performed a series of experiments that examined the conditions under which nitroprusside is degraded. These experiments include an examination of the release of cyanide and nitric oxide from nitroprusside in vitro, the release of cyanide in vivo, and a comparison of the biologic activity of intact and degraded nitroprusside. Nitroprusside in aqueous solution degraded when exposed to white or blue light but not to red light. While light at 20 microW X cm-2 produced 40% apparent photodegradation after 6 h exposure, while white light at 220 microW X cm-2 produced 100% apparent photodegradation after 2 h exposure. At 10% apparent photodegradation, 10% of the nitrosyl ligand was recovered as free nitric oxide, and 0.4% of the cyanide ligand was recovered as free cyanide. Following a 2-h infusion of light-protected nitroprusside in seven patients, cyanide concentrations ranged from 1.4 to 45.5 microM and 0.09 to 3.2 microM in blood and plasma, respectively. These values were not changed by exposing the samples to white light (220 microW X cm-2) for 4 h. Intact and photodegraded nitroprusside produced identical hypotensive responses in rats as would be expected, since the nitrosyl ligand was detected in solution following degradation, and it mediates this action. Cyanide was released from nitroprusside, both on its exposure to light in vitro and also in vivo. The latter was not an artifact of the assay for cyanide. Nitroprusside releases cyanide in vivo, and cyanide toxicity is a true complication of its use.

Effects of infrarenal aortic cross-clamping on renal hemodynamics in humans.

Abstract: While the systemic cardiovascular consequences of infrarenal aortic cross-clamping during aortic abdominal surgery are well documented, its repercussions on renal hemodynamics in humans have not been reported. In 12 patients, scheduled for elective aortic surgery, renal clearances, using 51Cr EDTA a

Comparison of Histamine Release in Human Skin Mast Cells Induced by Morphine, Fentanyl, and Oxymorphone

Abstract: Human leukocyte and skin mast cell preparations were incubated with morphine sulfate in concentrations ranging from 1.5 X 10(-5) M to 4.5 X 10(-3) M. Skin mast cells also were incubated with oxymorphone and fentanyl in the same concentrations. Human leukocytes did not release histamine in response to any concentration of morphine. In skin mast cells, histamine release by morphine first was detected at 1.5 X 10(-4) M. Histamine release further increased at 5.0 X 10(-4) M with no incremental increase at higher concentrations. Oxymorphone and fentanyl failed to release histamine at any concentration. Histamine release by morphine required calcium but was not influenced by changes in the 1-4 mM range. Skin mast cell preparations were pretreated for 30 min in naloxone 5 X 10(-4) M and then morphine 5 X 10(-4) M was added for 30 min without removing naloxone. Naloxone neither released histamine nor inhibited morphine-induced histamine release. The release of histamine by morphine but not equimolar concentrations of fentanyl and oxymorphone indicates that histamine release by narcotics is not a nonspecific effect of high drug concentration. The failure of naloxone to inhibit morphine-induced histamine release suggests that histamine release by morphine is not dependent on opiate receptor binding or activation. These results indicate that this human mast cell preparation will be useful in further understanding the mechanism of histamine release induced by morphine and other agents.