Mind-body response and neurophysiological changes during stress and meditation: central role of homeostasis.

Stress profoundly impacts quality of life and may lead to various diseases and conditions. Understanding the underlying physiological and neurological processes that take place during stress and meditation techniques may be critical for effectively treating stress-related diseases. The article examines a hypothetical physiological homeostatic response that compares and contrasts changes in central and peripheral oscillations during stress and meditation, and relates these to changes in the autonomic system and neurological activity. The authors discuss how cardiorespiratory synchronization, which occurs during the parasympathetic response and meditation, influences and modulates activity and oscillations of the brain and autonomic nervous system. Evidence is presented on how synchronization of cardiac and respiratory rates during meditation may lead to a homeostatic increase in cellular membrane potentials in neurons and other cells throughout the body. These potential membrane changes may underlie the reduced activity in the amygdala, and other cortical areas during meditation, and research examining these changes may foster better understanding of the restorative properties and health benefits of meditation.

Acute chest syndrome after abdominal surgery in children with sickle cell disease: Is a laparoscopic approach better?

BACKGROUND/PURPOSE: Acute chest syndrome (ACS) is the leading cause of hospitalization and death among patients with sickle cell disease (SCD). Surgery is a risk factor for the development of ACS. It has been suggested that laparoscopic surgery could diminish the risk of sickle-related complications; therefore, more procedures may be encouraged in asymptomatic patients. The goal of the authors was to determine the incidence of postoperative ACS and assess for predisposing factors in all sickle cell patients undergoing abdominal surgery. METHODS: A retrospective analysis of all sickle cell patients receiving abdominal surgery (open and laparoscopic) between 1994 and 1998 was conducted. Data pertaining to demographics, perioperative clinical status, postoperative care, and outcome were collected and analyzed using Student's t test or chi(2) where appropriate. RESULTS: Fifty-four children underwent 62 procedures (35 abdominal and 27 extracavitary). All abdominal cases were either cholecystectomy or splenectomy (22 laparoscopic and 13 open). ACS occurred in 7 of 62 (11.3%) overall, and all were in abdominal cases 7 of 35 (20%). ACS occurred in 5 of 22 (22.7%) laparoscopic cases and 2 of 13 (15.4%) open cases. Operating time was significantly longer in the laparoscopic group compared with open cases (P <.05). A higher percentage of patients who had ACS had at least 1 previous episode (71.4% v 39.3%; P value not significant) and a smaller percentage of ACS patients received a preoperative blood transfusion (14.3% v 32.1%; P value not significant). Postoperative hospitalization was prolonged if ACS occurred (9 +/- 2 v 3 +/- 2 days; P <.05). CONCLUSIONS: Abdominal surgery carries a significantly high risk (20%) of ACS. Laparoscopy does not decrease the incidence of ACS compared with open approach. Predisposing factors were not significant in predicting postoperative ACS. There is considerable morbidity and potential cost implications in patients with ACS.

The effect of magnesium deficiency on volatile anaesthetic requirement in the rat: the role of central noradrenergic neuronal activity.

Volatile anaesthetic minimum alveolar concentration (MAC, a measure of anaesthetic requirement) increased in a time-dependent manner in rats fed a Mg2+-deficient diet. MAC values in hypomagnesemic rats were 22-30 per cent greater than those in age-matched controls at 12 and 17 days after starting the diet (p < 0.01). Noradrenergic neuronal activity, as assessed from the ratio of the concentration of 3,4-dihydroxyphenylethylene-glycol (DHPG) to that of norepinephrine (NE), decreased in the brain stem and cerebrum-cerebellum in hypomagnesemic rats owing to an increase in NE concentration in both regions of the brain (p < 0.025). We conclude that prolonged hypomagnesemia (> or = 12 days) increases volatile anaesthetic MAC in the rat. The concomitant decrease in the ratio of DHPG/NE suggests that this increase in MAC cannot be attributed to an increase in noradrenergic neuronal activity in brain.

Dose-response relationship and infusion requirement of cisatracurium besylate in infants and children during nitrous oxide-narcotic anesthesia.

BACKGROUND: To determine the effect of age on the dose-response relation and infusion requirement of cisatracurium besylate in pediatric patients, 32 infants (mean age, 0.7 yr; range, 0.3-1.0 yr) and 32 children (mean age, 4.9 yr; range, 3.1-9.6 yr) were studied during thiopentone-nitrous oxideoxygen-narcotic anesthesia. METHODS: Potency was determined using a single-dose (20, 26, 33, or 40 microg/kg) technique. Neuromuscular block was assessed by monitoring the electromyographic response of the adductor pollicis to supramaximal train-of-four stimulation of the ulnar nerve at 2 Hz. RESULTS: Least-squares linear regression analysis of the log-probit transformation of dose and maximal response yielded median effective dose (ED50) and 95% effective dose (ED95) values for infants (29+/-3 microg/kg and 43+/-9 microg/kg, respectively) that were similar to those for children (29+/-2 microg/kg and 47+/-7 microg/kg, respectively). The mean infusion rate necessary to maintain 90-99% neuromuscular block during the first hour in infants (1.9+/-0.4 microg x kg(-1) x min(-1); range: 1.3-2.5 microg x kg(-1) x min(-1)) was similar to that in children (2.0+/-0.5 microg x kg(-1) x min(-1); range: 1.3-2.9 microg x kg(-1) x min(-1)). CONCLUSION: The authors conclude that cisatracurium is equipotent in infants and children when dose is referenced to body weight during balanced anesthesia.

Development through self-assessment: strategies used during clinical nursing placements.

The question asked for this small research project was 'how do senior students judge their progress towards being a "good nurse"?' A qualitative approach was taken and a convenience sample of 10 student midwives identified. Interviews were the main source of data collection. Since the method of analysis was that of grounded theory, the interviews became more focused as themes emerged. Results demonstrated that each student developed a range of self-assessment strategies which were used in any clinical placement. Some techniques were used only at a certain stage in a clinical placement while others were used throughout. Cyclical techniques were related to the achievement of short-term goals; strategies used for the duration of the placement had more long-term significance. Highlights of the findings were explored in the literature. These features included models of professional development, the need to feel part of a team, the necessity of identifying a role model, and the significance of the length of a clinical placement. Conclusions related to the duration of a clinical placement and the necessity for the student to have the opportunity to complete the cycle. The value of acquainting new students with self-assessment strategies is suggested.

Dose-response of rocuronium bromide in children anesthetized with propofol: a comparison with succinylcholine.

BACKGROUND: The aim of this study was to determine the potency of rocuronium during propofol/fentanyl/N2O anesthesia in children and to compare the time course of action of rocuronium at doses of two and three times the ED95 with that of succinylcholine. METHODS: Rocuronium (120, 160, 200, or 240 microg/kg) was administered to 48 children aged 2-10 yr. Neuromuscular block was assessed by monitoring the electromyographic response of the adductor digiti minimi to supramaximal stimulation of the ulnar nerve at 2 Hz for 2 s every 10 s. Potency was determined by log-probit transformation and least-squares linear regression analysis of dose and response. In a second group of 30 children, the onset and recovery profile of rocuronium at doses of two and three times the ED95 was compared with that of succinylcholine (2 mg/kg). RESULTS: Values for ED50 and ED95 were 210 +/- 24 and 404 +/- 135 microg/kg, respectively. The time to 90% neuromuscular block after 1.2 mg/kg rocuronium (three times the ED95), 33 +/- 5 s (mean +/- SD), did not differ significantly from that after succinylcholine, at 30 +/- 7 s; however, both were significantly less than that after 0.8 mg/kg rocuronium, 46 +/- 8 s (P < 0.05). The time to 25% recovery from 1.2 microg/kg rocuronium, 41 +/- 13 min, was approximately 50% greater than that after 0.8 mg/kg, at 27 +/- 6 min (P < 0.001), and eight times greater than that after succinylcholine, at 5.2 +/- 1.9 min (P < 0.001). CONCLUSIONS: Both 1.2 mg/kg rocuronium (three times the ED95) and 2 mg/kg succinylcholine provide 90% neuromuscular block within 45 s in 95% of children. The present dose-response data support the use of rocuronium at a dose of 1.2 mg/kg when rapid onset and intermediate-duration neuromuscular block are needed in children.

The neuromuscular effects of mivacurium chloride during propofol anesthesia in children.

Previous studies examined the neuromuscular effects of mivacurium in doses up to, but not exceeding, 2.5 times 95% effective dose (ED95) in children. To determine whether larger doses offer clinical advantages, we compared the onset and duration of neuromuscular block, intubating conditions, and changes in plasma histamine concentration (PHC) after mivacurium (0.2, 0.3, or 0.4 mg/kg) with those after succinylcholine (2.0 mg/kg) during propofol/N2O anesthesia in 48 children aged 3-10 yr. The evoked electromyograph (EMG) of the adductor digiti minimi after supramaximal train-of-four (TOF) stimulation was recorded. When T1 was 10% of control, laryngoscopy and intubation were performed. PHC was measured immediately before and at 2 and 5 min after administration of the relaxant. Venous blood was sampled for determination of plasma cholinesterase activity. Axillary temperature was measured. Increasing the dose of mivacurium from 0.2 to 0.3 mg/kg accelerated the onset of block (time to 90% block, 1.6 +/- 0.2 vs 1.2 +/- 0.2 min) (P < 0.001), but did not significantly prolong recovery (time to 95% recovery, 16.0 +/- 3.8 vs 18.6 +/- 3.6 min). A further increase in dose to 0.4 mg/kg produced no significant decrement in onset time, but did prolong recovery (time to 95% recovery, 23.8 +/- 5.0 min) (P < 0.001). The duration of action of mivacurium 0.3 and 0.4 mg/kg correlated inversely with plasma cholinesterase activity. PHC increased significantly after mivacurium 0.3 and 0.4 mg/kg; however, mean arterial pressure did not change significantly. We conclude that mivacurium 0.3 mg/kg provides a relatively rapid onset and short duration of neuromuscular block in healthy children. Increasing the dose to 0.4 mg/kg does not significantly accelerate the onset of neuromuscular block.

Additive contribution of nitrous oxide to sevoflurane minimum alveolar concentration for tracheal intubation in children.

BACKGROUND: To study the interaction between nitrous oxide and sevoflurane during trachea intubation, the authors determined the minimum alveolar concentration of sevoflurane for tracheal intubation (MAC(TI)) with and without nitrous oxide in children. METHODS: Seventy-two children aged 1-7 yr were assigned randomly to receive one of three end-tidal concentrations of nitrous oxide and one of four end-tidal concentrations of sevoflurane: 0% nitrous oxide with 2.0, 2.5, 3.0, or 3.5% sevoflurane: 33% nitrous oxide with 1.5, 2.0, 2.5, or 3.0% sevoflurane; or 66% nitrous oxide with 1.0, 1.5, 2.0, or 2.5% sevoflurane. After steady state end-tidal anesthetic concentrations were maintained for at least 10 min, laryngoscopy and intubation were attempted using a straight-blade laryngoscope and an uncuffed tracheal tube. The interaction between nitrous oxide and sevoflurane was investigated using logistic regression analysis of the responses to intubation. RESULTS: Logistic regression curves of the probability of no movement in response to intubation in the presence of sevoflurane and 0, 33, and 66% nitrous oxide were parallel. The interaction coefficient between nitrous oxide and sevoflurane did not differ significantly from zero (P = 0.89) and was removed from the logistic model. The MAC(TI) (+/- SE) of sevoflurane was 2.66+/-0.16%, and the concentration of sevoflurane required to prevent movement in 95% of children was 3.54+/-0.25%. Thirty-three percent and 66% nitrous oxide decreased the MAC(TI) of sevoflurane by 18% and 40% (P<0.001), respectively. CONCLUSIONS: We conclude that nitrous oxide and sevoflurane suppress the responses to tracheal intubation in a linear and additive fashion in children.

The effect of adenosine-induced hypotension on systemic and splanchnic hemodynamics during halothane or sevoflurane anesthesia in the rat.

BACKGROUND: It has been suggested that the liver may be at risk for ischemic damage during adenosine-induced hypotension. This notion, however, is somewhat inconsistent with the understanding that adenosine is a powerful vasodilator of the splanchnic circulation. To help clarify the effect of adenosine-induced hypotension on splanchnic hemodynamics, we studied the systemic and splanchnic hemodynamic responses to adenosine, both alone and in the presence of halothane or sevoflurane. METHODS: Systemic and splanchnic hemodynamics were determined during the infusion of adenosine in 36 rats allocated randomly to one of three study groups: (1) awake, (2) halothane anesthesia (1.0 MAC), or (3) sevoflurane anesthesia (1.0 MAC). Adenosine was infused at a rate sufficient to decrease the mean arterial pressure by 35-38% from awake control values. Cardiac output and organ blood flows were measured using the radiolabeled microsphere technique. RESULTS: Adenosine infusion produced stable hypotension of rapid onset due to a reduction in systemic vascular resistance. Stroke volume increased, but cardiac output remained unchanged in the awake and sevoflurane groups because of a decrease in heart rate. Infusion of adenosine during halothane anesthesia increased cardiac output enough to compensate for the decrease in cardiac output due to halothane alone. In the splanchnic circulation, there was an increase in portal tributary (42%, P < 0.01) and hepatic arterial (38%, P < 0.05) blood flows during adenosine infusion in awake rats. This resulted in an overall increase in total liver blood flow (42%, P < 0.01). Halothane anesthesia was associated with a decrease in portal tributary blood flow (28%, P < 0.05). In contrast, sevoflurane anesthesia was associated with an increase in hepatic arterial flow (35%, P < 0.05) but with no change in portal tributary blood flow. During halothane anesthesia, adenosine infusion increased portal tributary (90%, P < 0.01) and hepatic arterial (37%, P < 0.05) blood flows, thereby increasing total liver blood flow to values similar to those in awake adenosine-infused rats. During sevoflurane anesthesia, adenosine infusion increased portal tributary blood flow (48%, P < 0.01), but hepatic arterial blood flow did not increase beyond the values observed during sevoflurane anesthesia alone. CONCLUSIONS: These findings demonstrate that adenosine is a potent vasodilator of portal tributary and hepatic arterial vasculature in the rat and that the splanchnic hemodynamic effects of adenosine predominate over those of halothane and sevoflurane.

Hemodynamic and organ blood flow responses to halothane and sevoflurane anesthesia during spontaneous ventilation.

This study compared systemic hemodynamic and organ blood flow responses to equipotent concentrations of halothane and sevoflurane during spontaneous ventilation in the rat. The MAC values for halothane and sevoflurane were determined. Cardiac output and organ blood flows were measured using radiolabeled microspheres. Measurements were obtained in awake rats (control values) and at 1.0 MAC halothane or sevoflurane. The MAC values (mean +/- SEM) for halothane and sevoflurane were 1.10% +/- 0.05% and 2.40% +/- 0.05%, respectively. The PaCO2 increased to a similar extent in both groups compared with control values. During halothane anesthesia, heart rate decreased by 12% (P < 0.01), cardiac index by 26% (P < 0.01), and mean arterial blood pressure by 18% (P < 0.01) compared with control values. Stroke volume index and systemic vascular resistance did not change. During sevoflurane anesthesia, hemodynamic variables remained unchanged compared with control values. Coronary blood flow decreased by 21% (P < 0.01) and renal blood flow by 18% (P < 0.01) at 1.0 MAC halothane, whereas both remained unchanged at 1.0 MAC sevoflurane. Cerebral blood flow increased to a greater extent with halothane (63%; P < 0.01) than with sevoflurane (35%; P < 0.05). During halothane anesthesia, hepatic arterial blood flow increased by 48% (P < 0.01), whereas portal tributary blood flow decreased by 28% (P < 0.01). During sevoflurane anesthesia, hepatic arterial blood flow increased by 70% (P < 0.01) without a concomitant reduction in portal tributary blood flow. Total liver blood flow decreased only with halothane (16%; P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of hypoxia and isoflurane on liver blood flow: the role of adenosine.

We investigated the role of endogenous adenosine in mediating the effects of hypoxia and isoflurane on portal tributary blood flow (PTBF) and hepatic arterial blood flow (HABF) in rats. Liver blood flows were determined using radiolabelled microspheres. Hypoxia resulting from the exposure of rats to an atmosphere containing 15% oxygen for 30 min decreased PTBF (23%) (P<0.05) and cardiac index (15%) (P<0.05), and increased HABF (78%) (P<0.05). Isoflurane (1.4 vol%) increased HABF in both normoxic and hypoxic conditions but did not affect PTBF. The adenosine receptor antagonist 8-phenyltheophylline attenuated the hypoxia-induced increase in HABF but did not affect that resulting from the administration of isoflurane. In conclusion, in contrast to the increase in HABF induced by hypoxia, that induced by isoflurane appears to be independent of endogenous adenosine.

Recovery characteristics of propofol anaesthesia, with and without nitrous oxide: a comparison with halothane/nitrous oxide anaesthesia in children.

Few studies have examined whether nitrous oxide influences the recovery characteristics of propofol anaesthesia. The present study examined the effect of nitrous oxide on the recovery characteristics of propofol anaesthesia, and compared these data with those for halothane/nitrous oxide anaesthesia. Sixty children aged 3-12 years were assigned at random to receive one of three maintenance regimens: propofol with or without nitrous oxide (70%) or halothane/nitrous oxide (70%). During propofol/N2O anaesthesia, the infusion rate of propofol (180 +/- 39 micrograms.kg-1.min-1) required to maintain the mean arterial pressure and heart rate within 20% of the baseline values was significantly less than that during propofol/O2 (220 +/- 37 micrograms.kg-1.min-1; P < 0.005). The time from discontinuation of anaesthesia to eye-opening (11 +/- 6 min), to response to commands (12 +/- 6 min), and to return of full wakefulness (21 +/- 10 min) after propofol/N2O were similar to those after propofol/O2, but significantly less (by approximately 30%) than those after halothane (P < 0.05). The overall incidence of emesis after propofol/N2O (53%) was greater than that after propofol/O2 (17%, P < 0.05) and comparable to that after halothane/N2O (58%). These data suggest that N2O has little effect on the rate of recovery after propofol, but significantly increases the incidence of postoperative emesis, thereby attenuating one of the main attributes of propofol anaesthesia.

An evaluation of the quality of clinical trials in anesthesia.

BACKGROUND: The authors evaluated the quality of clinical trials published in four anesthesia journals during the 20-yr period from 1981-2000. METHODS: Trials published in four major anesthesia journals during the periods 1981-1985, 1991-1995, and the first 6 months of 2000 were grouped according to journal and year. Using random number tables, four trials were selected from all of the eligible clinical trials in each journal in each year for the periods 1981-1985 and 1991-1995, and five trials were selected from all of the trials in each journal in the first 6 months of 2000. Methods and results sections from the 160 trials from 1981-1985 and 1991-1995 were randomly ordered and distributed to three of the authors for blinded review of the quality of the study design according to 10 predetermined criteria (weighted equally, maximum score of 10): informed consent and ethics approval, eligibility criteria, sample size calculation, random allocation, method of randomization, blind assessment of outcome, adverse outcomes, statistical analysis, type I error, and type II error. After these trials were evaluated, 20 trials from the first 6 months of 2000 were randomly ordered, distributed, and evaluated as described. RESULTS: The mean (+/- SD) analysis scores pooled for the four journals increased from 5.5 +/- 1.4 in 1981-1985 to 7.0 +/- 1.1 in 1991-1995 (P < 0.00001) and to 7.8 +/- 1.5 in 2000. For 7 of the 10 criteria, the percentage of trials from the four journals that fulfilled the criteria increased significantly between 1981-1985 and 1991-1995. During the 20-yr period, the reporting of sample size calculation and method of randomization increased threefold to fourfold, whereas the frequency of type I statistical errors remained unchanged. CONCLUSION: Although the quality of clinical trials in four major anesthesia journals has increased steadily during the past two decades, specific areas of trial methodology require further attention.

Haemodynamic and organ blood flow responses to sevoflurane during spontaneous ventilation in the rat: a dose-response study.

To determine the systemic haemodynamic and organ blood flow responses to the administration of sevoflurane during spontaneous ventilation, heart rate, cardiac index, mean arterial pressure, arterial blood gases, and blood flows to the brain, spinal cord, heart, kidneys and splanchnic organs were measured awake (control values) and after 30 min of anaesthesia with 0.5, 1.0, 1.2 or 1.5 MAC sevoflurane in rats. Cardiac output and organ blood flows were measured using radiolabelled microspheres. The MAC (mean +/- SEM) of sevoflurane was found to be 2.30 +/- 0.05%. At each concentration, haemodynamic variables were similar to awake values with the exception of a 12% reduction in mean arterial pressure at 1.5 MAC (P less than 0.01). Arterial PCO2 increased in a dose-related fashion. Cerebral and spinal cord blood flows increased at 1.2 and 1.5 MAC whereas coronary and renal blood flows did not change significantly. Portal tributary blood flow and preportal vascular resistance were unaffected. Hepatic arterial flow increased by 63% at 1.5 MAC (P less than 0.05) but total liver blood flow remained unchanged compared with awake values. In conclusion, the administration of sevoflurane during spontaneous ventilation produces a high degree of cardiovascular stability and maintains blood flow to major organs in the rat.

Effect of propofol infusion on splanchnic hemodynamics and liver oxygen consumption in the rat. A dose-response study.

BACKGROUND: Propofol has been used for the maintenance of anesthesia. The effects of propofol infusion on splanchnic hemodynamics and liver oxygen consumption, however, have not been reported. In the current investigation, the authors studied the effects of a continuous infusion of propofol on systemic and splanchnic hemodynamics using a new method to measure liver oxygen consumption in awake control and anesthetized rats. METHODS: Cannulas were inserted into the left ventricle, femoral artery, portal vein, and hepatic vein during ether anesthesia, and the rats were allowed to awaken and recover for 3-4 h before study. Animals were infused for 30 min with either saline (controls) or propofol at a rate of 300, 600, 900, or 1,200 micrograms.kg-1 x min-1. Cardiac output and organ blood flows were measured using radiolabelled microspheres, and blood samples from the femoral artery, portal vein, and hepatic vein were used to determine liver oxygen consumption. RESULTS: Mean arterial pressure decreased in a dose-dependent manner with a 25% reduction at the highest infusion rate. Systemic vascular resistance similarly decreased, whereas cardiac output remained unchanged at all the infusion rates. Hepatic arterial blood flow increased in a dose-dependent fashion over the dose range studied, to a maximum increase of 120%. Portal tributary blood flow increased by 30% at the highest infusion rate. Total liver blood flow increased in a dose-dependent manner to a maximum of 38%. Total oxygen delivery to the liver by the hepatic artery and portal vein increased in a dose-dependent fashion. Liver oxygen consumption increased in a dose-dependent fashion to a maximum increase of 51% at an infusion rate of 1,200 micrograms.kg-1 x min-1. The percent of oxygen extracted by the liver was not altered by propofol infusion, and hepatic venous oxygen saturation did not decrease at any dose studied. Coronary and renal blood flows were not altered. Arterial PaCO2, increased from 31 +/- 2 mmHg in awake control rats to 41 +/- 2 mmHg in spontaneously breathing rats infused with 1,200 micrograms.kg-1 x min-1 propofol. CONCLUSIONS: The maintenance of anesthesia using an infusion of propofol resulted in an increase in liver oxygen consumption that was fully compensated for by an increase in oxygen delivery to the liver. Splanchnic hemodynamics and liver oxygenation are not adversely affected during maintenance of anesthesia with propofol in the normal rat.