Effects of acute plasma volume expansion on renal perfusion, filtration, and oxygenation after cardiac surgery: a randomized study on crystalloid vs colloid.

BACKGROUND: In the present randomized study, we evaluated the differential effects of a colloid and a crystalloid fluid on renal oxygen delivery (RD(O2)), glomerular filtration (GFR), renal oxygen consumption ((RV(O2))), and the renal oxygen supply-demand relationship (i.e., renal oxygenation) after cardiac surgery with cardiopulmonary bypass. METHODS: Thirty patients with normal preoperative renal function, undergoing uncomplicated cardiac surgery, were studied in the intensive care unit in the early postoperative period. Patients were randomized to receive a bolus dose of either a crystalloid (Ringers-acetate 20 ml kg(-1), n=15) or a colloid solution (Venofundin) 10 ml kg(-1), n=15). Systemic haemodynamics were measured via a pulmonary artery catheter. Renal blood flow and GFR were measured by the renal vein retrograde thermodilution technique and by renal extraction of 51Cr-EDTA (=filtration fraction). Arterial and renal vein blood samples were obtained for measurements of renal oxygen delivery (RD(O2)) and RV(O2). Renal oxygenation was estimated from the renal oxygen extraction. RESULTS: Despite an increase in cardiac index and renal blood flow with both fluids, neither of the fluids improved RD(O2), because they both induced haemodilution. The GFR increased in the crystalloid (28%) but not in the colloid group. The crystalloid increased the filtration fraction (24%) and renal oxygen extraction (23%), indicating that the increase in GFR, the major determinant of RV(O2), was not matched by a proportional increase in RD(O2). CONCLUSIONS: Neither the colloid nor the crystalloid improved RD(O2) when used for postoperative plasma volume expansion. The crystalloid-induced increase in GFR was associated with impaired renal oxygenation, which was not seen with the colloid. CLINICAL TRIAL REGISTRATION: NCT01729364.

Low-dose vasopressin increases glomerular filtration rate, but impairs renal oxygenation in post-cardiac surgery patients.

BACKGROUND: The beneficial effects of vasopressin on diuresis and creatinine clearance have been demonstrated when used as an additional/alternative therapy in catecholamine-dependent vasodilatory shock. A detailed analysis of the effects of vasopressin on renal perfusion, glomerular filtration, excretory function and oxygenation in man is, however, lacking. The objective of this pharmacodynamic study was to evaluate the effects of low to moderate doses of vasopressin on renal blood flow (RBF), glomerular filtration rate (GFR), renal oxygen consumption (RVO2) and renal oxygen extraction (RO2Ex) in post-cardiac surgery patients. METHODS: Twelve patients were studied during sedation and mechanical ventilation after cardiac surgery. Vasopressin was sequentially infused at 1.2, 2.4 and 4.8 U/h. At each infusion rate, systemic haemodynamics were evaluated by a pulmonary artery catheter, and RBF and GFR were measured by the renal vein thermodilution technique and by renal extraction of 51chromium-ethylenediaminetetraacetic acid, respectively. RVO2 and RO2Ex were calculated by arterial and renal vein blood samples. RESULTS: The mean arterial pressure was not affected by vasopressin while cardiac output and heart rate decreased. RBF decreased and GFR, filtration fraction, sodium reabsorption, RVO2, RO2Ex and renal vascular resistance increased dose-dependently with vasopressin. Vasopressin exerted direct antidiuretic and antinatriuretic effects. CONCLUSIONS: Short-term infusion of low to moderate, non-hypertensive doses of vasopressin induced a post-glomerular renal vasoconstriction with a decrease in RBF and an increase in GFR in post-cardiac surgery patients. This was accompanied by an increase in RVO2, as a consequence of the increases in the filtered tubular load of sodium. Finally, vasopressin impaired the renal oxygen demand/supply relationship.

Preload changes by positive pressure ventilation can be used for assessment of left ventricular systolic function.

BACKGROUND: Assessment of preload independent left ventricular function with conductance volumetry is traditionally accomplished by inflating a balloon in the inferior caval vein. Our aim was to investigate if a similar change in preload could be achieved by positive pressure ventilation with large tidal volume. METHODS: Conductance volumetry generating left ventricular pressure-volume loops was used in seven pentobarbital-anesthetized pigs. Changes in preload recruitable stroke work were studied, comparing the effects of inferior vena cava occlusion (IVCO) or large tidal volume (LTV). Cardiodepression was induced by halothane anesthesia and halothane + phenylephrine, and stimulation by epinephrine infusion. RESULTS: Although the decreasis in left ventricular end diastolic volume was slightly less with LTV (16.5 +/- 1.7 ml, mean +/- SEM) than with IVCO (22.4 +/- 1.7 ml) (P < 0.0001) the PRSW-slopes showed a high degree of correlation (r=0.80, P < 0.0001). Although peak tracheal pressures increased significantly to 27.8 +/- 0.9 mmHg during LTV, esophageal pressures (used as an indicator of pericardial pressure) were unchanged. CONCLUSIONS: Positive pressure ventilation with LTV is similar to IVCO in creating transient changes in preload, necessary for assessment of left ventricular systolic function. This observation was valid also during drug-induced cardiac depression and stimulation. The preload recruitable stroke work used for this validation was shown to be a reliable and stable method.

Interpretation of radial pulse contour during fentanyl/nitrous oxide anesthesia and mechanical ventilation.

BACKGROUND: Peripheral arterial blood pressure is not a reliable substitute for proximal aortic pressure. Recognition of this phenomenon is important for correct appreciation of cardiac afterload. Our aim was to evaluate the utility of the radial pulse wave to better understand ventriculo-vascular coupling during anesthesia. METHODS: We observed the differences between aortic systolic pressure (AoSAP, tipmanometry) and radial systolic pressure in 15 patients, (including two women) aged 53-78 years, before coronary artery bypass surgery. We studied the induction of anesthesia with fentanyl (20 microg kg-1), moderate volume loading, and thereafter the addition of 70% nitrous oxide. The circulatory effects of mechanical ventilation were studied by doubling the tidal volumes. Pulse wave contours were assessed by calculation of radical and aortic augmentation indices (AI), which measure the second systolic pressure peak. RESULTS: Radial systolic pressure was higher than AoSAP in the control situation (8+/-2 mmHg), and this SAP gradient increased further with fentanyl (12+/-2 mmHg). The gradient persisted throughout the study, but was partially reduced by volume loading and nitrous oxide, respectively. Radial augmentation index was the only parameter remaining in a stepwise multivariate model to explain the variance in the SAP gradient (r2=0.48). Radial augmentation index also correlated with aortic pulse pressure (r2=0.71). Mechanical ventilation had significant and similar effects on pulse wave augmentation both in the aorta and in the radial artery, and did not affect the radial to aortic SAP gradient. CONCLUSION: These elderly coronary patients had stiff vasculature (high aortic AI) and considerable pulse wave reflection, which was beneficially delayed by fentanyl. Changes in the radial pulse wave augmentation during mechanical ventilation were mainly a result of cyclic changes in the stroke volume, and were seldom associated with an increased systolic pressure gradient from the aorta to the radial artery.

Can a clinically useful aortic pressure wave be derived from a radial pressure wave?

BACKGROUND: The information contained in arterial pressure waveforms is probably underused by most clinicians who manage critically ill patients. It is not generally known that an aortic pressure wave can be synthesized by applying a generalized transfer function to the radial arterial pressure wave. We validated a commercially available system, SphygmoCo (PWV Medical, Sydney). METHODS: Ascending aortic pressure waves were synthesized and comparisons were made between the synthesized aortic waveforms, the measured aortic and radial arterial waveforms. Ascending aortic pressure waves (catheter-tip manometer) and radial artery pressure waves (short fluid-filled catheter) were recorded simultaneously in 12 patients with angina pectoris (age 62-76 years) undergoing cardiac catheterization. Patients were studied at rest, following midazolam, sublingual nitroglycerin and during Valsalva manoeuvres. RESULTS: Both midazolam and nitroglycerin lowered mean arterial pressure but nitroglycerin caused a more selective decrease in the measured and synthesized aortic systolic pressures than in the radial artery pressure. The synthesized aortic systolic pressure was less, by 6-8 mm Hg (SD 2-3) and the synthesized aortic diastolic pressure greater, by 4 mm Hg (SD 2). Despite these differences in pulse pressure, the synthesized waveform tracked the measured waveform before and during interventions. CONCLUSIONS: By deriving an aortic waveform from the radial pulse, monitoring of left ventricular afterload can improve without more invasive means.

Is skeletal muscle luxury perfusion the main hemodynamic effect of high-dose insulin in cardiac surgery?

Insulin, in combination with glucose and potassium (GIK), can be used in heart surgery to improve hemodynamic performance. This study evaluates the role of skeletal muscle vasodilation in hemodynamic effects of high-dose GIK therapy early after coronary surgery. Thirty-three male patients undergoing coronary artery bypass grafting were included in a prospective, randomized and controlled study. Eleven patients received infusions of mixed amino acids (11.4 g) and insulin solution (225 IU insulin, glucose with the glucose clamp technique, and potassium), 11 patients received infusions of mixed amino acids (11.4 g) and 11 patients served as control subjects. During combined insulin and amino acid infusion, cardiac output increased by 13+/-3% (+0.6+/-0.2 L x min(-1)) and systemic vascular resistance decreased by 24+/-3% (-320+/-46 dyn x s x cm(-5)). The changes differed from those in the control group (CO: -0.2+/-0.1 L x min(-1), p < 0.05; SVR: +136+/-42 dyn x s x cm(-5), p < 0.05). Changes in skeletal muscle perfusion and leg vascular resistance did not differ significantly among the groups. At most, changes in leg blood flow could explain 40% of the changes in cardiac output. Skeletal muscle luxury perfusion is not the main hemodynamic effect of high-dose insulin in the early postoperative period after coronary surgery.

Aortic and radial pulse contour: different effects of nitroglycerin and prostacyclin.

UNLABELLED: Through vasorelaxation, nitroglycerin is considered to reduce arterial wave reflection and to cause a more pronounced decrease in systolic pressure in the aorta (AoSAP) than in the radial artery (RaSAP). Our aim was to study how radial and aortic pulse wave configurations and the gradient (RaSAP-AoSAP) were affected by nitroglycerin and by prostacyclin, and how these changes correlated to stroke volume, vascular resistance/impedance, and wave reflection. Prostacyclin has not been studied in this context and was chosen because, in contrast to nitroglycerin, it does not reduce stroke volume and reduces afterload by arteriolar dilation. In 18 patients (53-81 yr old; heavily premedicated before coronary artery surgery), blood pressure was measured in both the radial artery and the ascending aorta (tipmanometry), and cardiac output was measured by thermodilution. Mean arterial pressure was reduced stepwise with each drug (mean total decrease 10-12 mm Hg). The initial RaSAP-AoSAP gradient (6 mm Hg) was increased 10 mm Hg by nitroglycerin and was not affected by prostacyclin. The nitroglycerin-induced increase in systolic gradient RaSAP-AoSAP correlated to decreases in stroke volume index, mean arterial pressure, and arterial elastance, but not to decrease in pulse wave augmentation. Thus, decreases in stroke volume index, not wave reflection, seem to be the main reason for an increased RaSAP-AoSAP when nitroglycerin is used in the elderly, hypertensive patient. IMPLICATIONS: We studied ascending aortic and radial pulse contours in patients scheduled for coronary artery surgery. The radial pulse wave can be used for interpretation of central hemodynamic changes during nitroglycerin-, but not prostacyclin-, induced hypotension.

Quality of life after cardiac surgery complicated by multiple organ failure.

OBJECTIVE: To evaluate quality of life after prolonged multiple system intensive care treatment in cardiac surgical patients. DESIGN: A case-control study. SETTING: Adult 12-bed thoracic intensive care unit (ICU) at a university teaching hospital. PATIENTS: Forty-seven patients surviving multiple organ failure requiring intensive care treatment for > or = 5 days (ICU group). Patients with a completely uncomplicated postoperative course were matched to the study group with respect to gender, age, and type and date of surgery. The Nottingham Health Profile was used to assess quality of life at least 1 yr after complicated cardiac surgery. INTERVENTIONS: Quality of life measures were collected at least 1 yr after discharge from the ICU. MEASUREMENTS AND MAIN RESULTS: Seventy-five percent of the patients in the ICU group suffered from multiple organ failure involving at least three organ systems, with a mean stay in the ICU of 9.0 +/- 1.2 (SEM) days. Quality of life was considerably reduced in the ICU group, with a higher total mean score of all dimensions of quality of life (22.7 +/- 2.6) compared with the control group (13.2 +/- 2.4 [SEM])(p < .01). The Nottingham Health Profile score was higher in three of six dimensions of health--i.e., energy (p < .05), physical mobility (p < .05), and emotional reactions (p < .05)--compared with the control group. A higher percentage of patients reported problems in three of six important activities of daily life--housework (p < .05), hobbies (p < .01), and sex life (p < .01)--compared with the control group. CONCLUSION: Patients treated with prolonged multiple system intensive care after heart surgery have a poor outcome with respect to quality of life measured at least 1 yr after discharge from the ICU.

Depressed baroreflex sensitivity in patients with obstructive sleep apnea.

Muscle nerve sympathetic activity (MSA), the interval between two R-waves in the ECG, or the interbeat interval (RR-interval), and blood pressure (BP) were recorded in 10 awake patients with obstructive sleep apnea (OSA) and in nine sex- and age-matched controls. Changes in RR-interval and MSA, evoked by sodium nitroprusside-induced reduction of BP, were used to quantitate baroreflex sensitivity. Both the cardiac (expressed as the RR-interval versus mean arterial BP slope) and the muscle sympathetic (mean MSA area versus diastolic BP slope) baroreflex sensitivity were depressed in patients as compared with controls. Cardiac baroreflex slope sensitivity (expressed as a regression coefficient) was 5.5 +/- 1.2 (mean +/- SEM) in patients and 9.6 +/- 0.96 in controls (p < 0.05). The corresponding figures for the sympathetic slope sensitivity were -4.9 +/- 0.9 and -13.1 +/- 2.3, respectively (p < 0.05). Differences remained after stepwise correction for age, body mass index (BMI), and to some extent BP. Resting MSA correlated with cardiac (r = 0.67, p < 0.003) and sympathetic (r = 0.56, p < 0.025) baroreflex sensitivity in the entire study group. We conclude that OSA patients exhibit an impaired baroreflex sensitivity to a hypotensive stimulus, which may represent an adaptive response to changes in BP or hypoxemia occurring in association with nocturnal apneas. Baroreflex adaptation may also contribute to the augmentation of resting MSA observed in OSA patients in this as well as in a previous study.

Insulin increases forearm vascular resistance in obese, insulin-resistant hypertensives.

OBJECTIVE: To determine whether acutely lowering insulin levels with somatostatin in obese, insulin-resistant hypertensive individuals reduces arterial pressure and forearm vascular resistance; and whether these changes are reversed by restoring insulin levels during continuing somatostatin infusion. SUBJECTS: Subjects were 11 obese (body mass index 36 +/- 4 kg/m2) insulin-resistant, hypertensive men (systolic/diastolic blood pressures 153 +/- 6/94 +/- 2 mmHg, aged 51 +/- 7 years, fasting insulin level 17 +/- 8 mU/l). METHODS: Arterial pressure, forearm blood flow and vascular resistance were measured during 2 h of somatostatin infusion and during 2h of somatostatin plus insulin infusion (hyperinsulinemic or euglycemic clamp). RESULTS: Somatostatin infusion decreased plasma insulin levels from 17 +/- 2 to <3 mU/l. Insulin infusion raised plasma insulin levels to 86 +/- 7 mU/l. The forearm vascular resistance decreased significantly during somatostatin infusion and increased significantly during infusion of somatostatin plus insulin. Somatostatin also caused small but significant reductions in arterial pressure whereas insulin infusion during somatostatin infusion increased arterial pressure. Control experiments in six obese hypertensives indicated that the changes in forearm vascular resistance (but not in arterial pressure) were caused neither by time nor by vehicle. Control studies in six young normotensives indicated that somatostatin does not block the vasodilator response to insulin previously demonstrated in this group. CONCLUSIONS: The present results suggest that insulin causes forearm vasoconstriction in obese, insulin-resistant hypertensive humans.

Anesthetic modulation of the cardiovascular response to microlaryngoscopy. A comparison of propofol and methohexital with special reference to leg blood flow, catecholamines and recovery.

The modulating effects of propofol versus methohexital on the cardiovascular response to microlaryngoscopy were studied in 35 patients divided into four equal groups (one patient participated twice). Heart rate (HR), mean arterial blood pressure (MAP, cardiac output (CO; impedance cardiography), leg blood flow (LBF; occlusion plethysmography) and concentrations of arterial catecholamines were measured. After administration of atropine and fentanyl (2 micrograms.kg-1), anesthesia was induced by either an injection of propofol (2.0 mg.kg-1) followed by a low (6 mg.kg-1.h-1; n = 9) or a high (12 mg.kg-1.h-1; n = 9) dose propofol infusion or an injection of methohexital (1.5 mg.kg-1) followed by a low (5 mg.kg-1.h-1; n = 9) or a high (10 mg.kg-1.h-1; n = 9) dose methohexital infusion. The low methohexital infusion dose was insufficient to control MAP, which increased 41% during microlaryngoscopy compared to the awake state. The HR increased in all groups but the increase was most prominent in the low dose methohexital group. There were no statistically significant changes in CO in any group, whereas LBF increased consistently in all groups except in patients anesthetized with the low dose of methohexital. The increases of LBF in the propofol groups were intermediate and not dose dependent. The methohexital low dose group showed increases in norepinephrine levels compared to awake values and in epinephrine levels compared to the other groups. Propofol seems to differ from methohexital in modulation of peripheral vascular tone.(ABSTRACT TRUNCATED AT 250 WORDS)

Sympathetic muscle nerve activity, peripheral blood flows, and baroreceptor reflexes in humans during propofol anesthesia and surgery.

BACKGROUND: With percutaneous recordings of muscle nerve sympathetic activity (MSA), it is possible to study interactions between the autonomic nervous system and anesthetics. This study describes the effects of propofol infusion both before and during microlaryngoscopy. METHODS: Nine patients participated. MSA was recorded, muscle and skin blood flows were measured. Sodium nitroprusside-induced decreases in blood pressure were used to quantitate baroreceptor reflex sensitivity. RESULTS: During steady state propofol anesthesia (0.1 mg.kg-1.min-1), "total MSA" (MSA burst area per minute) was 37% (P < 0.05) of awake control value; leg blood flow recorded by strain-gauge plethysmography was 227% (difference not significant); and skin blood flow recorded by laser Doppler flowmetry and finger pulse plethysmography was 300% (P < 0.05) and 376% (P < 0.05) of respective awake control values. During microlaryngoscopy, when mean arterial blood pressure was controlled as close as possible to mean arterial blood pressure in the awake state by individually adjusted propofol infusion rates (average 0.33 mg.kg-1.min-1) MSA was restored to 93% of the activity before anesthesia, and leg blood flow increased further. Both cardiac and muscle sympathetic baroreflex sensitivities were depressed by propofol. During surgery the cardiac baroreflex sensitivity decreased further, whereas the muscle sympathetic baroreflex sensitivity was unchanged. CONCLUSIONS: Propofol is a potent inhibitor of sympathetic neuronal activity and decreases the sensitivity of the baroreflex. When used to control the pressor response during surgery, the vasodilatating effect of propofol overrides the neural vasoconstriction induced by surgery, and a further inhibition of the cardiac baroreflex is observed.

Possible genetic influence on the strength of human muscle nerve sympathetic activity at rest.

Large reproducible interindividual differences in the strength of human muscle nerve sympathetic activity have been demonstrated previously without satisfactory explanation. We undertook the present study to investigate whether a genetic influence may be a factor of importance. Microneurographic recordings of sympathetic impulse traffic were made in the peroneal nerve in nine pairs of monozygotic male twins and eight pairs of age-matched male subjects without family relationship. The strength of the sympathetic activity was quantitated as number of sympathetic bursts per 100 heart beats and bursts per minute. Group mean values of muscle sympathetic activity, heart rate, and blood pressure were similar in the two groups. Intrapair differences (mean +/- SEM) of sympathetic activity were 5.4 +/- 1.7 bursts per 100 heart beats (1.7 +/- 0.5 bursts per minute) for the twins and 19.4 +/- 3.2 bursts per 100 heart beats (11.8 +/- 2.5 bursts per minute) for the control subjects (P < .01 for both). The degree of reproducibility between twins is similar to that reported previously between repeated recordings in the same subject. The finding may indicate that the strength of sympathetic outflow to muscle is controlled genetically. If so, we speculate that this may contribute to the heritability of blood pressure in both normotensive and hypertensive subjects.

Augmented resting sympathetic activity in awake patients with obstructive sleep apnea.

Muscle nerve sympathetic activity (MSA) was recorded during wakefulness in 11 patients with obstructive sleep apnea (OSA) and in 9 sex- and age-matched healthy control subjects. Plasma levels of norepinephrine (NE) and neuropeptide Y were analyzed. Five patients had established hypertension (resting supine systolic BP/diastolic BP > or = 160/95 mm Hg). The investigation was performed after a minimum of 3 weeks' washout period of antihypertensive medication. Muscle sympathetic activity during supine rest was higher in patients compared with controls (p < 0.01) with no difference between normotensive and hypertensive patients. However, systolic, but not diastolic, BP was positively related to resting MSA (n = 20, p < 0.01). There was no significant correlation between body mass index and MSA. Resting MSA was unrelated to disease severity expressed as apnea frequency or minimum SaO2 during the overnight recording. Both the arterial and venous plasma norepinephrine was higher in patients compared with controls (p < 0.05). Plasma levels of NE correlated to resting MSA (p < 0.01) in the whole study group (patients and controls) but not within the respective subgroups. No significant correlation, however, was found between plasma NE (arterial and venous) and BP. Plasma neuropeptide Y-like immunoreactivity was similar in patients and controls. However, one patient with hypertension had approximately twice this level in repeated samples. It is concluded that neurogenic sympathetic activity as well as circulating plasma NE is increased in patients with OSA. This increased sympathetic activity during awake supine rest may reflect a pathophysiologic adaptation to hypoxia and hemodynamic changes occurring at repetitive apneas during sleep. The correlation between MSA and systolic BP implies that this mechanism may be directly or indirectly involved in the development of cardiovascular complications in OSA.

The effects of propofol, methohexitone and isoflurane on the baroreceptor reflex in the cat.

The effects of propofol (P), methohexitone (M) and isoflurane (I) on the baroreceptor reflex were studied in a cat model in which the blood pressure in a bilateral isolated carotid sinus preparation was artificially varied between 50-200 mmHg. The influence from aortic and cardiopulmonary baroreceptors was excluded by vagotomy. With basal chloralose anaesthesia as control, the investigated anaesthetics were used in doses corresponding to MAC 0.5 and 1.0. The maximum change in systemic mean arterial pressure (MAP) and heart rate (HR) following a defined increase in carotid sinus pressure was used as an index of baroreceptor reflex sensitivity. Compared to control, M and I anaesthesia were associated with significant depression of baroreceptor reflex sensitivity at the high dose (corresponding to MAC 1.0), and during I anaesthesia also at the low dose (MAC 0.5). The baroreceptor reflex sensitivity was maintained during propofol anaesthesia. The carotid sinus pressure interval at which the maximum changes in MAP could be elicited, was significantly higher during M than during P. This indicates resetting of the baroreflex.

Characteristics of muscle nerve sympathetic activity during general anaesthesia in humans.

General anaesthesia influences the cardiovascular system at different levels. To increase our knowledge of how sympathetic outflow is affected by anaesthetic interventions, we used direct microelectrode recordings of muscle sympathetic activity (MSA) in the peroneal nerve in 18 patients scheduled for ENT-surgery. During induction of anaesthesia (propofol 2.1 mg/kg or methohexitone 1.4 mg/kg), all patients showed reductions in MSA (from 41 +/- 4 to 20 +/- 4 bursts/min). With endotracheal intubation there was a sudden increase of activity and in several patients the normal pulse-synchrony of MSA was lost temporarily. Maintenance of anaesthesia with nitrous oxide (n = 12) increased MSA and methohexitone (n = 2), propofol (n = 3) and isoflurane (n = 8) decreased MSA, while the effect of halothane (n = 3) varied. Baroreflex mechanisms were still operative but seemed to be depressed in relation to anaesthetic agent and depth. Laryngeal and surgical stimuli caused increases in MSA and blood pressure, lasting several minutes after the stimulation. It is concluded that the strength of MSA is profoundly influenced by the choice of anaesthetic agent. A suppression of activity is more common than an increase. Qualitatively, several sympathetic reflexes operate in a similar way during light anaesthesia as in awake subjects, but are depressed or absent during deep anaesthesia.

Percutaneous recording of muscle nerve sympathetic activity during propofol, nitrous oxide, and isoflurane anesthesia in humans.

The effects of propofol, nitrous oxide, and/or isoflurane on efferent activity of sympathetic muscle nerve fibers (MSA) were studied using percutaneous microneurographic recordings from the peroneal nerve. Eight ASA Physical Status 1 patients (30-70 yr of age) scheduled for otorhinolaryngeal surgery entered the study. The effects of propofol (2-2.5 mg.kg-1.min-1) induction, tracheal intubation, and maintenance of anesthesia with isoflurane (0.3%, 0.6%, and 1.2% end-tidal concentrations) and/or 70% nitrous oxide were studied with respect to MSA, arterial blood pressure, heart rate, and indices of skin blood flow (laser doppler photometry and finger pulse plethysmography). Induction of anesthesia with propofol decreased MSA to 34 +/- 2% (mean +/- SEM) (P less than 0.05), and subsequent tracheal intubation increased MSA rapidly to 151 +/- 23% (P less than 0.05) of the control level. Isoflurane administration both with and without nitrous oxide led to a decrease of MSA (P less than 0.05). However, during nitrous oxide/isoflurane anesthesia (1.0 MAC) MSA was 76 +/- 38% higher than when isoflurane was used alone, although this implied a decrease in anesthetic depth to 0.5 MAC. This indicates that nitrous oxide and isoflurane have opposite effects on sympathetic outflow. During undisturbed propofol, nitrous oxide, and/or isoflurane administration (up to 1.0 MAC), MSA retained its normal pulse synchronous pattern, indicating that modulation of sympathetic outflow from arterial baroreceptors was still present. Skin blood flow increased sevenfold to tenfold in association with propofol induction (P less than 0.05) and was maintained at an 11- to 19-fold increase during nitrous oxide and/or isoflurane anesthesia, without any difference between the two anesthetics.(ABSTRACT TRUNCATED AT 250 WORDS)

Is high and fluctuating muscle nerve sympathetic activity in the sleep apnoea syndrome of pathogenetic importance for the development of hypertension?

Muscle nerve sympathetic activity was recorded in six patients with the sleep apnoea syndrome (SAS). Compared with age- and sex-matched control patients, an increased activity during wakefulness was found. Sleep apnoic events were associated with sequencies of progressively increasing sympathetic activity followed by a sudden reduction of activity. The high sympathetic activity associated with SAS may be important in the development of the systemic hypertension commonly seen in these patients.