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Biomedical subjects

A Grünert

Publications and source records attributed to A Grünert.

At least 37 records · Page 2Linked to original sources

Water turnover and body composition during long-term exposure to high altitude (4,900-7,600 m).

Thirteen healthy subjects (11 men and 2 women; 30.2 +/- 5.4 yr; 73.5 +/- 10.3 kg; 178.9 +/- 10.4 cm; body mass index, 22.9 +/- 1.6 kg/m2) participated at the 62-day expedition to the Broad Peak (8,047 m), Pakistan. Weight, body water, and water turnover (deuterium dilution and elimination) were measured eight times to assess long-term changes. Body weight fell during the ascent to the base camp [from 73.2 +/- 9.8 (baseline) to 71.7 +/- 9.7 kg; P < 0.05] and decreased until the end of the base camp stay (66.7 +/- 7.2 kg; P < 0.0001). Body compartments changed at different rates. Total body water decreased during the ascent (from 43.1 +/- 7.3 to 41.0 +/- 7.7 liters; P < 0.05) and remained unchanged until the base camp was reached (41.2 +/- 6.9 liters; P < 0.01) but decreased further during the base camp stay (40.6 +/- 5.2 liters). Water content of the body (total body water-to-body weight ratio) fell during the ascent (from 58.6 +/- 3.4 to 55.8 +/- 4.4%; P < 0.01), approached the baseline value during the base camp (57.4 +/- 4.0 and 58.3 +/- 5.1%), and increased again until the end of the base camp (60.6 +/- 3.4 and 60.9 +/- 4.3%). The compartment of the solids increased during the ascent (from 30.2 +/- 3.4 to 32.2 +/- 4.9 kg; P < 0.01) and approached the baseline value on arrival at the base camp (30.5 +/- 4.7 kg). Until the end of the base camp, the compartment of the solids fell (26.9 +/- 2.6 and 26.1 +/- 4.0 kg), indicating that weight loss was due to a loss of body solids, presumably mostly fat mass. Water turnover during the pretest period (sea level) was 45 +/- 7 ml.kg-1.day-1; it increased during the ascent (56 +/- 11 and 60 +/- 10 ml.kg-1.day-1) but remained constant during the base camp stay (63 +/- 12, 58 +/- 9, and 56 +/- 10 ml.kg-1.day-1). It increased during the ascent to Broad Peak (73 +/- 20 ml.kg-1.day-1; P < 0.05) and even more during the descent to civilization (83 +/- 17 ml.kg-1.day-1; P < 0.05).

Adult↗

Are the effects of noradrenaline, adrenaline and dopamine infusions on VO2 and metabolism transient?

OBJECTIVE: To determine whether noradrenaline, adrenaline and dopamine have persistent actions on VO2 and metabolism. DESIGN: Descriptive laboratory investigation. SETTING: Laboratory of the Department of Anaesthesiology at a University Hospital. SUBJECTS: 9 volunteers. INTERVENTION: VO2 and the plasma concentration of glucose and free fatty acids were measured prior to and during a 4 h infusion of saline (control), noradrenaline (0.14 microgram/kg min) adrenaline (0.08 microgram/kg min) or dopamine (7 micrograms/kg min), n = 9 each. VO2 was measured using an open circuit gas exchange system. MEASUREMENTS AND MAIN RESULTS: VO2 increased from 250 +/- 22 ml/min to 280 +/- 38 ml/min during noradrenaline, to 298 +/- 30 ml/min during adrenaline and to 292 +/- 39 ml/min during dopamine infusion. The plasma glucose concentration increased from 6.2 +/- 0.6 mmol/l to 8.8 +/- 0.8 mmol/l, 13.2 +/- 1.4 and 7.3 +/- 0.4 mmol/l during infusion of noradrenaline, adrenaline or dopamine, respectively. The plasma free fatty acid concentration increased from 0.28 +/- 0.10 mmol/l to 0.79 +/- 0.21 mmol/l during noradrenaline and to 0.52 +/- 0.09 mmol/l during dopamine. In contrast, free fatty acid values averaged baseline values at the end of the adrenaline infusion after an initial increase to 0.72 +/- 0.31 mmol/l. CONCLUSIONS: Administration of noradrenaline, adrenaline or dopamine resulted in persistent increases in VO2 in volunteers. With the exception of the transient adrenaline effect on fatty acids the metabolic actions were steady during 4 h of adrenergic stimulation. Since the adrenergic effect on VO2 is persistent over time a similar action in patients (e.g. septic shock) during treatment with adrenoceptor agonists may be important. Thus, an increase in VO2 during therapy may not only reflect an oxygen debt but also a pharmacodynamic action of adrenoceptor mediated calorigenic and metabolic induction.

Adult↗

Unchanged 5'-deiodinating activity during the induction of a nonthyroidal illness.

We investigated the formation of a "nonthyroidal illness" (NTI) in pigs undergoing ventricular fibrillation (VF) and resuscitation. Seven minutes after VF twenty-one pigs received either Epinephrine (E: 45 micrograms/kg B.W.; n = 7), Norepinephrine (NE: 45 micrograms/kg B.W.; n = 7), or Vasopressin (VP: 0.8 U/kg B.W.; n = 7). We determined the serum concentrations (sc) of total T4 (TT4), FT4, total T3 (TT3) and rT3 120 min before, during (t0), and 5, 15, 60 and 120 min after VF. At the end of the observation period we figured out the in-vitro T3-generation (kM, Vmax), the in-vitro rT3-generation, the in-vitro rT3-decomposition (kM, Vmax) and the content of cytosolic sulfhydryls (total sulfhydryls, non-protein bound sulfhydryls) in liver and kidney specimen. Animals not undergoing VF served as controls (C) for parameters measured in the intracellular compartment. TT4- and TT3-sc decreased to 3.3 +/- 0.6 micrograms/dl (p < 0.05, vs. t0) and 15.2 +/- 4.1 ng/dl (p < 0.05, vs t0), resp. FT4-sc remained stable for five minutes (2.63 +/- 0.41 ng/dl) before declining to 1.8 +/- 0.39 ng/dl (p < 0.05, vs. t0). The rT3-sc raised finally to 46.9 +/- 7.3 ng/dl (p < 0.05, vs t0). Iodothyronine sc did not exhibit differences between E-, NE- and VP-treatment. Neither in-vitro T3-generation, nor in-vitro rT3-generation, nor in-vitro rT3-decomposition nor intracellular sulfhydryl content were affected by the events of VF and resuscitation as compared to the controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Elevated plasma endothelin concentrations in cyclosporine-treated patients after bone marrow transplantation.

Administration of cyclosporine is often associated with the development of renal dysfunction and hypertension. Since recent data from animal experiments provide evidence that endothelin, a potent vasoconstrictive peptide, might play a role in mediating cyclosporine-related renal and cardiovascular side-effects, the present study was designed to investigate whether plasma endothelin concentrations are elevated in cyclosporine-treated patients. Plasma endothelin concentrations, determined by radioimmunoassay after Sep Pak C18 extraction, were significantly elevated in cyclosporine-treated patients after bone marrow transplantation (8.3 +/- 1.4 ng/l, n = 28) compared to patients not treated with cyclosporine after bone marrow transplantation (3.9 +/- 0.2* ng/l, n - 11), patients with haematological disorders (3.9 +/- 0.3** ng/l, n = 11) not treated with bone marrow transplantation and to normal control subjects (3.1 +/- 0.2*** ng/l, n = 33) (*P < 0.05, **P < 0.01, ***P < 0.001). Furthermore, plasma endothelin levels exhibited a significant correlation with cyclosporine concentrations (r = 0.57, P < 0.01). The present data, demonstrating elevated plasma endothelin concentrations in cyclosporine-treated patients, suggest that the cyclosporine-associated renal and cardiovascular side-effects might in part be mediated by cyclosporine-induced stimulation of endothelin release.

Adult↗

Cyclosporine A stimulates endothelin release.

Administration of cyclosporine A is often associated with the development of renal dysfunction and hypertension. Because recent data provide evidence that endothelin (ET) might be involved in mediating cyclosporine-associated cardiovascular and renal side effects, the present study aimed to investigate the influence of cyclosporine A on ET release from cultured smooth-muscle cells and whether ET plasma concentrations are elevated in cyclosporine-treated patients. Addition of cyclosporine A to the medium of cultured human smooth-muscle cells, isolated from atherosclerotic iliac arteries, induced a dose-dependent increase in ET release. ET plasma levels were significantly elevated in cyclosporine-treated patients after bone marrow transplantation, compared to control groups. These data suggest that enhanced ET release might be involved in mediating the cyclosporine-associated side effects.

Cells, Cultured↗

Increased brain natriuretic peptide and atrial natriuretic peptide plasma concentrations in dialysis-dependent chronic renal failure and in patients with elevated left ventricular filling pressure.

Brain natriuretic peptide (BNP) and atrial natriuretic peptide (ANP) plasma concentrations were measured in patients with dialysis-dependent chronic renal failure and in patients with coronary artery disease exhibiting normal or elevated left ventricular end-diastolic pressure (LVEDP) (n = 30 each). Blood samples were obtained from the arterial line of the arteriovenous shunt before, 2 h after the beginning of, and at the end of hemodialysis in patients with chronic renal failure. In patients with coronary artery disease arterial blood samples were collected during cardiac catheterization. BNP and ANP concentrations were determined by radioimmunoassay after Sep Pak C18 extraction. BNP and ANP concentrations decreased significantly (P < 0.001) during hemodialysis (BNP: 192.1 +/- 24.9, 178.6 +/- 23.0, 167.2 +/- 21.8 pg/ml; ANP: 240.2 +/- 28.7, 166.7 +/- 21.3, 133.0 +/- 15.5 pg/ml). The decrease in BNP plasma concentrations, however, was less marked than that in ANP plasma levels (BNP 13.5 +/- 1.8%, ANP 40.2 +/- 3.5%; P < 0.001). Plasma BNP and ANP concentrations were 10.7 +/- 1.0 and 60.3 +/- 4.0 pg/ml in patients with normal LVEDP and 31.7 +/- 3.6 and 118.3 +/- 9.4 pg/ml in patients with elevated LVEDP. These data demonstrate that BNP and ANP levels are strongly elevated in patients with dialysis-dependent chronic renal failure compared to patients with normal LVEDP (BNP 15.6-fold, ANP 2.2-fold, after hemodialysis; P < 0.001) or elevated LVEDP (BNP 6.1-fold, ANP 2.0-fold, before hemodialysis; P < 0.001), and that the elevation in BNP concentrations was more pronounced than that in ANP plasma concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Changes in brain natriuretic peptide and atrial natriuretic peptide plasma concentrations during hemodialysis in patients with chronic renal failure.

The present study aimed to investigate whether brain natriuretic peptide (BNP), atrial natriuretic peptide (ANP), cortisol and thyroid hormone concentrations change during hemodialysis in patients with chronic renal failure. Blood samples were withdrawn in 30 patients with chronic renal failure before hemodialysis, 2 hours after the beginning and at the end of hemodialysis. ANP and BNP concentrations were determined by radioimmunoassay after Sep Pak C18 extraction. Cortisol, T3, T4, FT4 and TSH serum concentrations were measured by enzyme immunoassay. BNP and ANP plasma levels were strongly elevated in patients with renal failure (BNP 22.4 fold, ANP 4.7 fold versus controls [n = 20]) and decreased significantly (p < 0.001) during hemodialysis (BNP [pg/ml]: 192.1 +/- 24.9, 178.6 +/- 23.0, 167.2 +/- 21.8; ANP [pg/ml]: 240.2 +/- 28.7, 166.7 +/- 21.3, 133.0 +/- 15.5). BNP plasma concentrations showed a stronger elevation than ANP plasma levels and a less pronounced decrease during hemodialysis (BNP: 13.5 +/- 1.8%, ANP: 40.2 +/- 3.5%, p < 0.001) which might in part be due to the longer half-life of BNP. Cortisol and TSH levels did not change significantly whereas T3, T4 and FT4 levels increased significantly (p < 0.001) during hemodialysis. Since corticosteroids and thyroid hormones stimulate natriuretic peptide release, these data suggest that the dialysis-induced decrease of ANP and BNP plasma concentrations is not augmented by a loss of cortisol or thyroid hormones during hemodialysis. The present data provide support that BNP and ANP plasma concentrations are sensitive indicators of the extracellular fluid volume status.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

[Artificial oxygen carriers--perfluorocarbons].

The paper summarizes chemical, physical and physiological qualities of modern perfluorinated carbons. The indications for the application of these artificial oxygentransporting substances in the biological and medical field are summarized and discussed. The characteristics of perfluorocarbons are looked at from historical and current points of view in order to indicate the fields of application and especially the limitations of their applicability. Without any doubt application as a full replacement of blood will be impossible because blood with its multifunctional property cannot be replaced by systems which cover only one or few aspects. Besides this general statement it is also clear that the special qualities of perfluorocarbons make them highly suitable for application in biological and medical fields; their low viscosity allows to improve disturbancies in perfusion. Immunological problems do not occur, and the danger of infection is eliminated compared to biological material. The most important fields of application for perfluorocarbons are the organ perfusion in organ banks for transplantation, the oxygenation of cell cultures and the diagnosis with imaging procedures.

Animals↗

Effect of corticotropin releasing factor on atrial natriuretic peptide release from the isolated perfused rat heart.

The effect of corticotropin releasing factor (CRF) on atrial natriuretic peptide (ANP) release and its possible modulation by indomethacin, norepinephrine, propranolol and nitro-L-arginine (an inhibitor of the endothelium-derived relaxing factor (EDRF) release) was investigated, using an isolated perfused rat heart preparation. Bolus injection of 5 micrograms CRF, dissolved in 100 microliters perfusion buffer, provoked a significant (p < 0.01 vs. control) short-time increase of ANP release. Indomethacin (3 x 10(-5) mol/l) inhibited the CRF-stimulated increase of ANP release and decreased the basal ANP secretion (p < 0.01 vs. CRF group). Norepinephrine (10(-9) mol/l) slightly, but not significantly, decreased the CRF-stimulated ANP release and did not change the basal ANP output. Propranolol (3 x 10(-6) mol/l) did not alter ANP release. Nitro-L-arginine (3 x 10(-5) mol/l) increased the basal ANP release (p < 0.01 vs. CRF group) and prolonged the CRF-induced rise of the ANP secretion. The present data suggest that prostaglandins are important mediators of basal and CRF-stimulated ANP release and that EDRF might be a physiological inhibitor of ANP release.

Animals↗

Plasma brain natriuretic peptide and atrial natriuretic peptide concentrations correlate with left ventricular end-diastolic pressure.

The present study was designed to investigate whether brain natriuretic peptide (BNP) and atrial natriuretic peptide (ANP) plasma concentrations correlate with left ventricular end-diastolic pressure (LVEDP), pulmonary capillary wedge pressure (PCWP), diastolic pulmonary arterial pressure (DPAP), right atrial pressure (RAP), or ejection fraction (EF). Plasma BNP and ANP levels were determined by commercial radioimmunoassays (Peninsula) after Sep Pak C18 extraction in blood samples withdrawn from the pulmonary artery and the left ventricle or from the left ventricle and the femoral vein in 85 patients undergoing diagnostic cardiac catheterization. Linear and nonlinear regression analysis and the paired sample t-test were applied to the data. Pulmonary arterial plasma BNP and ANP levels showed a close nonlinear correlation with LVEDP (BNP: r = 0.94, p < 0.001; ANP: r = 0.81, p < 0.001), a significant linear correlation with PCWP, DPAP, and RAP, and a significant negative correlation with EF. ANP concentrations decreased significantly from the pulmonary artery to the left ventricle and from the left ventricle to the femoral vein (p < 0.001). BNP levels also decreased significantly between the left ventricle and the femoral vein (p < 0.001), but there was no significant difference between pulmonary arterial and left ventricular BNP concentrations. BNP and ANP concentrations correlated significantly between pulmonary arterial and left ventricular blood samples (BNP: r = 0.99, ANP: r = 0.93, p < 0.001) and between left ventricular and peripheral blood samples (BNP: r = 0.99, ANP: r = 0.94, p < 0.001). The present data suggest that peripheral plasma BNP and ANP levels are useful non-invasive indices of cardiac performance.

Atrial Function, Right↗

Metabolic and haemodynamic effects of dopamine plus domperidone in volunteers.

There are no studies of the relationship between infusion rate of dopamine and the arterial and venous dopamine plasma concentration and the resulting haemodynamic and metabolic effects. Dopamine was administered to seven volunteers using five infusion rates (1, 3, 6, 9, 13 micrograms/kg per minute) in an escalating sequence lasting for 30 min for each step. Since dopamine can cause nausea and vomiting, this relationship was investigated after administration of domperidone for infusion rates above 3 micrograms/kg per minute. Haemodynamic effects were assessed using 2-dimensional echocardiography. During the highest infusion rate the arterial plasma dopamine concentration reached 1,379 +/- 181 nmol/l. There was a linear correlation between the dopamine infusion rate and both the arterial and the venous plasma concentration. There was no significant change in heart rate or diastolic blood pressure. Systolic blood pressure, ejection fraction and cardiac index increased in a dose-dependent manner. Systemic vascular resistance decreased during the two low doses of dopamine and was not different from baseline values during the three high infusion rates. The plasma concentrations of glucose and non-esterified fatty acids increased from 5.3 +/- 0.4 to 0.68 +/- 0.9 nmol/l, and from 360 +/- 119 to 971 +/- 307 mumol/l, respectively, during the 13 micrograms/kg per minute infusion rate. As the plasma noradrenaline concentration increased up to 7.84 +/- 2.46 nmol/l in correlation to the dopamine plasma concentration, an indirect sympathomimetic effect may contribute to the actions of dopamine plasma concentration.

Adult↗

Effects of norepinephrine, epinephrine, and dopamine infusions on oxygen consumption in volunteers.

OBJECTIVE: To determine the relationships between plasma concentrations of norepinephrine, epinephrine, and dopamine and oxygen consumption (VO2) during infusion of these catecholamines. DESIGN: Prospective, randomized variable dose, pharmacologic study in which a noncumulative infusion-rate design was used. SETTING: Laboratory of the Department of Anesthesiology at a University Hospital. PATIENTS: Twenty-one normal volunteers. INTERVENTIONS: After a control period of 20 mins, norepinephrine (three infusion rates; 0.06 to 0.2 microgram/kg/min; n = 7), epinephrine (four infusion rates; 0.02 to 0.2 microgram/kg/min; n = 7), or dopamine (three infusion rates; 3 to 12 micrograms/kg/min; n = 7) was administered to normal volunteers (n = 21) for the purpose of constructing plasma concentration/VO2 response curves. MEASUREMENTS AND MAIN RESULTS: Systolic and diastolic blood pressure, heart rate, plasma concentrations of norepinephrine, epinephrine, and dopamine, and VO2 were measured at the end of the control period and at the end of each catecholamine infusion. VO2 was measured using a ventilated canopy system and a differential oxygen sensor. Typical hemodynamic responses to vasopressors were seen during adrenergic receptor agonist infusions. VO2 increased from 132 +/- 7 to 153 +/- 10 mL/min/m2 during the highest infusion rate of norepinephrine, from 133 +/- 7 to 182 +/- 11 mL/min/m2 during the highest infusion rate of epinephrine, and from 132 +/- 13 to 163 +/- 8 mL/min/m2 during the highest infusion rate of dopamine (p < .05; paired t-test). Increases in VO2 were correlated with the logarithms of the corresponding plasma catecholamine concentrations. Effects on VO2 and hemodynamic responses occurred at similar plasma concentrations for each of the three catecholamines. CONCLUSIONS: Administration of norepinephrine, epinephrine, or dopamine results in marked increases in VO2 in volunteers. In patients, the administration of catecholamines or sympathomimetics to attain optimal values of cardiac index, oxygen delivery (DO2), and VO2 may increase the oxygen demand and thus obscure the DO2-VO2 relationship.

Blood Pressure↗

Relationship between arterial and peripheral venous catecholamine plasma catecholamine concentrations during infusion of noradrenaline and adrenaline in healthy volunteers.

Noradrenaline and adrenaline were infused IV at 5 different rates (0.01-0.2 micrograms.kg.min-1) for 30 min to volunteers. The plasma catecholamine concentrations were determined by HPLC and electro-chemical detection. At the highest infusion rate, the arterial and venous plasma concentrations of noradrenaline increased from 1.18 to 44.1 nmol.l-1 and from 1.14 to 31.9 nmol.l-1, respectively, and of adrenaline from 0.29 to 23.9 nmol.l-1 and from 0.28 to 19.3 nmol.l-1, respectively. The peripheral venous plasma concentration of noradrenaline averaged 76% of the arterial concentration, and of adrenaline it was 73%. There was a linear relationship between the peripheral venous and arterial plasma noradrenaline and adrenaline concentrations at therapeutic doses.

Adult↗

Plasma catecholamine concentrations after successful resuscitation in patients.

OBJECTIVES: To measure plasma catecholamine concentrations after cardiopulmonary resuscitation (CPR) and to correlate catecholamine concentrations with heart rate (HR), BP, and plasma glucose and lactate concentrations. DESIGN: Prospective, descriptive study. SETTING: Emergency medical service at a University Hospital. PATIENTS: Ten patients (58 to 85 yrs) with out-of-hospital cardiac arrest. INTERVENTIONS: At 1, 5, 15, 30, and 60 mins after restoration of spontaneous circulation, blood samples were drawn and BP and HR were measured. Plasma catecholamine concentrations were measured by high-pressure liquid chromatography and plasma glucose and lactate concentrations were measured by enzymatic methods. MAIN RESULTS: Median plasma epinephrine and norepinephrine concentrations were 136.3 micrograms/L (136,300 pg/mL), range 27.6 to 397.6 micrograms/L (27,600 to 397,600 pg/mL), and 4.7 micrograms/L (4700 pg/mL), range 1.8 to 14.5 micrograms/L (1800 to 14,500 pg/mL), respectively, at 1 min. Median plasma epinephrine and norepinephrine concentrations decreased to 8.7 micrograms/L (8700 pg/mL), range 1.2 to 55.0 micrograms/L (1200 to 55,000 pg/mL) and 1.9 micrograms/L (1900 pg/mL), range 1.3 to 5.8 micrograms/L (1300 to 5800 pg/mL), respectively, at 60 mins after restoration of spontaneous circulation. Epinephrine concentrations decayed with a semilogarithmic decay pattern. The half-life for the alpha phase was 2.2 mins and was 38.7 mins for the beta phase. Mean values of systolic arterial pressure were between 136 +/- 23 mm Hg at 1 min and 120 +/- 15 mm Hg at 30 mins. Median plasma glucose concentrations were between 8.2 mmol/L (147.7 mg/dL; range 5.8 to 11.2 mmol/L [104.5 to 201.8 mg/dL]) at 1 min and 13.9 mmol/L (250.4 mg/dL; range 9.7 to 16.6 mmol/L [174.8 to 299.1 mg/dL]) at 30 mins. Lactate values were between 11.4 mmol/L (range 4.7 to 16.5) at 1 min and 5.2 mmol/L (range 2.7 to 12.5) at 60 mins. No significant correlations were found between circulating catecholamine concentrations and the other variables. CONCLUSIONS: After CPR, plasma catecholamine concentrations remained at high values but they did not lead to increases in BP, HR, or circulating glucose concentrations.

Aged↗

Relationship between infusion rates, plasma concentrations, and cardiovascular and metabolic effects during the infusion of norepinephrine in healthy volunteers.

OBJECTIVE: To determine the relationship between iv infusion rate, plasma concentrations, and hemodynamic and metabolic actions of norepinephrine. DESIGN: Norepinephrine was administered by using five iv infusion rates (0.01 to 0.2 micrograms/kg/min) for 30 mins each to eight volunteers, for the purpose of constructing cumulative plasma concentration-response curves. SETTING: Laboratory of the Department of Anesthesiology at a university hospital. MEASUREMENTS AND MAIN RESULTS: Systolic and diastolic BP, heart rate, and the plasma concentrations of norepinephrine, glucose, nonesterified fatty acids, and insulin were measured at the end of each infusion rate. During the highest infusion rate, plasma norepinephrine concentrations increased from 199 +/- 75 to 7475 +/- 1071 pg/mL (1.18 +/- 0.44 to 44.18 +/- 6.33 nmol/L). Typical hemodynamic responses, such as increases in BP and decreases in heart rate, were seen, while the plasma concentrations of glucose and nonesterified fatty acids increased from 92 +/- 10 to 132 +/- 17 mg/dL (5.1 +/- 0.6 to 7.3 +/- 0.9 mmol/L) and 11 +/- 4 to 34 +/- 6 mg/dL (0.11 +/- 0.04 to 0.34 +/- 0.06 g/L), respectively, during the 0.2 micrograms/kg/min infusion rate (p less than .05). Despite the increase in glucose concentration, insulin remained at baseline values. Metabolic and hemodynamic effects occurred at similar plasma concentrations throughout the study. CONCLUSIONS: Administration of norepinephrine showed no selective hemodynamic actions. The metabolic responses observed in this investigation were similar to those responses seen during increased endogenous sympathetic nervous system activity, such as stress, exercise, or trauma.

Adult↗

Measurement of mucociliary transport velocity in ventilated patients. Short-term effect of general anesthesia on mucociliary transport.

OBJECTIVES: The objectives of this study were to evaluate a method for measuring BTV in ventilated patients and to study the short-term effect of general anesthesia with midazolam, Fentanyl, pancuronium and O2:N2O on BTV. DESIGN: The study included phantom measurements on a bronchoscopy model and the determination of BTV in patients in a convenience sample trial. SETTING: The study took place in a university hospital. PATIENTS: Fourteen patients undergoing major abdominal surgery with planned postoperative mechanical ventilation were included in the study. All patients gave their written informed consent to participate in the study. INTERVENTIONS: Bronchial mucus transport velocity was measured with a small volume (0.05 to 0.08 ml) of technetium 99m-labeled albumin microspheres with an activity of 3 MBq. The radiolabeled bolus was deposited on the dorsal mucosal surface at the distal end of the right and left main bronchus via flexible bronchoscopy. The movement of the microspheres toward the trachea was visualized and recorded using a scintillation camera; quantitative evaluation utilized the condensed image. MAIN MEASUREMENTS AND RESULTS: The technique was validated in a bronchoscopy model and in an intubated patient by moving a radioactive drop in a catheter through the main bronchi at velocities from 0 to 20 mm/min. The velocities determined by the image processing technique correlated well with the data by the model and patient determination (right bronchus, r = 1.0; left bronchus, r = 1.0). In seven ventilated patients, mechanical irritation by the fiberscope produced no significant effect on BTV. The BTV was measured preoperatively in seven conscious patients one day before surgery while they received local anesthesia with 10 ml of 1 percent lidocaine and postoperatively while they received intubation anesthesia. The preoperative and postoperative BTV values showed no significant differences (10.5; 5.7 to 13.7 mm/min; vs 9.7 (3.7 to 15.3) (median with range). CONCLUSION: By this method, bronchial transport velocity can be determined in a relatively short time in ventilated patients. General anesthesia with midazolam, Fentanyl, pancuronium and O2:N2O does not influence BTV.

Adult↗