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Biomedical subjects

H Groeben

Publications and source records attributed to H Groeben.

31 records · Page 2Linked to original sources
PubMed1998

Combined intravenous lidocaine and inhaled salbutamol protect against bronchial hyperreactivity more effectively than lidocaine or salbutamol alone.

BACKGROUND: Airway instrumentation in persons with asthma is linked to the risk of life-threatening bronchospasm. To attenuate the response to airway irritation, intravenous lidocaine is recommended (based on animal experiments) and mitigates the response to histamine inhalation in asthmatic volunteers. However, the effects of lidocaine have not been compared with standard prophylaxis with beta-sympathomimetic aerosols. Therefore, the effect of lidocaine, salbutamol, combined treatment, and placebo control were tested in awake volunteers with bronchial hyperreactivity. METHODS: After approval from the local ethics committee, 15 persons, who were selected because they showed a decrease in forced expiratory volume in 1 s (FEV1) more than 20% of baseline in response to inhaled histamine in a concentration less than 18 mg/ml (PC20), were enrolled in a placebo-controlled, double-blind, and randomized study. The challenge was repeated on four different days and the volunteers were pretreated with either intravenous lidocaine, inhalation of salbutamol, inhalation of salbutamol plus intravenous lidocaine, or placebo. Lidocaine plasma concentrations were also measured. Statistical analyses included the Friedman test and Wilcoxon's rank sum. RESULTS: The baseline PC20 was 6.4 +/- 4.3 mg/ml. Intravenous lidocaine and salbutamol aerosol both significantly increased the histamine threshold to 14.2 +/- 9.5 mg/ml and 16.8 +/- 10.9 mg/ml, respectively (mean +/- SD). However, the combination of lidocaine and salbutamol significantly increased the PC20 even further to 30.7 +/- 15.7 mg/ml than did salbutamol or lidocaine alone. CONCLUSIONS: In volunteers with bronchial hyperreactivity, both lidocaine and salbutamol attenuate the response to an inhalational histamine challenge, and their combined administration has much greater effects than does either drug alone. Accordingly, pretreatment of patients with bronchial hyperreactivity with both beta-mimetic aerosol and intravenous lidocaine is recommended before airway irritation.

Administration, Inhalation↗
PubMed1997

Dermal and airway responses to monoclonal antibodies specific for canine IgE.

In order to understand mechanisms underlying variability of IgE-mediated responses in vivo, we compared effects of different monoclonal antibodies of IgE on dermal and airway responses in a group of atopic dogs. Using intradermal testing, fourteen antibodies were screened in Basenji-Greyhound dogs. For further comparisons between dermal and airway responses, we selected the two antibodies that stimulated the greatest and least dermal responses, respectively. These antibodies bound to IgE with similar affinities (4.1 +/- 0.2 x 10(9) and 1.5 +/- 0.2 x 10(10) M-1). Dose-response curves to intradermal testing were constructed for these two antibodies. On a separate occasion, peripheral airway resistance (Rp) was determined before and after aerosol challenge with an antibody or saline in the same dogs. For one antibody (affinity 4.1 +/- 0.2 x 10(9) M-1), Rp reached a maximum (407 +/- 142% above baseline; mean +/- SE, n = 6) 10 to 15 min after challenge, while maximum responses to saline (62 +/- 16% above baseline, p < 0.01) occurred immediately after aerosol delivery. Responses to the other antibody were similar (p = 0.068) to responses to saline. The magnitude of skin responses did not predict the magnitude of airway responses. These findings suggest that differences in affinities, alone, do not predict magnitude of responsiveness to the anti-IgE antibody and that mechanisms underlying skin and airway responses may differ qualitatively and/or quantitatively.

Airway Resistance↗
PubMed1996

Intravenous lidocaine and bupivacaine dose-dependently attenuate bronchial hyperreactivity in awake volunteers.

BACKGROUND: In standard textbooks, intravenous lidocaine is recommended for intubation of patients with bronchial hyperreactivity. However, whether and to what extent intravenous local anesthetics attenuate bronchial hyperreactivity in humans is unknown. Accordingly, nine awake volunteers with known bronchial hyperreactivity were subjected to an inhalational challenge with acetylcholine before and during intravenous infusion of lidocaine, bupivacaine, or placebo in a randomized, double-blinded fashion. METHODS: Baseline acetylcholine threshold concentrations were determined 3-5 days before initiation of the investigation. The response to the acetylcholine challenge was defined as hyperreactive, if forced expiratory volume in 1 s decreased by at least 20%. In addition, the acetylcholine threshold for a 100% increase in airway resistance was obtained by body plethysmography. On seven different days, the acetylcholine challenge was repeated at the end of a 30-min intravenous infusion period of three doses of lidocaine (1, 3, and 6 mg.min(-1)) or bupivacaine (0.25, 0.75, and 1.5 mg.min(-1)), during saline placebo infusion, respectively. Acetylcholine-threshold concentrations were presented with the respective plasma concentrations of the local anesthetic. RESULTS: The infusion of lidocaine and bupivacaine resulted in plasma concentrations (means +/- SD) of 0.29 +/- 0.11, 1.14 +/- 0.39, and 2.02 +/- 0.5 microg.ml(-1) for lidocaine and 0.11 +/- 0.04, 0.31 +/- 0.09, and 0.80 +/- 0.18 microg.ml(-1) for bupivacaine, respectively. Compared to baseline, the acetylcholine threshold for a 20% decrease of forced expiratory volume in 1 s as well as the threshold for a 100% increase in total airway resistance increased significantly with increasing plasma concentrations of both local anesthetics. Compared to placebo, acetylcholine threshold was almost quadrupled for lidocaine and tripled for bupivacaine with the highest plasma concentration of each local anesthetic. CONCLUSIONS: In awake humans, intravenous lidocaine and bupivacaine both dose-dependently attenuated the hyperreactive response to a nonspecific inhalational challenge with acetylcholine.

Adult↗
PubMed1996

Ipratropium decreases airway size in dogs by preferential M2 muscarinic receptor blockade in vivo.

BACKGROUND: Two major groups of drugs are available to prevent bronchoconstriction: beta-agonists and muscarinic blocking agents. Ipratropium is the most commonly used anticholinergic agent to treat chronic obstructive pulmonary disease. The authors studied anti-muscarinic agents to determine if they are as effective bronchodilators as beta-adrenergic agents and if not to identify the mechanism of their reduced effectiveness. METHODS: Six anesthetized dogs were studied using high-resolution computed tomography to measure changes in the cross-sectional area of conducting airways induced by cumulative doses of ipratropium with and without gallamine, a selective M2 muscarinic receptor blocker, and after metaproterenol. RESULTS: Metaproterenol dilated the airways and ipratropium constricted the airways. Ipratropium in concentrations of 0.01 and 0.1 mg/ml constricted the airways to 22 +/- 2% and 20 +/- 3% of control, respectively (P < 0.01), whereas larger concentrations caused bronchodilation. After complete blockade of the M2 receptors by pretreatment with intravenous gallamine, the bronchoconstrictor effect of ipratropium was abolished, and ipratropium dilated the airways by 16 +/- 8% and 27 +/- 10% of pre-gallamine baseline after doses of 0.01 and 0.1 mg/ml, respectively (P < 0.01). CONCLUSION: Low-dose ipratropium can decrease airway size by the initial, preferential blockade of neuronal M2 muscarinic receptors, whereas a larger dose of ipratropium blocks M3 muscarinic receptors on airway smooth muscle, resulting in bronchodilation.

Adrenergic beta-Agonists↗
PubMed1996

Intravenous lidocaine and oral mexiletine block reflex bronchoconstriction in asthmatic subjects.

Stimulation of the airways of asthmatic individuals causes severe bronchoconstriction, which is in part neurally mediated via the vagus nerve. Local anesthetics are commonly administered to prevent this reflex-induced bronchoconstriction. Therefore, in a double-blind, placebo-controlled prospective study, we tested the effectiveness of oral mexiletine and intravenous lidocaine at blocking histamine-induced reflex bronchoconstriction. Fifteen subjects with mild asthma were selected (for whom the provocative concentration of histamine aerosol causing a 20% decrease in FEV1 (PC20) was less than 18 mg/ml). Subsequently, the subjects were pretreated with oral mexiletine, intravenous lidocaine, or placebo, and the histamine challenges were repeated. The baseline PC20 for histamine was 8.8 +/- 1.8 mg/ml. Mexiletine and lidocaine at therapeutic serum concentrations blocked reflex bronchoconstriction. Oral mexiletine increased the PC20 to 21.1 +/- 5.0 mg/ml (serum concentration: 0.7 +/- 0.05 microg/ml). Likewise, intravenous lidocaine increased the PC20 to 24.5 +/- 4.9 mg/ml (serum concentration: 2.6 +/- 0.15 microg/ml). Oral mexiletine and intravenous lidocaine block reflex-induced bronchoconstriction. Furthermore, mexiletine may have additional airway benefits when selected for the treatment of dysrhythmias or chronic pain in patients with coexisting lung diseases.

Adult↗
PubMed1995

Pulmonary sympathetic denervation does not increase airway resistance in patients with chronic obstructive pulmonary disease (COPD).

Whether or not neural blockade of pulmonary sympathetic innervation is of relevance for airway resistance in patients with chronic obstructive pulmonary disease (COPD) is unknown. Accordingly we evaluated airway resistance during sympathetic blockade by high thoracic epidural anaesthesia in patients with COPD. Before and 45 min after thoracic epidural injection of bupivacaine 0.75% (6-8 ml; n = 10) total respiratory resistance (oscillometry, ROS), vital capacity (VC), forced expiratory vital capacity in 1 s (FEV1, [%VC]), functional residual capacity (FRC; helium dilution method), and arterial blood gases were measured. Three additional patients received bupivacaine intravenously (1.2 mg.min-1 for 45 min), another three received saline epidurally. Sensory blockade covered segment C5 through T8. As an indicator of widespread sympathetic blockade including the lungs, skin temperature increased significantly on thumb and little toe. Despite pulmonary sympathetic denervation ROS, FEV1, and FRC remained unchanged, while VC decreased slightly, probably due to intercostal muscle blockade. Blood gases remained constant. Neither intravenous bupivacaine nor epidural saline evoked directional changes. Since, in contrast to beta-adrenoceptor blockade, pulmonary sympathetic denervation did not increase airway resistance in patients with COPD, neural sympathetic blockade seems to be of no relevance for airway resistance in these patients.

Airway Resistance↗
PubMed1994

High thoracic epidural anesthesia does not alter airway resistance and attenuates the response to an inhalational provocation test in patients with bronchial hyperreactivity.

BACKGROUND: The functional relevance of an intact pulmonary sympathetic innervation for airway resistance is unknown. We therefore evaluated whether or not pulmonary sympathetic denervation by thoracic epidural anesthesia decreases the threshold of an inhalational provocation with acetylcholine in 20 patients with documented bronchial hyperreactivity scheduled for elective upper abdominal or thoracic surgery. METHODS: Baseline inhalational provocation with acetylcholine was performed 2-4 days before surgery. The acetylcholine threshold concentration for a hyperreactivity response (i.e., for a 20% decrease in forced expiratory volume in 1 s and a 100% increase in total respiratory resistance by oscillometry) was determined. On the day of surgery a second inhalative provocation with acetylcholine was performed 45 min after the patients had received 6-8 ml epidural bupivacaine 0.75% (n = 10), intravenous bupivacaine (1.2 mg.min-1, n = 6), or 6-8 ml epidural saline (n = 4). The acetylcholine threshold concentration for a hyperreactive response was again determined. We also measured vital capacity, forced expiratory volume in 1 s as a percentage of vital capacity, spread of sensory blockade (pin prick), skin temperature on hand and foot (telethermography). RESULTS: During thoracic epidural anesthesia, C4-T8 skin temperature increased significantly on hand and foot indicating widespread sympathetic blockade including the lungs. Compared to values obtained immediately before pulmonary sympathetic blockade, forced expiratory volume in 1 s as a percentage of vital capacity, and total respiratory resistance by oscillometry remained unchanged, while vital capacity decreased. Compared to baseline the acetylcholine threshold concentration for the hyperreactive response increased threefold after epidural as well as after intravenous bupivacaine. Epidural saline evoked no directional changes in the acetylcholine threshold concentration. CONCLUSIONS: We conclude that in patients with bronchial hyperreactivity 1. blockade of pulmonary sympathetic innervation seems to be of no relevance for airway resistance and 2. both epidural and intravenous bupivacaine substantially attenuate the response to an inhalational provocation with acetylcholine.

Acetylcholine↗
PubMed1992

[Pathophysiologic and anesthesiologic characteristics of patients with leukemia].

Leukaemia and its associated therapy result in pathophysiological peculiarities relevant to anaesthesia. Leukaemic patients suffer from anaemia, coagulation disorders, and the consequences of immunosuppression. In addition, some patients show infiltrations of the oropharynx, potentially resulting in difficult intubation and/or pharyngeal haemorrhage. Mediastinal masses can induce complete airway obstruction during general anaesthesia. Patients with a white blood cell count (WBC) greater than 100,000/mm3 (hyperleukocytosis) can suffer from the leukostasis syndrome with acute respiratory failure as well as cerebral vascular occlusions and bleeding due to increased blood viscosity and disturbed microvascular perfusion. Since this syndrome may be triggered by surgery, the WBC should be reduced prior to general anaesthesia in patients with hyperleukocytosis. To avoid development of the leukostasis syndrome, transfusion of packed red cells should be restricted in these patients. Hyperleukocytosis can simulate in-vitro hypoxaemia due to the excessive oxygen consumption of the mass of leukaemic blood cells during routine blood gas analysis. Therapy of leukaemia can lead to the tumor-lysis syndrome with hyperuricaemia, hyperphosphataemia, hyperkalaemia, hypocalcaemia, and hypoglycaemia, and may induce acute renal failure. Since drug interactions have only been evaluated for the combination of two or three drugs, interactions of cytotoxic agents with anaesthetics can hardly be predicted because of the large number of drugs simultaneously administered to leukaemic patients. The heart and lungs are target organs for the acute or chronic side effects of cytotoxic drugs, resulting in non-cardiogenic pulmonary oedema (e.g., cytosine-arabinoside), lung fibrosis (e.g., bleomycin), or arrhythmias and cardiac failure (e.g., adriamycin). The severity of these side effects depends on pre-existing organ disease and only in part on drug dosage. Only HLA- and CMV-compatible blood components should be administered to leukaemic patients. Hyperleukocytosis and the first days of cytotoxic treatment represent relative contraindications to general anaesthesia.

Airway Obstruction↗
PubMed1990

Comparative analysis of arterial oxygen saturations during exercise by pulse oximetry, photometric measurements, and calculation procedures.

Pulse oximetry allows non-invasive monitoring of arterial oxygen saturation (SO2). To study the validity of pulse oximetry, comparative measurements were performed. During exhaustion limited exercise SO2-values measured by pulse oximetry (SO2puls), calculated SO2-values (algorithms of Kelman, Severinghaus, and Siggaard-Andersen--SO2calc), and as "golden standard" photometric measured SO2-values (SO2meas) were compared. Fourteen triathletes performed a stepwise cycling exercise test in the supine position. SO2calc was determined on the basis of capillary actual blood gas values. SO2puls was measured continuously with a finger probe attached to the second finger. The SO2puls- and SO2calc-values differed from the SO2meas-values (p less than 0.05); however, the differences were of no clinical relevance. Performing linear regression analysis, only SO2puls correlated significantly (r = 0.47, p less than 0.001) with SO2meas. Pulse oximetry is able to replace invasive measurements of arterial oxygen saturation in athletes. It is superior to SO2-calculations and permits reliable, valid and non-invasive continuous monitoring of SO2.

Adult↗
PubMed1990

[Transcutaneous blood gas measurements in ergometry].

Blood gases were determined simultaneously both transcutaneously and arterially in 23 healthy male subjects during spiroergometric, exhaustion-limited stress. The individual correlation coefficient between arterially and transcutaneously measured pO2/pCO2 was 0.66 and 0.80, respectively. The median correlation coefficient between the individual correlation coefficients of the pO2 and pCO2 measurements was 0.85 (p less than 0.01). Hence, the validity of transcutaneous blood gas measurement under stress is significantly dependent on individual factors that influence both the pO2 and pCO2 measurements to an equal degree.

Blood Gas Monitoring, Transcutaneous↗
PubMed1990

[Validity of calculating oxygen saturation at rest and during exercise].

Oxygen saturation calculated with the formulae proposed by Heck, Kelman, Lutz, Marsoner, Severing-haus and Siggaard-Andersen, was compared with oxygen saturation measured photometrically. An analysis of 1350 peripheral venous, mixed venous and arterial blood samples obtained during bicycle ergometry revealed that only the calculations using the Kelman, Siggaard-Andersen and Severing-haus formulae had adequate validity and reliability over a wide measuring range. If, however, the oxygen saturation figures are to be used for further calculations, direct measurement should be given preference to avoid errors (for example, in shunt calculation).

Exercise Test↗
PubMed1989

Oxygen saturation calculation procedures: a critical analysis of six equations for the determination of oxygen saturation.

Photometrically measured values of O2-saturation (SO2) were compared with SO2 predictions on the basis of the equations proposed by Heck, Kelman, Lutz, Marsoner, Severinghaus, and Siggaard-Andersen on 1350 occasions. Capillary, venous and mixed venous blood samples from 23 healthy subjects and 30 patients, suffering from cardio-pulmonary diseases were analyzed at rest, during exhaustion, limited exercise and during the recovery phase of ergometric tests. Overall the best agreements with the measured values were found for the equations of Kelman, Severinghaus and Siggaard-Andersen. The results of Heck's, Lutz', and Marsoner's predictions were in reasonable agreement with the measured SO2 only under special physiological conditions. No calculation mode can be performed with constant accuracy and reliability when covering a wide range of acid-base values. If SO2 values are used for further calculations, e.g. for determination of cardiac output, measured values are preferred.

Adult↗