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Biomedical subjects

M Zaugg

Publications and source records attributed to M Zaugg.

15 recordsLinked to original sources
PubMed2002

Modulation of beta-adrenergic receptor subtype activities in perioperative medicine: mechanisms and sites of action.

This review focuses on the mechanisms and sites of action underlying beta-adrenergic antagonism in perioperative medicine. A large body of knowledge has recently emerged from basic and clinical research concerning the mechanisms of the life-saving effects of beta-adrenergic antagonists (beta-AAs) in high-risk cardiac patients. This article re-emphasizes the mechanisms underlying beta-adrenergic antagonism and also illuminates novel rationales behind the use of perioperative beta-AAs from a biological point of view. Particularly, it delineates new concepts of beta-adrenergic signal transduction emerging from transgenic animal models. The role of the different characteristics of various beta-AAs is discussed, and evidence will be presented for the selection of one specific agent over another on the basis of individual drug profiles in defined clinical situations. The salutary effects of beta-AAs on the cardiovascular system will be described at the cellular and molecular levels. Beta-AAs exhibit many effects beyond a reduction in heart rate, which are less known by perioperative physicians but equally desirable in the perioperative care of high-risk cardiac patients. These include effects on core components of an anaesthetic regimen, such as analgesia, hypnosis, and memory function. Despite overwhelming evidence of benefit, beta-AAs are currently under-utilized in the perioperative period because of concerns of potential adverse effects and toxicity. The effects of acute administration of beta-AAs on cardiac function in the compromised patient and strategies to counteract potential adverse effects will be discussed in detail. This may help to overcome barriers to the initiation of perioperative treatment with beta-AAs in a larger number of high-risk cardiac patients undergoing surgery.

Adrenergic beta-Antagonists↗
PubMed2001

Anabolic-androgenic steroids induce apoptotic cell death in adult rat ventricular myocytes.

We tested whether exposure to anabolic-androgenic steroids (AASs) would induce apoptosis in adult rat ventricular myocytes in vitro. Myocytes were exposed to stanozolol (STZ), testosterone enanthate (TE) and testosterone (T) (0.1 micromol/L, 1 micromol/L, 10 micromol/L, and 100 micromol/L) for 20 h. The percentage of myocytes undergoing apoptosis was determined by terminal deoxynucleotidyl transferase-mediated nick end labeling (TUNEL) and was found to be increased when compared to control myocytes at STZ 10 micromol/L 12 +/- 2% (mean +/- SD), STZ 100 micromol/L 42 +/- 3%; TE 1 micromol/L 11 +/- 2%, TE 10 micromol/L 21 +/- 3%, TE 100 micromol/L 62 +/- 2%; T 10 micromol/L 11 +/- 2%, T 100 micromol/L 40 +/- 3% (P < 0.001 vs. CTL 2 +/- 2%). The STZ-, TE- and T-induced dose-dependent apoptotic cell death was corroborated by a significantly increased DNA laddering in myocytes exposed to STZ and T > or = 10 micromol/L and TE > or = 1 micromol/L. Notably, STZ, TE, and T exposure markedly increased the expression of the pro-apoptotic oncogene Bax-alpha, as assessed by reverse transcription-polymerase chain reaction. Taken together, these results clearly show for the first time that AASs induce apoptotic cell death in a dose-dependent manner. This finding may have important implications in understanding the pathogenesis of ventricular remodeling, cardiomyopathy, and sudden cardiac death associated with AAS abuse.

Anabolic Agents↗
PubMed2000

Beta-adrenergic receptor subtypes differentially affect apoptosis in adult rat ventricular myocytes.

BACKGROUND-Catecholamine-induced apoptosis is mediated by activation of the beta-adrenergic signaling pathway. We tested the hypothesis that beta(1)- and beta(2)-adrenergic receptor (AR) subtypes differentially affect apoptosis in adult rat ventricular myocytes in vitro. METHODS AND RESULTS-Myocytes were first exposed to norepinephrine (NE) alone (10 mcmol/L) or NE+atenolol (AT) (10 mcmol/L) for 12 hours. AT, a beta(1)-selective AR antagonist, abolished the NE-induced increase in nick end-labeling (TUNEL)-positive cells compared with control (NE, 33+/-3% versus control, 3+/-1%, P<0.0001; NE+AT, 4+/-2% versus control, 3+/-1%, P=0. 98). Annexin V staining, DNA laddering, and caspase activity determinations corroborated these results. Subsequent experiments under prazosin treatment established the apoptosis dose-response curves for the increasingly beta(2)-selective AR agonists isoproterenol (ISO) (beta(1) approximately beta(2)) and albuterol (ALB) (beta(2)>beta(1)). ISO and ALB induced significantly less apoptosis than NE (beta(1)>beta(2)) at equimolar concentrations as assessed by TUNEL staining [1 mcmol/L: NE (8+/-2%) approximately ISO (7+/-1%)>ALB (2+/-1%); 10 mcmol/L: NE (35+/-2%)>ISO (23+/-1%)>ALB (3+/-1%); 100 mcmol/L: NE (50+/-2%)>ISO (29+/-2%)>ALB (14+/-1%), P<0.0001 except for NE versus ISO at 1 mcmol/L with P=0.62]. ALB-induced apoptosis at 100 mcmol/L was abolished by AT (10 mcmol/L), indicating a beta(1)AR-mediated effect. Importantly, ICI 118551 (0.1 mcmol/L), a highly selective beta(2)AR antagonist, did not decrease the percentage of NE-, ISO-, and ALB-induced apoptosis. Reverse transcription-polymerase chain reaction studies revealed that AT completely reversed the beta-adrenergic signaling-induced changes in the Bcl-2-to-Bax ratio. CONCLUSIONS-These observations provide evidence that beta AR-mediated apoptotic death signaling is largely dissociated from beta(2)ARs and selectively mediated by beta(1)ARs in adult rat ventricular myocytes.

Adrenergic beta-Antagonists↗
PubMed2000

Respiratory function in the elderly.

Aging reduces the reserve capacity of virtually all pulmonary functions. Age-related alterations in the respiratory system are based on structural changes that lead to functional impairment of gas exchange. Pulmonary complications during anesthesia and the postoperative period are significantly increased in elderly patients with pre-existing diseases. The physiologic changes in the aged respiratory system and their anesthetic implications are reviewed in this article.

Aged↗
PubMed2000

Norepinephrine-induced apoptosis is inhibited in adult rat ventricular myocytes exposed to volatile anesthetics.

BACKGROUND: Volatile anesthetics are used to provide anesthesia to patients with heart disease under heightened adrenergic drive. The purpose of this study was to test whether volatile anesthetics can inhibit norepinephrine (NE)-induced apoptosis in cardiomyocytes. METHODS: Rat ventricular cardiomyocytes were exposed to NE (10 microm) alone or in the presence of increasing concentrations of isoflurane and halothane. RESULTS: Isoflurane at 1.6 minimum alveolar concentration (MAC) (4 +/- 2% [SD]) and halothane at 1.2 MAC (3 +/- 2%) abolished the percentage of cardiomyocytes undergoing NE-induced apoptosis (34 +/- 8%), as assessed by terminal deoxynucleotidyl transferase-mediated nick end labeling (TUNEL) (P < 0.0001). Lower concentrations of isoflurane and halothane markedly decreased the number of TUNEL-positive cells. Similarly, isoflurane at 1.6 MAC (5 +/- 3%) and halothane at 1.2 MAC (6 +/- 3%) prevented the increase in annexinV-staining cardiomyocytes (38 +/- 7%; P < 0. 0001). These findings were corroborated with a decreased quantity of NE-induced DNA laddering by volatile anesthetics. Halothane at 1.2 MAC abolished the increase in TUNEL-positive cardiomyocytes exposed to the dihydropyridine Ca2+-channel agonist BAY K-8644 (1 microm) (BAY K-8644 + halothane: 3 +/- 2% vsBAY K-8644: 34 +/- 6%; P < 0. 0001) and the Ca2+-ionophore 4-bromo-A23187 (1 microm) (4-bromo-A23187 + halothane: 2 +/- 2% vs4-bromo-A23187: 13 +/- 4%; P = 0.03). NE treatment increased caspase-9 activity to 197 +/- 62% over control myocytes (P < 0.0001), whereas no caspase-8 activation was detectable. This increase in caspase-9 activity was blocked by isoflurane at 1.6 MAC and halothane at 1.2 MAC. CONCLUSIONS: Volatile anesthetics offer significant protection against beta-adrenergic apoptotic death signaling in ventricular cardiomyocytes. The authors present evidence that this protection is mainly mediated through modulation of cellular Ca2+ homeostasis and inhibition of the apoptosis initiator caspase-9.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1999

Beneficial effects from beta-adrenergic blockade in elderly patients undergoing noncardiac surgery.

BACKGROUND: Perioperative beta-blockade has been shown to improve long-term cardiac outcome in noncardiac surgical patients. A possible mechanism for the reduced risk of perioperative myocardial infarction is the attenuation of the excitotoxic effects of catecholamine surges by beta-blockade. It was hypothesized that beta-blocker-induced alteration of the stress response was responsible for the reported improvements in cardiovascular outcome. Several variables associated with the perioperative use of beta-blockade were also evaluated. METHODS: Sixty-three patients were randomly assigned to one of three groups: group I, no atenolol; group II, pre- and postoperative atenolol; group III, intraoperative atenolol. Hormonal markers of the stress response (neuropeptide Y, epinephrine, norepinephrine, cortisol, and adrenocorticotropic hormone) were evaluated preoperatively and for 72 h after surgery. RESULTS: Perioperative beta-blockade did not significantly alter the hormonal stress response. However, the beta-blocked patients showed improved hemodynamic stability during emergence and postoperatively. They also received less fentanyl intraoperatively (27.7%, P < 0.0001), experienced faster early recovery, had lower pain scores, and required less analgesia in the postanesthesia care unit. Cardiac troponin I release was detected in 8 of 19, 4 of 20, and 5 of 20 patients in groups I, II, and III, respectively (not significant). Three patients in group I had cardiac troponin I levels consistent with myocardial infarction. CONCLUSION: Beta-blockade does not reduce the neuroendocrine stress response, suggesting that this mechanism is not responsible for the previously reported improved cardiovascular outcome. However, it confers several advantages, including decreased analgesic requirements, faster recovery from anesthesia, and improved hemodynamic stability. The release of cardiac troponin I suggests the occurrence of perioperative myocardial damage in this elderly population, which appears to be independent of the neuroendocrine stress response.

Adrenergic beta-Antagonists↗
PubMed1998

Substantial changes in arterial blood gases during thoracoscopic surgery can be missed by conventional intermittent laboratory blood gas analyses.

UNLABELLED: Substantial and clinically relevant changes in arterial blood gases are likely to occur during thoracoscopic surgery with one-lung ventilation (OLV). We hypothesized that they may be missed when using the conventional intermittent blood gas sampling practice. Therefore, during 30 thoracoscopic procedures with OLV, the sampling intervals between consecutive intermittent laboratory blood gas analyses (BGA) were evaluated with respect to changes of PaO2, PaCO2, and pHa ([H+]) using a continuous intraarterial blood gas monitoring system. Frequency and timing of BGA were based on the clinical judgment of 16 experienced anesthesiologists who were blinded to the continuously measured values. Extreme fluctuations of PaO2 (37-625 mm Hg), PaCO2 (27-56 mm Hg), and pHa (7.24-7.51) were observed by continuous blood gas monitoring. During 63% of all sampling intervals, PaO2 decreased >20% compared with the preceding BGA value, which remained undetected by intermittent analysis. In 10 patients with a continuously measured minimal PaO2 value < or = 60 mm Hg, the preceding BGA overestimated this minimal PaO2 by > 47%. Correspondingly, PaCO2 increases of > 10% were observed in 35% of all sampling intervals, and [H+] increases of > 10% were observed in 24% of all sampling intervals. Because these blood gas changes were not reliably detected by using noninvasive monitoring and their magnitude is not predictable during OLV, intermittent BGA with short sampling intervals is warranted. In critical cases, continuous blood gas monitoring may be helpful. IMPLICATIONS: The magnitude of blood gas changes during thoracoscopic surgery with one-lung ventilation is not predictable and not reliably detected by noninvasive monitoring. Using a continuous intraarterial blood gas monitoring device, we demonstrated that intermittent laboratory blood gas analysis with short sampling intervals is warranted to detect arterial hypoxemia.

Adolescent↗
PubMed1998

Accidental pleural puncture by a thoracic epidural catheter.

We report the occurrence of an accidental pleural puncture by an epidural catheter that happened during the attempted induction of thoracic epidural anaesthesia using a paramedian approach in an awake patient. The incorrect placement of the catheter was recognised while the patient was undergoing thoracoscopic surgery. The possibility of accidental pleural puncture during attempted thoracic epidural catheter placement by either the paramedian or the midline approach should be borne in mind. A misplaced catheter may injure lung tissue and result in a potentially dangerous intra-operative tension pneumothorax.

Aged↗
PubMed1998

Fatal air embolism in an airplane passenger with a giant intrapulmonary bronchogenic cyst.

Considering the large number of airplane passengers with a variety of medical conditions, the incidence of in-flight emergencies on commercial airline flights is low. Only few cases of pulmonary barotrauma in airplane passengers with prior lung pathologies have been reported. We present the unusual case of a female airplane passenger with a previously diagnosed asymptomatic giant intrapulmonary bronchogenic cyst who experienced fatal air embolism on a commercial airline flight. We believe that preventive surgical resection is mandatory in asymptomatic patients with large intrapulmonary cysts prior to exposure to even small alterations in ambient pressure as, for instance, prior to airplane flight or use of mountain cable cars. However, screening for pre-existent lung pathologies in the growing mass of commercial airline travelers is not justified.

Adult↗
PubMed1997

Video-assisted thoracoscopic volume reduction surgery in patients with diffuse pulmonary emphysema: gas exchange and anesthesiological management.

Arterial blood gases were studied prospectively using continuous intraarterial blood gas monitoring during thoracoscopic volume reduction surgery (VRS) in 24 patients with advanced diffuse pulmonary emphysema. Additionally, the early postoperative course (48 h) of arterial blood gases was studied retrospectively. Twenty-six operations were performed using a combination of thoracic epidural and general anesthesia with left-sided double-lumen intubation for one-lung ventilation (OLV). Arterial blood gases were determined awake, during two-lung ventilation prior to surgery, during OLV (extreme values), and after tracheal extubation. Additionally, the extremes during the whole procedure were determined: avoiding excessive peak inspiratory pressures (26.4 +/- 7.0 cm H2O), minimum PaO2 was 77 +/- 39 mm Hg (mean +/- SD), maximum PaCO2 65 +/- 14 mm Hg (P < 0.0001 versus preoperative values), and minimum pHa 7.22 +/- 0.08 (P < 0.0001). One tension pneumothorax occurred during OLV. Immediate postoperative extubation was performed in 25 of 26 cases, reintubation was necessary in two cases. One patient with coronary artery disease died 36 h after surgery. Hypercapnia (maximum PaCO2 49 +/- 8 mm Hg, minimum pHa 7.37 +/- 0.04, P < 0.01) was still observed 48 h after surgery. These results demonstrate that adequate oxygenation can be preserved during OLV for VRS, but CO2 elimination is impaired. However, intraoperative hypercapnia and immediate postoperative tracheal extubation are well tolerated.

Adult↗
PubMed1995

External irradiation of macroinvasive pituitary adenomas with telecobalt: a retrospective study with long-term follow-up in patients irradiated with doses mostly of between 40-45 Gy.

PURPOSE: Published dose recommendations for radiotherapy in patients with pituitary macroadenomas vary. Therefore, we retrospectively analyzed the results in our patients from the treatment period 1973-1992. METHODS AND MATERIALS: From a total of 89 patients with macroinvasive adenomas, 66 received radiation therapy immediately following subtotal surgical removal (combined treatment modality), and 22 were irradiated as primary treatment or after surgical recurrence. Only one patient was reirradiated. The surgical interventions have been performed by the same surgeon. For the majority of patients (79 out of 89) with a mean follow-up of 8.1 years (0.5-19 years) the total tumor dose ranged between 40-45 Gy at a dose per fraction of 1.8-2.25 Gy. All patients had bilateral opposed fields with telecobalt. Eleven patients had an additional arc rotation. RESULTS: The 10-year progression-free survival for all 89 patients independent of treatment modality was 88.1%. The 10-year progression-free survival for patients treated by surgery and adjuvant radiation therapy (40-45 Gy at 1.8-2.25 Gy, 60 out of 79) was 90.3%, and for radiation therapy alone (40-45 Gy at 1.8-2.25 Gy, 19 out of 79), 100% (p = 0.32). The prognostic factors for progression-free survival were the subtype of adenoma, the presence of visual symptoms at the time of diagnosis, the suprasellar extension, and the initial hormone levels. The presence of infiltration of adenoma cells in the basal dura or in the mucosa of the sinus sphenoidalis do not represent prognostic factors showing the special biological behavior of pituitary adenomas. Signs of x-ray-induced cerebral necrosis have not been observed in any patient. Long-term visual complications developed in four patients. This could be due to scar formation in the treated region, which can compress the optic nerve and provoke disturbance similar to an empty-sella syndrome. The latter occurred prevalently years after treatment, even though surgical methods of sellar plugging were used. The incidence of hypopituitarism after combined treatment modality at time of last follow-up (irradiated between 40-45 Gy at 1.8-2.25 Gy) was low (36%, 21 out of 60). CONCLUSION: In patients with pituitary macroadenomas, radiotherapy with a total dose of 40-45 Gy at 1.8-2.25 Gy per fraction resulted in a high local tumor control without serious morbidity.

Adenoma↗
PubMed1993

Extrapulmonary and disseminated infections due to Mycobacterium malmoense: case report and review.

Mycobacterium malmoense is a potentially pathogenic species that was first described in 1977. During the past decade M. malmoense has been recognized with increasing frequency as a pulmonary pathogen. More than 180 cases of M. malmoense infection have been reported. Most of these infections affected a previously damaged lung. Other infection sites included the skin, lymph nodes, and bursae. Five cases of disseminated infection have been reported. The antituberculous drugs associated with the most favorable susceptibility patterns are rifampin and ethambutol. Because of the slow growth of M. malmoense on conventional, egg-based bacteriologic media, the incubation time should be > 6 weeks; special solid and liquid media are recommended. We report a case of disseminated pulmonary and gastrointestinal infection due to M. malmoense in a patient with AIDS, who was treated successfully with a combination of rifabutin (ansamycin), clofazimine, and isoniazid. In addition, we review the characteristics of extrapulmonary and disseminated infections due to M. malmoense.

AIDS-Related Opportunistic Infections↗