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Biomedical subjects

Claus-Martin Muth

Publications and source records attributed to Claus-Martin Muth.

6 recordsLinked to original sources
PubMed2006

Effects of 15-deoxy-Delta12,14-prostaglandin-J2 during hyperdynamic porcine endotoxemia.

OBJECTIVE: To investigate the hemodynamic and metabolic effects of the peroxisome proliferator-activated receptor (PPAR)-gamma ligand and nuclear-factor (NF)-kappa B inhibitor 15-deoxy-Delta12,14-prostaglandin-J2 (15d-PGJ2) during long-term, hyperdynamic porcine endotoxemia. DESIGN: Prospective, randomized, controlled experimental study with repeated measures. SETTING: Investigational animal laboratory. SUBJECTS: 19 anesthetized, mechanically ventilated and instrumented pigs. INTERVENTIONS: At 12 h of continuous intravenous endotoxin and hydroxyethylstarch to keep mean arterial pressure (MAP)>60 mmHg, swine randomly received vehicle (control group, n=10) or 15-deoxy-Delta12,14-prostaglandin-J2 (15d-PGJ2 group, n=9; 1 microg kg(-1) min(-1) loading dose during 1 h; thereafter,0.25 microg kg(-1) min(-1) for 11 h). MEASUREMENTS AND RESULTS: Hemodynamic, metabolic and organ function parameters were assessed together with parameters of nitric oxide production and oxidative stress. 15d-PGJ2 prevented the endotoxin-induced progressive hypotension, due to a positive inotropic effect, which resulted in a significantly higher blood pressure during the treatment phase and prevented the rise in hepatic vein alanine-aminotransferase activity. It did not affect, however, any other parameter of organ function nor of nitric oxide production, proinflammatory cytokine release or lipid peroxidation (8-isoprostane). CONCLUSIONS: 15d-PGJ2 stabilized systemic hemodynamics, due to improved myocardial performance, and resulted in an only transient effect on alanine-aminotransferase activity, without further beneficial effect on endotoxin-induced metabolic and organ function derangements. Low tissue 15d-PGJ2 concentrations and/or the delayed drug administration may explain these findings.

Animals↗
PubMed2005

Interaction of hyperbaric oxygen, nitric oxide, and heme oxygenase on DNA strand breaks in vivo.

Hyperbaric oxygen (HBO), e.g. pure oxygen breathing at supra-atmospheric pressures, represents a well-suited model for investigating oxidative stress-induced DNA damage as well as protective mechanisms. While the induction of heme oxygenase-1 (HO-1) seems to be crucial for this protection against this DNA damage, the role of nitric oxide (NO) remains unclear. HO-1 expression is a major regulator of the inducible NO synthase (iNOS), and therefore we investigated the effect of the interaction between HBO, NO, and HO-1 on DNA damage. Prior to exposure to HBO (3 h at 3 bar ambient pressure) rats randomly received vehicle (HBO alone, 1 mL 0.9% saline, n=8), the NO donor molsidomine (SIN-10, 40 mg/kg, n=8) or the HO-1 blocker tin-mesopophyrin (Sn-MP, 50 micromol/kg, n=8). Additional groups received SIN-10 without exposure to HBO, i.e. breathing air under normobaric conditions for 3h (SIN-10 alone, 40 mg/kg, n=6), vehicle without HBO (negative controls, n=6), and ethylmethanesulfonate without HBO (EMS, 200 mg/kg) (positive controls n=4). Immediately after the 3 h HBO or air breathing period blood was analysed for DNA strand breaks (tail moment in the alkaline comet assay) and nitrite+nitrate (chemoluminescence). Whereas the tail moment was ten-fold higher after EMS than in the negative controls, there was no effect of HBO nor SIN-10 alone. Together with HBO, pretreatment with SIN-10 doubled the tail moment, and Sn-MP increased it by 50%. In contrast to Sn-MP or HBO alone, SIN-10 resulted in a five-fold increase of nitrite+nitrate concentrations. We conclude that both HO-1 blockade and excess NO release promote DNA damage during HBO exposure in vivo. The effect of HO-1 inhibition is probably independent of the regulatory function of HO-1 for iNOS.

Animals↗
PubMed2005

Physiological and clinical aspects of apnea diving.

Apnea diving is a fascinating example of applied physiology. The record for apnea diving as an extreme sport is 171 meters, 8:58 minutes. The short time beneath the surface induces profound cardiovascular and respiratory effects. Variations of blood-gas tensions result from the interaction of metabolism and the rapid sequence of compression and decompression. Decompression sickness is possible. Apnea divers can reach depths beyond the theoretic physiologic limit by using the lung-packing maneuver. Apnea divers exhibit a fall in heart rate, which can be trained and is an oxygen-conserving effect, but increases the incidence of ventricular arrhythmia.

Apnea↗
PubMed2004

[Scuba diving and the heart. Cardiac aspects of sport scuba diving].

Diving with self-contained underwater breathing apparatus (scuba) has become a popular recreational sports activity throughout the world. A high prevalence of cardiovascular disorders among the population makes it therefore likely that subjects suffering from cardiovascular problems may want to start scuba diving. Although scuba diving is not a competitive sport requiring athletic health conditions, a certain medical fitness is recommended because of the physical peculiarities of the underwater environment. Immersion alone will increase cardiac preload by central blood pooling with a rise in both cardiac output and blood pressure, counteracted by increased diuresis. Exposure to cold and increased oxygen partial pressure during scuba diving will additionally increase afterload by vasoconstrictive effects and may exert bradyarryhthmias in combination with breath-holds. Volumes of gas-filled body cavities will be affected by changing pressure (Figure 1), and inert gas components of the breathing gas mixture such as nitrogen in case of air breathing will dissolve in body tissues and venous blood with increasing alveolar inert gas pressure. During decompression a free gas phase may form in supersaturated tissues, resulting in the generation of inert gas microbubbles that are eliminated by the venous return to the lungs under normal circumstances. Certain cardiovascular conditions may have an impact on these physiological changes and pose the subject at risk of suffering adverse events from scuba diving. Arterial hypertension may be aggravated by underwater exercise and immersion. Symptomatic coronary artery disease and symptomatic heart rhythm disorders preclude diving. The occurrence of ventricular extrasystoles according to Lown classes I and II, and the presence of atrial fibrillation are considered relative contraindications in the absence of an aggravation following exercise. Asymptomatic subjects with Wolff-Parkinson-White syndrome may be allowed to dive, but in case of paroxysmal supraventricular tachycardia they must refrain from diving. Pacemakers will fail with increasing pressure, but some manufacturers have proven their products safe for pressure equivalents of up to 30 m of seawater, so that patients may dive uneventfully when staying within the 0-20 m depth range. Significant aortic or mitral valve stenosis will preclude diving, whereas regurgitation only will not be a problem. Right-to-left shunts have increasingly gained attention in diving medicine, since they may allow venous gas microbubbles to spill over to the arterial side of the circulation enabling the possibility of arterial gas embolism. Significant shunts thus preclude diving. The highly prevalent patent foramen ovale is considered a relative contraindication only when following certain recommendations for safe diving (Table 2). Metabolic disorders are of concern, since adiposity is associated with both, higher bubble grades in Doppler ultrasound detection after scuba dives when compared to normal subjects, and an increased epidemiologic risk of suffering from decompression illness. In conclusion, cardiovascular aspects are important in the assessment of fitness to dive, and certain cardiovascular conditions preclude scuba diving. Any history of cardiac disease or abnormalities detected during the routine medical examination should prompt to further evaluation and specialist referral.

Coronary Artery Disease↗