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Biomedical subjects

W Schlack

Publications and source records attributed to W Schlack.

60 records · Page 4Linked to original sources
PubMed1994

Left stellate ganglion block impairs left ventricular function.

Stellate ganglion block (SGB) is an established procedure for the diagnosis and treatment of chronic pain. SGB results in an acute sympathetic denervation of a part of the left ventricular (LV) wall innervated by the blocked ganglion, which may impair regional contractility. The resulting imbalance of myocardial contractility in different LV regions may affect LV function adversely by increasing LV asynchrony. Seven anesthetized open chest dogs were instrumented for measurement of aortic and LV pressure (tip manometers), cardiac output (CO, thermodilution), and regional LV wall thickness (WT, sonomicrometry) in the anteroapical (predominantly innervated by the right stellate ganglion) and posterobasal wall (left stellate ganglion). The contractility of both regions was assessed using the relationship between preload recruitable stroke work and end-diastolic WT relationship (MW). The timing of regional myocardial wall motion was evaluated by means of the phase of the first harmonic of the Fourier transform of the WT signals, LV asynchrony by the phase difference (PD) between both regions, and LV diastolic function by the time constant of isovolumic relaxation (tau). Measurements were performed before and after left SGB (LSGB). Mean arterial pressure was 105 +/- 25 (mean +/- SD) before and 97 +/- 10 mm Hg after LSGB (not significant). CO remained unchanged (3.09 +/- 1.03 vs 2.93 +/- 1.07 L/min). LSGB significantly reduced contractility in the posterobasal myocardium (MW -162 +/- 26 vs -80 +/- 7 mm Hg; P < 0.01), accompanied by a delay of regional wall motion within the cardiac cycle (phase 202 +/- 18 vs 223 +/- 17 degrees; P < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

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PubMed1993

Adenosine A2-receptor activation at reperfusion reduces infarct size and improves myocardial wall function in dog heart.

Reestablishment of blood supply to ischemic myocardium leads to biochemical and cellular changes which are believed to reduce the amount of potentially salvageable myocardium (reperfusion injury). In this situation, adenosine is known to have myocardial protective properties. Activation of adenosine A2-receptors may account for most of the beneficial effects of adenosine in reperfusion injury because A2-receptor activation mediates vasodilation, inhibits neutrophil adhesion to vascular endothelium and diminishes generation of free radicals by neutrophils, thus acting on some of the key mechanisms of reperfusion injury such as postischemic vascular dysfunction and neutrophil-mediated damage. Therefore, we investigated the effect of an intracoronary A2-agonist, CGS 21680, on regional postischemic myocardial function (measured as wall thickening) and infarct size [determined by triphenyltetrazolium chloride (TTC) staining]. Fourteen anesthetized open-chest dogs underwent 1-h left anterior descending artery (LAD) occlusion and 6-h reperfusion and were randomly assigned to receive intracoronary CGS 21680 or to serve as control. The drug was infused for 60 min starting 5 min before reperfusion with a concentration of 10(-7) M at a rate of 10 ml/min under anoxic conditions. The infusion was then continued for the first 55 min of reperfusion with 10(-6) M at a rate of 1 ml/min. Intracoronary infusion of CGS 21680 led to significant improvement in regional wall function in postischemic myocardium (p < 0.05 vs. control). Thickening fraction (percentage of baseline) increased from -13.1 +/- 13.7% (mean +/- SD) during occlusion to 15.3 +/- 29.8% at 30 min of reperfusion in the CGS 21680 treatment group and remained at this level throughout the reperfusion period.(ABSTRACT TRUNCATED AT 250 WORDS)

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PubMedDate not supplied

[Effect of bradykinin on pressure changes in the femur head epiphysis--an experimental and magnetic resonance tomography study].

AIM OF THE STUDY: The aim of this study was to evaluate the response of the femoral head to intraosseous pressure increases and to document blood flow of periarticular soft tissue after infusion of vasoactive substances. Beside that the value and imagery of native MRI after induced intraosseous pressure increase should be estimated for early detection of femoral head necrosis. METHODS: The alteration of intraosseous pressure and peripheral blood flow of the femoral head of beagle dogs was examined after administration of bradykinin as a vasoactive substance followed by subsequent magnetic resonance imaging (MRI). Bradykinin was injected into the arteriae circumflexae femoris lateralis and medialis of six beagle dogs. The administrations were made using a standard protocol with simultaneous measurement of venous blood flow and intraosseous pressure distribution in the epiphysis of the femoral head. Bradykinin was applied in regular time intervals followed by MRI. RESULTS: At a mean epiphyseal pressure 14.66 mmHg (sigma: 2.42) in the femoral head, a mean flow of 91.6 ml/min (sigma: 16.08) was measured in the vena femoralis. After an administration of a defined concentration of bradykinin an increased epiphyseal pressure was recorded in the measured area. An average increase blood flow of the vena femoralis was observed at the beginning of the bradykinin-injection, followed by a circulatory volume reduction. The post-experimental MRIs showed massive oedema in the femoral musculature after bradykinin-application, however without osseous signal alterations in T1- or STIR-weighted images. CONCLUSION AND CLINICAL RELEVANCE: Our results indicate that acute intraosseous pressure increases are not accompanied by signal alterations in MRI. Obviously more extensive pressure induced lesions are necessary for detectable signal alterations, as these have already been demonstrated in patients with diagnosed femoral head necrosis.

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