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Biomedical subjects

B Puschendorf

Publications and source records attributed to B Puschendorf.

At least 37 records · Page 2Linked to original sources
PubMed1998

Atrial natriuretic peptide-induced release of cyclic guanosine monophosphate by coronary bypass grafts.

BACKGROUND: Superior long-term patency rates of the internal mammary artery (IMA) versus saphenous vein (SV) after coronary artery bypass grafting are well documented. Higher production rates of vasodilating and platelet-inhibiting mediators (prostacyclin and nitric oxide) by the IMA seem to have a major impact on its long-term durability and resistance to coronary artery graft disease. For the right gastroepiploic artery (RGEA) marked release of protective mediators is reported as well. The vasodilating effect of cyclic guanosine monophosphate (cGMP) released after stimulation by atrial natriuretic peptide might serve as another graft protective system. The aim of the present study was to determine cGMP release by IMA, RGEA, and SV after atrial natriuretic peptide challenge. METHODS: Samples of human IMA (n = 19), RGEA (n = 7), and SV (n = 18) discarded during coronary artery bypass grafting were stimulated with 10(-6) mol/L atrial natriuretic peptide after a resting phase in nutrient medium. Release of cGMP was determined by 125-iodide radioimmunoassay. RESULTS: Basal cGMP production rates of the IMA (759.9 +/- 277.0 fmol/cm2) and RGEA (739.9 +/- 186.0 fmol/cm2) were higher than production rates of SV (281.2 +/- 64.0 fmol/cm2). Application of atrial natriuretic peptide led to a statistically significant increase of cGMP release in IMA grafts (1,939.3 +/- 778.0 fmol/cm2), whereas RGEA (618.4 +/- 141.3 fmol/cm2) and SV (221.7 +/- 64.5 fmol/cm2) remained at basal levels (p < 0.05). CONCLUSIONS: From these data we conclude that the IMA in comparison with the RGEA and SV produces more extracellular cGMP when stimulated by atrial natriuretic peptide. This effect might support the cGMP-mediated protective properties of nitric oxide and could underline the extraordinary suitability of the IMA as a bypass conduit.

Abdominal Muscles↗
PubMed1998

Stimulated prostacyclin release by conduits used for coronary artery bypass grafting.

A direct comparison of the three coronary artery bypass conduits internal mammary artery (IMA), right gastroepiploic artery (RGEA), and saphenous vein (SV) concerning arachidonic acid (AA) stimulated release of the vasodilating and platelet inhibiting mediator prostacyclin was the aim of the present study. Pieces of saphenous vein (n = 16), right gastroepiploic artery (n = 8), and internal mammary artery (n = 19) were obtained from patients undergoing coronary artery bypass grafting. After a resting phase of 30 min in HEPES medium arachidonic acid (AA) was added in order to stimulate prostacyclin release. Time-dependent production of the stable prostacyclin metabolite 6-keto-prostaglandin F1 alpha was determined following stimulation. Under basal conditions the IMA (12.4 ng/cm2) and RGEA (12.0 ng/cm2) released more prostacyclin than saphenous vein (4.0 ng/cm2). After AA stimulation 6-keto-prostaglandin F1 alpha release at 30 min was as follows: IMA 806.0 ng/cm2, RGEA 35.9 ng/cm2, SV 82.3 ng/cm2 (p < 0.0001 within grafts, p < 0.0001 between grafts, ANOVA for repeated measures). The internal mammary artery in comparison with the right gastroepiploic artery and saphenous vein seems to be better protected against local thrombotic events and development of coronary artery graft disease with the aid of the vasodilating and platelet inhibiting mediator prostacyclin.

Arachidonic Acid↗
PubMed1998

No release of cardiac troponin I during major orthopedic surgery after acute normovolemic hemodilution.

BACKGROUND: Normovolemic hemodilution is a well-accepted method for intraoperative blood salvage. However, some controversy exists concerning the possible risk of myocardial fiber injury as consequence of the reduced oxygen content. Laboratory diagnosis of perioperative myocardial fiber injury is difficult, since biochemical markers are elevated postoperatively due to the surgical trauma. Cardiac troponin I (cTnI) is a new, highly sensitive and specific marker for the detection of myocardial injury. The aim of our study was to investigate whether normovolemic hemodilution in patients with major orthopedic surgery (13 hemodiluted patients, 15 control) induces a release of cTnI. METHODS: cTnI as a highly specific and sensitive cardiac parameter, as well as total creatine kinase (CK), creatine kinase isoenzyme MB mass (CKMB mass) and myoglobin were measured after induction of anesthesia, after normovolemic hemodilution, prior to retransfusion of blood components, 3 h after surgery, and on the first and third postoperative days. RESULTS: Prior to retransfusion of blood components the hematocrit was decreased to 25.4 +/- 1.2% (mean +/- SEM; range: 18%-34%) in the control group and to 20.2 +/- 0.8% (mean +/- SEM; range: 17%-24%) in the hemodilution group. Total CK, CKMB mass as well as myoglobin concentration increased significantly in both groups, reaching their maxima within the first day of surgery. In contrast, cTnI was below the detection limit of assay (< 0.5 micrograms/L) at any time. CONCLUSIONS: We suggest that pre- and intraoperative hemodilution to a hematocrit of approximately 20% by maintaining normovolemia does not induce myocardial fiber injury in patients without preexisting cardiac diseases.

Adult↗
PubMed1998

Early assessment of exercise induced skeletal muscle injury using plasma fatty acid binding protein.

OBJECTIVE: To test whether fatty acid binding protein (FABP) is a useful plasma marker for the early detection of exercise induced skeletal muscle injury in healthy subjects. METHODS: Plasma concentrations of FABP and myoglobin (Mb) were measured in six healthy physical education teacher trainees after 20 minutes of downhill running (16% incline; mean lactate 4 mmol/l; 70% (VO2MAX). Creatine kinase (CK) was measured for comparison. RESULTS: Significant increases were found in plasma FABP (mean peak level 50 micrograms/l), Mb (823 micrograms/l), and CK (491 U/l). Mb and FABP concentrations were already significantly elevated (p < 0.05) at 30 minutes, but CK not until two hours after exercise. Whereas Mb and FABP decreased to normal levels within 24 hours, CK activity remained elevated until 48 hours. The Mb to FABP ratio in plasma after exercise induced muscle injury was 15.0 (1.3) (mean (SEM)) (range 7.4-31.1), which is within the range of ratios calculated for skeletal muscle tissue contents of Mb and FABP, but different from the reported plasma ratio after myocardial injury (4-6). CONCLUSIONS: After eccentric exercise induced muscle injury, plasma FABP and Mb increase and decrease more rapidly than CK, indicating that both FABP and Mb are more useful than CK for the early detection of such injuries and the monitoring of injury during repeated exercise bouts. In addition, the Mb to FABP ratio in the plasma identifies the type of muscle injured.

Adult↗
PubMed1998

Rebound increase of plasminogen activator inhibitor type I after cessation of thrombolytic treatment for acute myocardial infarction is independent of type of plasminogen activator used.

Plasma concentrations of tissue-type plasminogen activator (t-PA), plasminogen activator inhibitor type 1 (PAI-1), and D-dimer were investigated in 50 patients treated intravenously for acute myocardial infarction with either streptokinase (n = 23), urokinase (n = 17), or recombinant t-PA (rt-PA, n = 10). The fibrinolytic variables were measured by enzyme immunoassay on admission; 1, 2, 4, 6, 8, 12, and 24 h later; and then daily until day 7 after admission. In each subgroup of patients treated with different thrombolytic agents, PAI-1 increased significantly (P < 0.01) approximately 3 h after cessation of thrombolytic therapy. PAI-1 peak concentrations did not differ significantly (P = 0.82) among these three subgroups. t-PA and D-dimer did not differ significantly (P > 0.14) among subgroups except for higher t-PA in the rt-PA group attributable to detection of the therapeutically administered exogenous rt-PA by the t-PA assay. Our findings demonstrate a marked PAI-1 increase after thrombolytic therapy for acute myocardial infarction, which seems to be a common, drug-independent antifibrinolytic rebound phenomenon in response to thrombolytic treatment.

Adult↗
PubMed1998

Effects of prolonged strenuous endurance exercise on plasma myosin heavy chain fragments and other muscular proteins. Cycling vs running.

BACKGROUND: This study evaluates creatine kinase, myosin heavy chain, and cardiac troponin blood levels following three types of exercise: 1) short-distance uphill or downhill running; 2) alpine ultramarathon; and 3) alpine long-distance cycling. METHODS EXPERIMENTAL DESIGN: Comparative field study; follow-up up to 10 days. SETTING: Department of Sports Medicine. All biochemical markers were analysed at the Department of Medical Chemistry and Biochemistry. PATIENTS OR PARTICIPANTS: Subjects included healthy, trained males (N = 53). All subjects were nonsmokers and free from medication prior to and during the study. Each volunteer was an experienced runner or cyclist, who had at least once successfully finished the Swiss Alpine Marathon of Davos or the Otztal-Radmarathon before. INTERVENTIONS: Running or cycling. MEASURES: Plasma concentrations of creatine kinase, myosin heavy chain fragments and cardiac troponins were measured to diagnose skeletal and cardiac muscle damage, respectively. RESULTS: Skeletal muscle protein release is markedly different between uphill and downhill running, with very little evidence for muscle damage in the uphill runners. There is considerable muscle protein leakage in the ultramarathoners (67 km distance; 30 km downhill running). In contrast, only modest amounts of skeletal muscle damage are found after alpine long-distance cycling (230 km distance). CONCLUSIONS: This study proves that there is slow-twitch skeletal muscle fiber damage after prolonged strenuous endurance exercise and short-distance downhill running. Exhaustive endurance exercise involving downhill running and short-distance downhill running lead to more pronounced injury than strenuous endurance exercise involving concentric actions. From our results there is no reason for suggesting that prolonged intense exercise may induce myocardial injury in symptom-less athletes without cardiac deseases.

Adult↗
PubMed1998

Different intracellular compartmentations of cardiac troponins and myosin heavy chains: a causal connection to their different early release after myocardial damage.

We investigated the net myocardial release of creatine kinase isoenzyme MB (CKMB), myoglobin, cardiac troponin T (cTnT), cardiac troponin I (cTnI), and cardiac beta-type myosin heavy chain (beta-MHC) into the coronary circulation after cardioplegic cardiac arrest in humans. Cardiac markers were measured in paired arterial, central venous, and coronary sinus blood in 19 patients undergoing elective coronary artery bypass grafting (CABG) before aortic cross-clamping and 1, 5, 10, and 20 min after aortic declamping. cTnT and cTnI were released into the coronary sinus in parallel to each other and almost simultaneously to myoglobin and CKMB within 20 min of reperfusion. In contrast, no beta-MHC was released in the same patients during the study period. The average soluble cTnT and cTnI pools in right atrial appendages of 11 patients with right atrial and right ventricular pressures within reference values were comparable and were approximately 8% of total myocardial troponin content. The soluble beta-MHC pool was <0.1% in all patients. Our results demonstrate the impact of the different intracellular compartmention of regulatory and contractile proteins on their early release from damaged myocardium.

Adult↗
PubMed1997

Markers of activated coagulation for early diagnosis of acute myocardial infarction.

Intracoronary thrombosis plays a key role in the pathogenesis of acute myocardial infarction (AMI), and the formation of an occlusive thrombus usually precedes the development of myocardial damage. Therefore we evaluated and compared the early sensitivities of thrombin-antithrombin III complex (TAT), D-dimer, myoglobin, creatine kinase (CK) MB mass concentration, and cardiac troponin T (cTnT) on admission to a coronary care unit (CCU) before heparin or thrombolytic therapy was started. We investigated 31 consecutive patients admitted to CCU for evolving AMI within 6 hours from the onset of infarct-related symptoms; the median delay from chest pain onset to CCU admission was 135 minutes. Of all biochemical markers tested TAT had the highest early sensitivity on admission to the CCU, and TAT was significantly more sensitive than cTnT, CKMB mass, myoglobin, and D-dimer. However, TAT increases give no information about the location of clot formation in the body, and the diagnosis of AMI must be subsequently verified by an increase in more cardiac specific proteins, such as troponins or CKMB.

Acute Disease↗
PubMed1997

Cardiac troponin I to diagnose percutaneous transluminal coronary angioplasty-related myocardial injury.

The purposes of the present study were to evaluate cardiac troponin 1 (cTnl) in the diagnosis of percutaneous transluminal coronary angioplasty (PTCA)-related myocardial injury in comparison with cardiac troponin T (cTnT) and creatine kinase (CK) MB mass concentration, and to investigate the frequency of myocardial injury, as indicated by myocardial protein release, after clinically symptomless side-branch occlusion (SBO) which may occur in the proximity of the attempted stenosis. The final study population comprised 80 patients undergoing elective, single vessel PTCA. Blood samples were drawn before, 6, 24 and 48 h after PTCA. cTnI, cTnT and CKMB mass baseline values were within the reference intervals in all patients (cTnI < 0.1 microgram/l, cTnT < 0.2 microgram/l, CKMB < 5 micrograms/l). Two patients presented with primary failure of PTCA, and visually successful PTCA was performed in all remaining patients. Seven patients (four with SBO) subsequently developed acute myocardial infarction (AMI). Symptomless SBO occurred in 16 patients. In controls (n = 55) there were no significant increases in cTnI, cTnT, or CKMB concentrations compared with baseline values, and all markers stayed within their reference intervals. In half the patients with symptomless SBO (n = 8) all markers were slightly to moderately increased, in two additional patients only CKMB was elevated (cTnI: 0.1-1.0 microgram/l; cTnT: 0.25-0.81 microgram/l and CKMB: 7.9-25.6 micrograms/l). In the majority of patients with primary failure or AMI we found pronounced increases in all tested markers (cTnI: 0.2-12.0 micrograms/l; cTnT: 0.44-12.10 micrograms/l; CKMB: 19.2-423.0 micrograms/l). The results of this study indicate that cTnI is comparably useful to cTnT or CKMB mass for diagnosing myocardial injury in PTCA patients. From our results a preference for one of the tested parameters cannot be clearly derived. Post-procedural cTnI, cTnT, and CKMB mass values are not higher than baseline values in uncomplicated cases, whereas AMI after PTCA leads to pronounced marker increases. SBO, even when symptomless, leads frequently (in about half the patients) to slight marker increases.

Adult↗
PubMed1997

Augmented release of brain natriuretic peptide during reperfusion of the human heart after cardioplegic cardiac arrest.

The aim of the study was to investigate the release of natriuretic peptides during myocardial ischaemia and reperfusion associated with cardioplegic cardiac arrest. Brain natriuretic peptide (BNP) and atrial natriuretic peptide (ANP) concentrations were measured in paired arterial, central venous and coronary sinus blood samples in 19 patients undergoing elective coronary artery bypass grafting before aortic crossclamping and 1, 5, 10 and 20 min after aortic declamping. Peak myocardial BNP release after aortic declamping was significantly higher than baseline values before aortic crossclamping. Both peak and cumulative BNP release during reperfusion correlated significantly with the severity of ischaemia, as assessed by myocardial lactate production. In 3 patients with perioperative myocardial ischaemia, cumulative and peak myocardial BNP release after aortic unclamping was markedly higher than in the remaining 16 uneventful patients. Myocardial ANP release during reperfusion was not significantly different from baseline values before aortic crossclamping. In conclusion, our data demonstrate a significantly enhanced myocardial BNP release early during reperfusion of the human heart after global ischaemia associated with cardioplegic cardiac arrest.

Adult↗
PubMed1997

Muscular adaptation and strength during the early phase of eccentric training: influence of the training frequency.

We investigated the effects of different training frequencies on maximum isometric voluntary contraction (MVC) force and plasma concentrations of muscle proteins during the early phase of eccentric training. MVC and plasma concentrations of creatine kinase (CK) and slow-twitch skeletal (cardiac beta-type) myosin heavy chain (MHC) fragments were measured before and 4 and 7 d after performing the first and last training task. Training tasks, which comprised 70 high-force eccentric contractions involving the thigh muscles (single leg), were performed under supervision in three groups (A, B, C) at the beginning and at the end of the study period (7 wk). In addition, groups A (N = 10) and B (N = 10) trained during the study period starting 1 wk after the first training task. Group A performed one training task once a week for 5 wk and group B (N = 10) twice a week for 2 wk and three times a week during the subsequent 3 wk. In all three groups the first training task resulted in delayed CK and MHC peaks and decrements in MVC, which were comparable (P > 0.05). Only training regimen B resulted in a significant increase in the MVC. Compared with the first training task training regimens, A and B significantly (P < 0.01) reduced the increase in serum muscle protein and muscle function impairment. The responses to the last training task did not differ significantly between groups A and B. In group C the responses after the second training task did not differ significantly from those observed after the first task. Our results suggest that, compared with group A, additional eccentric exercise in group B is the essential basis for the increase in muscle strength during the early phase of eccentric training without further benefits for muscular adaptation. In group C we found no muscular adaptation.

Adaptation, Physiological↗
PubMed1997

Skeletal troponin I as a marker of exercise-induced muscle damage.

The utility of skeletal troponin I (sTnI) as a plasma marker of skeletal muscle damage after exercise was compared against creatine kinase (CK), myoglobin (Mb), and myosin heavy chain (MHC) fragments. These markers were serially measured in normal physical education teacher trainees after four different exercise regimens: 20 min of level or downhill (16% decline) running (intensity: 70% maximal O2 uptake), high-force eccentric contractions (70 repetitions), or high-force isokinetic concentric contractions of the quadriceps group (40 repetitions). Eccentrically biased exercise (downhill running and eccentric contractions) promoted greater increases in all parameters. The highest plasma concentration were found after downhill running (median peaks: 309 U/l CK concentration (-CK-)), 466 microgram/l Mb concentration (-Mb-), 1,021 microU/l MHC concentration (-MHC-), and 27.3 microgram/l sTnI concentration ([sTnI]). Level running produced a moderate response (median peaks: 178 U/l -CK-, 98 microgram/l -Mb-, 501 microU/l -MHC-, and 6.6 microgram/l [sTnI]), whereas the concentric contraction protocol did not elicit significant changes in any of the markers assayed. sTnI increased and peaked in parallel to CK and stayed elevated (>2.2 microgram/l) for at least 1-2 days after exercise. In contrast to MHC, sTnI is an initial, specific marker of exercise-induced muscle injury, which may be partly explained by their different intracellular compartmentation with essentially no (MHC <0.1%) or a small soluble pool (sTnI: median 3.4%).

Adult↗
PubMed1996

In vivo phosphorylation of histone H1 variants during the cell cycle.

In vivo phosphorylation of the five histone H1 variants H1a-H1e including H1(0) in NIH 3T3 mouse fibroblasts was examined during the cell cycle by using a combination of HPLC techniques and conventional AU gel electrophoresis. Phosphorylation starts during the late G1 phase and increases throughout the S phase. In the late S phase, the H1 variants exist as a combination of molecules containing 0 or 1 (H1a, H1c), 0-2 (H1d), or 0-3 (H1b, H1e) phosphate groups with a share of unphosphorylated protein ranging between 35% and 75%, according to the particular subtype. Pulse-chase experiments show that phosphorylation during the S phase is a dynamic phosphorylation process with a limited phosphorylation maximum. In most H1 subtypes, phosphorylation occurs very rapidly at the G2/M transition with only small amounts of intermediate phosphorylated molecules. Phosphorylation of mouse H1c, however, occurs stepwise during this transition. Phosphorylated mouse histone subtypes from cells in mitosis contain four phosphate groups in the case of H1a, H1c, and H1e and five in the case of H1b and H1d. Comparison of the mouse phosphorylation pattern to that in rat C-6 glioma cells showed differences for H1e and H1d. By comparing the different phosphorylation patterns of the individual H1 variants during the cell cycle, we were able to classify the H1 histones into subtypes with low (H1a, H1c, H1(0)) and high (H1b, H1d, H1e) phosphorylation levels.

3T3 Cells↗