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Biomedical subjects

J Schaper

Publications and source records attributed to J Schaper.

At least 199 records · Page 11Linked to original sources
PubMedDate not supplied

Tolerance to ischemia of hypertrophied human hearts during valve replacement.

This study evaluates the tolerance to ischemia during induced cardiac arrest in patients undergoing aortic valve replacement. In all patients cardiac standstill was of 45 minutes duration. Biopsies for electron microscopic study were taken from the left ventricle before induction of arrest, at the end of the ischemic period and 20 minutes after coronary perfusion had been reestablished. Structural ischemic damage was more pronounced in patients with severe hypertrophy and structural reconstitution was delayed. Degenerative changes of the myocardial cells, although observed frequency, apparently did not influence the tolerance to ischemia. It is concluded from this study that patients with severe hypertrophy represent a high-risk group in cardiac surgery because of their reduced tolerance to induced myocardial ischemia during cardiopulmonary bypass.

Adult↗
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Influence of repetitive coronary occlusions on myocardial adenine nucleosides, high energy phosphates and ultrastructure.

We compared the effects of repeated short periods of myocardial ischemia with those of permanent occlusion (canine open-chest) with regard to tissue content of adenine nucleotides, nucleosides, creatine phosphate, and ultrastructure. Coronary occlusion for 3 min followed by a reperfusion period of 7 min was repeated up to a cumulative occlusion time of either 45 or 90 min. After cumulative occlusions of 15, 30, 45, and 90 min, transmural needle biopsies were taken from the ischemic area to be analyzed for adenine nucleotides, nucleosides, creatine phosphate, and ultrastructural changes. At the end of each experiment, tetrazolium salt staining was used for macroscopic detection of myocardial necrosis. These data were obtained with those obtained from dogs with a permanent coronary occlusion of 45 and 90 min, respectively. After repeated coronary occlusions at a cumulative occlusion time of 45 min, macroscopic detection of necrosis was negative, and after 90 min of cumulative coronary occlusion, patchy subendocardial tissue necrosis was found in only one out of 13 dogs, whereas in the group with permanent coronary occlusion, small patchy subendocardial necrosis was found in 95% after 45 min, and after 90 min permanent coronary occlusion, large subendocardial necrotic areas spreading towards the epicardial layers were found in 90% of the hearts. Ultrastructural investigations showed only slight to moderate ischemic injury after 45 and 90 min intermittent coronary occlusion, whereas permanent coronary occlusion produced moderate to severe ischemic injury after 45 min; and 90 min permanent coronary occlusion produced irreversible ischemic injury in all subendocardial tissue samples and in 80% of the subepicardial tissue samples.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenine Nucleotides↗
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Loss of canine myocardial nicotinamide adenine dinucleotides determines the transition from reversible to irreversible ischemic damage of myocardial cells.

We investigated if the loss of nicotinamide coenzymes in ischemic-infarcted myocardium may be responsible for the transition from reversibly ischemic to irreversibly infarcted cell damage. The LAD was occluded in 6 dogs for 4 h. Transmural needle biopsies were taken from he ischemic-infarcted region after 1/2, 1, 11/2, 2, and 4 h of ischemia and further divided into subepicardial and subendocardial halves. At each time interval the concentration of the nicotinamide coenzymes NAD, NADH, and NADPH were measured, and the degree of cellular injury was evaluated by electron microscopy. The glycohydrolase activity (EC 3.2.2.5), the enzyme which splits NAD, was determined in brain, myocardium, kidney, and skeletal muscle of 4 rats. Total NAD, the sum of NAD and NADH, started to decrease significantly in the ischemic subendocardium 1 h after onset of ischemia. Degradation of NADPH occurred later. Loss ot total NAD was about 60-70% when electron microscopy diagnosed irreversible cell injury. The glycohydrolase activity was the highest in brain followed by myocardium, kidney, and skeletal muscle, reflecting the different tolerances of these tissues towards ischemia. The key mechanism for ischemic injury seems to be the tissue acidosis which activates the glycohydrolase leading to a loss of the vital coenzymes.

Animals↗
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Quantitative ultrastructure of the myocardium in chronic aortic valve disease.

Light and electron microscopic morphometry was carried out in tissue samples which were obtained from the left ventricular free wall in 29 patients with chronic aortic valve disease during open-heart surgery. 6 patients had aortic stenosis, 9 had aortic insufficiency and 14 had a mixed aortic valve lesion. Hemodynamics were studied before operation. Patients with mixed aortic valve disease had a higher left ventricular mass, a lower ejection fraction and mean circumferential fiber shortening rate than patients with aortic stenosis. Peak systolic wall stress was comparable between groups. The intracellular content of contractile material was lower and the sarcoplasmic volume was higher in mixed aortic valve disease than in aortic stenosis. Mitochondrial volume and interstitial fibrosis were not different between groups. Patients with aortic insufficiency showed no significant difference of parameters as compared to both other groups. We conclude that an intracellular deficiency of myofibrils causes lack of contractility in advanced hypertrophy due to mixed aortic valve disease.

Aortic Valve Insufficiency↗
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Ultrastructure of electrophysiologically identified human sinoatrial nodes.

The ultrastructure of freshly excised human sinus node tissue was studied. In three female patients (ages 20, 30, and 36 years) medically refractory disabling episodes of inappropriate sinus tachycardia were surgically treated by extirpation of the sinus node. Each patient underwent intraoperative electrophysiological mapping to determine the area of earliest atrial activation. This area corresponded anatomically to the region of the sinoatrial node and was excised in each patient, the defect repaired using a pericardial patch. The freshly excised SA nodes underwent ultrastructural study. Three types of myocardial cells were identified: pacemaker or polygonal cells with clear cytoplasm, few mitochondria and sparse numbers of contractile elements (P cells); a transitional cell with slightly increased numbers of myofibrils (T cells); and typical atrial myocardial cells with normal numbers of contractile elements. These cell types have previously been identified in post-mortem studies of presumed SA node. The current study confirms the cell types in electrophysiologically documented SA nodes. The one abnormal finding observed in transitional cells in all patients was an increased number of lipofuscin-laden vacuoles. These vacuoles are considered a sign of cell degeneration and their occurrence was totally unexpected in these young adults. In summary, ultrastructural study of electrophysiologically documented human SA nodes confirmed the cell types identified in post-mortem studies. Furthermore, lipofuscin-laden vacuoles were increased in these three patients and this finding may serve as an ultrastructural marker associated with the syndrome of inappropriate sinus tachycardia.

Adult↗
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Morphology and mitochondrial function of the surviving myocardium following myocardial infarction in the cat.

The surviving myocardium of the cat was studied 7 days and 6 weeks following experimental infarction. Seven days after infarction, ultrastructural alterations of the mitochondria indicative of slight hypoxic injury--clearing of the matrix and loss of dense matrix granules--were found. Together with intracellular edema and glycogen depletion this result was considered as a sign of relative hypoxia in the surviving myocardium 7 days after infarction. At the same time beta-glucuronidase activity of tissue homogenates was found to be elevated. Focal ischemic lesions in remote myocardium which have been described by other authors (5, 6, 23) were not detected in our experiments. Six weeks after infarction, the fractional volume occupied by myofibrils had increased whereas the fractional volume of mitochondria had remained unchanged (left ventricle) resp. had decreased (right ventricle). There were no qualitative changes detectable at the ultrastructural level. Based on the morphometric investigation of Anversa (1, 2), our results were regarded indicative of mild compensatory hypertrophy of the surviving myocardium. Glutamate dehydrogenase activity of tissue homogenates was shown to be increased when compared to control values. Furthermore our morphometric results showed that the unit mass of mitochondria has to render an enhanced amount of energy six weeks after infarction which might leave the surviving myocardium with a higher susceptibility to future hypoxic injury.

Animals↗
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The role of apoptosis in myocardial ischemia: a critical appraisal.

The role of apoptosis in cardiac ischemia is not clarified yet. Own data show that suicidal cell death is apparently not important in global ischemia where it only affects a small number of myocytes (8 %) while the majority of cells, i.e. 92 % die by oncosis. In acute regional ischemia it is most probably not a decisive factor. However, more solid data are needed to justify this statement. Human hibernating myocardium shows an activation of the apoptotic cascade, i.e., apoptosis might contribute to cell loss in this pathophysiological situation of multiple ischemic episodes. Manifold unresolved issues contribute to problems in determining the role of apoptosis in ischemia. These include 1) Uncertainty of the duration of the apoptotic cascade from activation of death receptors at the cellular membrane until DNA fragmentation occurs, 2) The role of the mitochondrial pathway, 3) The mode of removal of myocytes after cell death has occurred, 4) Technical problems such as specificity of the TUNEL method, detection of low abundance proteins such as activated caspases or cytochrome C, statistical considerations. These issues and many others should be clarified before any definite conclusion as to the role of apoptosis in ischemia may be drawn.

Animals↗
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Long-term intracoronary ethanol administration electrophysiologic and morphologic effects.

The long-term intracoronary infusion of ethanol was used to evaluate the potential of ethanol to produce myocardial injury and cardiac rhythm disturbances. In 22 dogs, electrophysiologic testing was performed 48 hr after cessation of alcohol administration. Multiple premature ventricular beats occurred spontaneously in 3 dogs with spontaneous sustained monomorphic ventricular tachycardia observed in 1 dog. Provocative ventricular pacing produced ventricular tachycardia lasting 20 or more beats in 13 animals with sustained tachycardia observed in 3 animals. Provocative ventricular pacing in the presence of lidocaine or epinephrine produced sustained ventricular tachycardia in an additional 4 dogs. The electrophysiologic properties of Purkinje fibers from the zone receiving ethanol were altered when compared to the control zone. The resting membrane potential was decreased (-76 +/- 2 mV vs. -85 +/- mV, p less than 0.001) with a decrease in action potential amplitude (91 +/- 4 vs. 109 +/- 2 mV, p less than 0.001) and phase 0 upstroke (231 +/- 27 vs. 456 +/- 25 V/sec, p less than 0.02). Prolonged refractoriness was observed in the ethanol zone without a prolongation of action potential duration. Intramural lesions observed within the left circumflex distribution varied from focal acute myofibrillar degeneration and necrosis to severe local scarring. The data suggest that intracoronary ethanol administration at human abuse levels of blood alcohol concentrations produces histologic and electrophysiologic injury in the canine heart. The electrophysiologic ch changes provide a substrate sufficient for the induction and maintenance of ventricular arrhythmia.

Action Potentials↗
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Bone marrow oedema and aseptic osteonecrosis in children and adolescents with acute lymphoblastic leukaemia or non-Hodgkin-lymphoma treated with hyperbaric-oxygen-therapy (HBO): an approach to cure? -- BME/AON and hyperbaric oxygen therapy as a treatment modality.

BACKGROUND: There is a striking need for additional therapies of bone marrow oedema (BME) and aseptic osteonecrosis (AON) in paediatric oncology patients. Hyperbaric oxygenation (HBO) therapy used in the treatment of osteoradionecrosis is demonstrated effectiveness. Aim of this retrospective analysis was to investigate whether HBO-therapy might lead to subjective as well as objective effects in the treatment of BME and/or AON in paediatric oncology patients with acute lymphoblastic leukaemia (ALL) or Non-Hodgkin lymphoma (NHL). PATIENTS AND METHODS: Between 11/1988 and 01/2001 27/291 (9.3 %) patients with ALL or NHL were diagnosed with a BME and/or AON in the Clinic for Paediatric Oncology, Haematology, and Immunology at University of Dusseldorf. 19/27 patients were submitted to HBO-therapy. Patients received average 45 HBO-treatments per patient (min. 13, max. 80 treatments). The affected regions were re-evaluated with MRI for radiological extent of lesions every 3 months. Pain in its intensity and localisation was serially recorded during HBO-therapy as key symptom in 11 of 19 patients. RESULTS: 27 patients (15 females, 12 males; mean age at diagnosis of malignancy 8.2 +/- 4.7 (SD) years, range 7 months to 16 years) presented with 138 lesions. 133/138 lesions were localised in the lower extremities. At diagnosis of BME and/or AON, 78/133 lesions were shown in females and 55/133 lesions in male. Girls < 10 years predominantly presented BME (33 BME vs. 6 AON), girls aged > 10 years predominantly offered AON (28 AON vs. 11 BME). BME was more often exhibited in boys < 10 years (34 BME vs. 10 AON) and rarely in boys > 10 years (4 BME vs. 6 AON). 11 patients treated with HBO-therapy were serially evaluated for pain intensity throughout their HBO-therapy courses by visual analogue scale (VAS) assessment. During the first 15 treatment courses the HBO-therapy a clear-cut reduction of pain was observed. The mean pain score before the first HBO-treatment unit was 2.4 +/- 2.7 (X +/- SD), decreased before the fifth to 1.6 +/- 1.7 and prior to the 35 (th) and 40 (th) HBO treatment to 0. Girls < 10 years treated with HBO showed an increase of BME (31 --> 46) and declining AON numbers (6 --> 2). Girls > 10 years with and without HBO-therapy showed decrease of BME lesions (7 --> 4 vs. 4 --> 0), whereas AON increased in the HBO-treated group (28 --> 29) as well as the non-treated group (0 --> 4). Males < 10 years showed an increase in BME lesion numbers despite HBO intervention (24 --> 26). The AON lesion numbers dropped in parallel (6 --> 3). Male patients not treated with HBO showed constant numbers of BME (11-->11) and a decreased numbers of AON (4 --> 2). All differences are statistically not significant. CONCLUSIONS: Children and adolescents diagnosed with ALL or NHL have a risk for accruement of BME and/or AON irrespective of the age, with an almost exclusive involvement of the lower extremities. Lesions of pedal bones and ankle joints predominantly affect children < 10 years. Lesions of knee and hip joints predominantly affect children > 10 years. In children < 10 years of age we demonstrate declining AON numbers and conversion of AON to BME thereby implicating possible beneficial effect of HBO in such patients. HBO failed to show beneficial effect on BME whether by preventing new lesions or by improving existent lesions in children > 10 years.

Adolescent↗
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[Effects of self-adapting G-DRG system 2004 to 2006 on in-patient services payment in pediatric hematology and oncology patients of a university hospital].

BACKGROUND: Reimbursement of inpatient treatment by daily constant charges is replaced by diagnosis- and procedure-related group system (G-DRG) in German acute care hospitals excerpt for psychiatry since 2004. Re-designs of G-DRG system were undertaken in 2005 and 2006. Parallel to implementation requirement- and resource-based self-adjustment of this new reimbursement system has been established by law. Adjustments performed in 2005 and 2006 are examined with respect to their effect on reimbursements in treatments of children with oncological, hematological, and immunological diseases. PATIENTS AND METHODS: An unchanged population of 349 patients associated with 1,731 inpatient stays of a Clinic of Pediatric Oncology, Hematology, and Immunology in 2004 was analyzed by methods and means of G-DRG systems 2004, 2005, and 2006. DRGs and additional payments for drugs and procedures eligible for all and/or individual hospitals were calculated. RESULTS: G-DRG system 2005 resulted in overall reimbursement loss of 3.77 % compared to G-DRG 2004. G-DRG 2006 leads to slightly improved overall reimbursements compared to G-DRG 2005 by increasing DRG-based revenues. G-DRG 2006 effects 2.40 % reduction in overall reimbursement compared to G-DRG 2004. This loss includes ameliorating effects of additional payments for drugs and blood products already. Despite introduction of additional payments especially designed for children and teenagers in 2006, additional payment volume is decreased by 21.71 % from 2005 to 2006. G-DRG 2006 yields over-all reimbursement losses of 1.45 % in comparison to G-DRG 2004. Overall reimbursements include introduced additional payments for drugs and blood products. (Reimbursements resulting out of DRG payment alone drop by 14.73 % from 2004 to 2005, and increase by 3.26 % from 2005 to 2006 (2004 vs. 2006 11.95 %). Introduction of additional payments for drugs and blood products on a Germany-wide basis introduced in 2005 dampens DRG-based reimbursement losses. Despite introduction of dosage intervals specifically designed for children and adolescents in 2006, reimbursement of additional payments for drugs and blood products decrease by 21.71 % from 2005 to 2006. An important revenue-balancing function is attributed to additional charges individual for each hospital according to Par. 6 Section 2 (New diagnostic and therapeutic methods) and Section 2 a KHEntgG (German Hospital Reimbursement Law) with respect to financing tertiary care focusses. If possible to attain, those charges may partially equalize losses. Including these additional charges per individual hospital balance of summarized additional charges is -3.89 % from 2005 to 2006. However, fraction of additional payments on total reimbursements increases from 0.64 % in 2004 to 11.98 % in 2005, and 11.24 % in 2006, respectively. CONCLUSIONS: The G-DRG system in its versions 2005 and 2006 results in lowering overall reimbursements of a pediatric hematology, oncology, and immunology department compared to initial status in 2004. The growing chargeability of additional payments ameliorate this effect.

Adolescent↗
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[Mastoiditis in childhood].

BACKGROUND: Despite new antibiotics mastoiditis in children still is a serious infection confronting the pediatrician and otolaryngologist with diagnostic and therapeutic problems. PATIENTS AND METHODS: In a retrospective study we reviewed the charts of 48 children who had a mastoidectomy from 1990 to 1995 in the Department of Oto-Rhino-Laryngology at the University of Essen. RESULTS: 60% of the patients presented with a retroauricular swelling, and a pathologic tympanic membrane was found in 89%. The erythrocyte sedimentation rate as the most valuable laboratory parameter was increased in 95% of cases. Larger osteodestructive lesions as a complication of mastoiditis could be predicted in three of ten cases by plain x-ray of the temporal bone. The most common bacteria to be isolated were Staphylococcus aureus, Streptococcus pneumoniae and Pseudomonas aeruginosa. CONCLUSION: Because of potential endocranial complications (10% in our patients) as well as difficult radiologic diagnosis of osteodestructive lesions by plain x-ray, we advocate mastoidectomy instead of a mere pharmacological therapy in the treatment of mastoiditis.

Adolescent↗
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Extending myocardial viability during heart preservation with cyclosporine A.

BACKGROUND AND AIM OF STUDY: Hypothermic preservation (PRES) of donor hearts is limited to 12-14 hours for complete functional recovery after reperfusion. In a canine heterotopic heart transplant model, 50% to 60% functional recovery returned after 18 hours of PRES with University of Wisconsin (UW) solution. Concomitant with functional changes were marked increases in apoptotic cells at 2 (2.69%) and 6 (5.98%) hours of reperfusion with a concomitant decrease in lamin B1 (2% and 7.6%, respectively) with no evidence of necrotic cells. These results suggested that blockade of apoptosis may prolong myocardial viability during PRES and reperfusion. METHODS: Donor hearts were subjected to 18 and 24 hours of PRES (2 degrees C to 4 degrees C) with and without cyclosporine A (CyS) treatment (apoptosis blocker). CyS was given to the donor animal (10 mg/kg), in the PRES solution (10(-5) mol/L), slowly infused during the PRES period (1 mL/min), and also to the recipient animal (2.5 mg/kg). RESULTS: After 18 hours of PRES with CyS, function returned to 100% within 1 hour and stayed at this level throughout a 6-hour recovery period. Apoptotic myocytes were reduced (55%) after 18 hours PRES with CyS treatment, and 6-hour reperfusion lamin B1 was reduced to only 3.7%. Twenty-four hour PRES in UW resulted in no functional recovery. However, after CyS treatment, functional recovery returned to 100% after 4 hours of reperfusion. Adenosine triphosphate (ATP) and creatine phosphate (CP) concentrations were surprisingly the same with or without CyS treatment at 18 hours and lower with 24 hours. CONCLUSIONS: Use of CyS in the PRES solution prolongs myocardial viability during donor heart PRES. The mechanism of action may be associated with the mitochondrial permeability transition (MPT) pore via cyclophilin D binding.

Adenosine↗
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Ischemia-tolerance following cardioplegic arrest in human patients and in experimental animals.

Cardiac biopsies were taken from the hearts of 40 patients undergoing open heart surgery for acquired and congenital disease. Tissue samples were taken prior to aortic cross-clamping, at the end of the ischemic period, and 20 minutes after reperfusion. Cardiac arrest was induced with Kirsch's cardioplegic solution at mild hypothermia (28-30 degrees C). Electron-microscopy of these tissue samples showed that cardioplegic arrest allows safe recovery with a tolerable degree of cellular alterations following ischemic periods of approximately 45 minutes. This period of reversible ischemia agreed well with similar studies in dogs that were completed by metabolic studies. ATP4-time in these dogs was 60 minutes under conditions closely resembling those at operationmin spite of the similarity between ischemia tolerance times, marked discrepancies existed on the ultrastructural level. Human hearts showed, generally, a much more marked degree of cellular alterations. The good correlation between ultrastructural alterations and the metabolic status of the canine heart can, therefore, not be used to predict levels of metabolites from human electron-micrographies.

Adenosine Triphosphate↗
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Tolerance to ischemia in the human heart.

The tolerance to ischemic cardiac arrest during open-heart surgery depends on the degree of hypertrophy and on the functional impairment of the heart. The angiographically determined muscle mass is a good indicator of the susceptibility of the myocardium to ischemic injury and of its ability to quickly restore myocardial structure upon reperfusion. Tissue from extremely hypertrophied hearts exhibited numerous degenerative alterations.

Adult↗