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Biomedical subjects

K Metze

Publications and source records attributed to K Metze.

At least 73 records · Page 4Linked to original sources
PubMed1991

[Coronary microcirculation in myocardial reperfusion. The phenomenon of no-reperfusion].

PURPOSE: The study of the ultrastructural features of the coronary microvessels in postischemic reperfusion. MATERIAL AND METHODS: Five mongrel dogs of either sex, weighing 2 to 17 kg were studied Each dog was anesthetized with 30 mg. of pentobarbital and ventilated with room air. A thoracotomy was done and the left descendent coronary artery was isolated. Aorta and right atria pressures, electrocardiogram and coronary blood flow was measured. After 90 minutes of coronary occlusion and 20 minutes of reperfusion carbon black was injected into the anterior descending coronary artery to identify the area of impaired perfusion. The heart was excised and placed in a ice-cold saline. The left ventricle was cut transversely in six slices of 1 cm thickness parallel to the atrioventricular sulcus. Tissue specimens were taken from the subendocardial, mid-myocardial (in the non reperfused area) subepicardial and control layers for electron microscopic examination. Each slice was then incubated in a 1% solution of triphenyltetrazolium chloride (TTC) at 37 degrees C for 10 minutes. RESULTS: The infarcted areas showed widespread tissue damage with relaxed myofibrils cellular edema, swollen mitochondria with fractured cristae and nuclear changes. The vascular endothelium demonstrated severe injury with edema, cytoplasmic clearing, loss of pinocytotic vesicles, nuclear changes, formation of blebs into the vascular lumen and intravascular neutrophil. In the mid-myocardial layer, near the non reperfused vessels, a striking contrast was observed between the vessel and myocardium cells patterns. The usual picture was a severe vascular damage without myocyte injury. CONCLUSION: This study showed that prominent capillary damage with coagulation necrosis was the morphologic pattern observed in areas of myocardial infarction. In the mid-myocardium, near the non reperfused vessel, severe capillary damage was found in areas of preserved myocytes. Obstruction of flow at the capillary level, correlates well with the decrease of the coronary flow reserve observed during the post-ischemic reperfusion.

Animals↗
PubMed1991

[Immunohistochemical detection of rabies virus antigen in the cardiac ganglia of dogs in paraffin sections].

The hearts of five naturally infected rabid dogs were studied by immunohistochemistry on paraffin sections using a monoclonal antibody and the peroxidase labelled streptavidin-biotin method to detect rabies ribonucleoprotein. In all cases distinct small granular and ring-shaped antigen deposits were found within the nerve cells of the cardiac ganglia thus reflecting the early centrifugal spread of virus along the pathway of the vagal nerve to the heart. Histologic findings consisted only of single small eosinophilic inclusions in some nerve cell bodies. These findings may be of diagnostic value.

Animals↗
PubMed1991

Nucleolar organizer regions in normal hematopoiesis: relationship to cellular proliferation and maturation.

The pattern of nucleolar organizer regions (NORs) in normal interphase hematopoietic cells was studied employing the Ag-NOR technique in bone marrow smears. A characteristic pattern of clusters and dots was observed for each cell type. The presence of clusters correlated with cells in proliferation, while in non-proliferating cells only dots were seen. In granulopoiesis, as in erythropoiesis, the number of clusters was highest in the most immature cells, decreasing as maturation took place. Conversely, the number of dots was lowest in the most immature cells, increasing with maturation. In the mature endstage cells, only few dots were seen. The results justify separate counting of clusters and dots, which probably represent different physiologic activities. The present study offers basic data for the study of benign and malignant hematologic disorders where alterations of cellular proliferation and/or maturation occur.

Bone Marrow↗
PubMed1990

[The coronary flow reserve during reperfusion in myocardial infarction].

PURPOSE: The study of coronary flow reserve on the reperfused myocardium damaged by 90 minutes of severe ischemia. MATERIAL AND METHODS: Nine mongrel dogs of either sex, weighing 12 to 17 kg were studied. Each dog was anesthesiated with 30 mg of pentobarbital and ventilated with room air. A thoracotomy was done and the left descendent coronary artery was isolated. Aorta and right atria pressures was measured using a Siemmens-Elema transducers and mingograf recording-804 (Siemmens Instruments). Coronary blood flow was measures with a Caroline Medical Electromagnetic flowmeter, 501D. The index studied was the coronary resistance, calculated as the quotient of the diastolic aortic pressure and the diastolic blood flow. The coronary reserve was studied during reactive hyperemia produced by 10 seconds of coronary occlusion in the 5, 10, 15 and 20 minutes of reperfusion. The infarcted area was detected by TTC (triphenyltetrazolium) method. RESULTS: All the hearts examined showed infarcted area. The diastolic coronary resistance during the reactive hyperemia in the 20 minutes of reperfusion was higher than the control value. CONCLUSION: The coronary vascular reserve was decreased during reperfusion, in the myocardial infarction.

Animals↗
PubMed1990

[Significance of intramural vascular injuries in myocardial revascularization. A case report].

The authors report the case of 59 year-old hypertensive woman, suffering from angina pectoris, who died 24 hours after coronary by pass surgery due to cardiogenic shock. Autopsy revealed a small recent postero-lateral infarction. The venous by pass, however, were inconspicuous. Histologic examination showed extensive microarteriopathy with stenosing intimal fibro-elastosis and hyperplasia of the media, affecting 73% of the vessels with a diameter greater than 150 micra. The authors believe that the diffuse microangiopathy could have affected the myocardial reperfusion, and participated of the mechanical dysfunction.

Angina Pectoris↗
PubMed1990

[Coronary flow reserve during myocardial reperfusion, after 15 minutes of ischemia].

PURPOSE: To study the coronary resistance reserve on the reperfused myocardium, damaged by 15 minutes of severe ischemia. MATERIAL AND METHODS: Eight mongrel dogs, of either sex, weighing 14.4 to 21 kg were used. The index studied was the late diastolic coronary resistance. The coronary reserve was studied through reactive hyperemia produced by 10 seconds of coronary occlusion in the 5, 10, 15 and 20 minutes of reperfusion. Histological studies were done in the reperfused and control areas. RESULTS: The myocardial structure in the reperfused area was essentially normal, without any lesion on the capillaries or intra-myocardial vessels. The diastolic coronary resistance, after reactive hyperemia, during the reperfusion 20 minutes, have no differences with the control values. The coronary resistances in the reperfusion time, improved progressively until normal control, considering the perfusion pressure. CONCLUSION: The coronary vascular reserve is preserved after 15 minutes of ischemia, followed by 20 minutes of reperfusion, considering the perfusion pressure.

Animals↗
PubMed1987

Size dependent enzyme activities of multinucleated (osteoclastic) giant cells in bone tumors.

In osteoclastic giant cells of six different tumors of bones and joints (fibrous dysplasia, proliferating giant cell tumor, malignant giant cell tumor, osteosarcoma after chemotherapy, malignant synovioma and Ewing's sarcoma) activities of tartrate-resistant acid phosphatase, NADH-tetrazolium-oxidoreductase and, in three of them, of non-specific esterase are determined by enzyme histochemical methods. Quantitative microphotometry makes it possible to determine relative enzyme activities in the cut sections of giant cells of different sizes. Giant cells of the various tumors reveal similar trends: With an increase in cell size, mean extinctions of NADH-tetrazolium-oxidoreductase and non-specific esterase decrease. Mean extinctions of tartrate-resistant acid phosphatase increase in cells of medium size, whereas the large cells reveal in part low activities. An additional ultrastructural examination of the giant cells in the proliferating giant cell tumor as well as in the osteosarcoma shows morphological signs of degeneration in the large cells. Electron probe microanalysis of the proliferating giant cell tumor exhibits evidence of phagocytosis of Ca and/or Fe containing particles. The similar size dependent reaction pattern of enzymes in osteoclastic giant cells of different tumors favors the concept of a common histogenesis, i.e. a host reaction.

Acid Phosphatase↗
PubMed1985

Microphotometric quantitation of enzyme activities in giant cell tumor of bone. A case study.

In a proliferating giant cell tumor of bone the activities of tartrate-resistant acid phosphatase (acPase) and of NADH-tetrazolium reductase were demonstrated by enzyme histochemical methods. Quantitative microphotometry made it possible to determine the relative enzyme activities per given volume unit in the cytoplasm of giant cells of several sizes. The activity of tartrate-resistant acid phosphatase increases with increasing cell size, whereas the activity of tetrazolium reductase will decrease in proportion. This coincidence of high acPase activity and low tetrazolium reductase activity in larger giant cells is interpreted as an expression of degenerative change.

Acid Phosphatase↗
PubMed1981

Copper and zinc content of liver, heart, skeletal muscle, and brain, in acute thioacetamide intoxication of rats.

It has been demonstrated that acute thioacetamide intoxication causes a significant increase in copper and zinc in the dystrophic liver of rats. Heart, skeletal muscle, cerebrum and cerebellum showed neither significant deviations of copper and zinc content, nor noticeable histopathologic changes in comparison with controls. Thus, hepatotropia in thioacetamide intoxication receives minimal pathological confirmation.

Acetamides↗
PubMed1980

Secondary athrocytotic cardiomyopathy--heart damage due to Wilson's disease.

Post-mortem atomic absorption spectrophotometry of the myocardium of a 14-year-old boy revealed a hundred-fold increase in copper. Further electrolyte analysis of the myocardium showed changes corresponding to metabolic heart muscle damage. Ultrastructural examination showed all the feature of a cardiomyopathy at the cellular level. Laser-Microprobe-Mass-Analysis demonstrated an inhomogeneous distribution of copper. An essential factor in the mechanism of death is heart damage.

Adolescent↗
PubMedDate not supplied

Chronic nitric oxide inhibition as a model of hypertensive heart muscle disease.

We have compared the myocardial alterations in rats made hypertensive by the chronic inhibition of nitric oxide biosynthesis with those having renal hypertension (two kidney-one clip model). Male Wistar rats were chronically administered the nitric oxide synthase inhibitor N omega-nitro-L-arginine methyl ester (L-NAME) for 2, 4 and 8 weeks. Both groups initially developed a similar increase in blood pressure but only the 2K-1C rats developed myocardial hypertrophy after 2-4 weeks. L-NAME-treated animals developed a similar degree of hypertrophy following 8 weeks of treatment. As observed by light microscopy, the myocardial alterations in the latter animals consisted of extensive areas of fibrosis and myocardial necrosis, especially in regions of the subendocardium. The histological alterations induced by L-NAME were not caused by the accompanying hypertension, since the 2K-1C animals had a similar increase in arterial blood pressure without any significant alterations in the heart morphology. 2K-1C rats treated chronically with L-NAME behaved in a manner similar to the L-NAME-treated animals with regard to both the blood pressure increases and cardiac morphological alterations. Animals which received the inactive enantiomer D-NAME did not develop hypertension nor did they have any morphological abnormalities. Both the coronary flow and the contractile capacity of hearts isolated from rats treated with L-NAME for 8 weeks were impaired compared to control animals. These results indicate that the chronic inhibition of NO biosynthesis causes cardiac ischemia associated with a mechanical dysfunction that is unrelated to cardiac hypertrophy which is similar to those seen in some patients suffering from chronic arterial hypertension.

Analysis of Variance↗
PubMedDate not supplied

[Surgical treatment of fungal bolus in acute lymphoid leukemia].

Case report of a 24 year old female patient with ALL that developed pulmonary invasive aspergillosis during aplastic phase of induction chemotherapy. She was treated with antibiotics and amphotericin B. After recovering from neutropenia, she developed a mycetoma in the inferior lobe of the right lung, which required lobectomy. Nine months after surgery the patient is well, in complete remission of ALL and with no evidence of infection. One month after lobectomy, chemotherapy had been reintroduced. Attention should be called to this form of therapy of Aspergillosis, as a successful way to eradicate this fungal infection that responds poorly to antifungal drugs currently used.

Adult↗