Increased diameter and enhanced myogenic response of saphenous vein induced by two-week experimental orthostasis are reversible.

Previously, increased diameter and enhanced myogenic tone were seen after 2-week 45o head-up (HUT2) in the rat. We studied the reversibility and the effect of extended tilt on this phenomenon using two experimental groups: HUT2 plus 2-week horizontal (HUT2HOR2), and 4-week tilting (HUT4). 4-weeks in normal cages (NC4) served as control. Diameter of saphenous vein (SV) in 2-20 mm Hg pressure range, wall and media thickness, endothelial and smooth muscle cell densities, and cell proliferation were measured. The diameter of SV from HUT4 was significantly larger compared with HUT2HOR2 or NC4 within the whole pressure range both in Krebs-Ringer (870.4+/-21.3 vs. 778.2+/-24.9 and 771.6+/-28.1 microm at 10 mm Hg, respectively) and in Ca(2+)-free solution. Myogenic and norepinephrine-induced vascular tone, wall and media thickness did not differ among the three groups. Endothelial cell density decreased in HUT4 (10.7+/-1.2) vs. HUT2HOR2 (15.1+/-1.0) and NC4 (15.3+/-0.6), while that of smooth muscle was unchanged. No cell proliferation marker was seen. In conclusion, both increased diameter and enhanced myogenic tone of SV seen in HUT2 proved to be reversible. HUT4 resulted in increased SV diameter, similarly to HUT2, however, vascular tone was not amplified. This suggests that a prolonged orthostatic load may readjust the function of smooth muscle.

Hypercalcitoninemia in a patient with a recurrent goitre and insulinoma: a case report.

Serum calcitonin has become a very sensitive and specific marker for medullary thyroid carcinoma that should be determined in patients with nodular thyroid disease. However, a few earlier reports indicated that tumors other than medullary thyroid carcinoma including insulinomas arising from pancreatic islet cells may also produce calcitonin. Of the few cases of calcitonin-producing insulinomas previously reported, most had incomplete data or lack of documentation of the association between raised serum calcitonin concentration and immunohistochemical detection of calcitonin in pancreatic islet cell tumors. In this paper we are reporting a 54-year-old woman with a history of partial thyroidectomy for multinodular goitre at the age of 50 yrs, she was evaluated for a 2-months history of fasting hypoglycemia (plasma glucose 1.9 mmol/L during a supervised fast), raised serum insulin (at the time of hypoglycemia 88.8 microU/ml; normal, 5 - 35 microU/ml) and C-peptide levels (at the time of hypoglycemia 6.1 ng/ml; normal, 1.37 - 3.51 ng/ml), markedly increased serum calcitonin concentration (481 pg/ml; normal, < 9.9 pg/ml), and an enlarged residual thyroid gland. Aspiration biopsy of the thyroid was negative for parafollicular C-cell hyperplasia or medullary thyroid carcinoma. Abdominal ultrasound and CT scan revealed a tumor in the head of the pancreas, which was surgically removed. Histopathological evaluation of the pancreatic tumor showed typical features of a neuroendocrine neoplasm with strong immunostaining for both insulin and calcitonin. After removal of the pancreatic tumor, clinical symptoms resolved and biochemical markers normalized (serum insulin, 14.9 microU/ml; C-peptide, 3.0 ng/ml; calcitonin, 2.9 pg/ml) confirming the causal relationship between insulinoma and markedly increased serum calcitonin levels.

Six regimens for the eradication of Helicobacter pylori (Hp) in duodenal ulcer patients: three consecutive trials (1995-1999).

AIM: to present our experience in eradicating Hp in three consecutive trials performed between 1995 and 1999. METHODS: 320 duodenal ulcer outpatients have been enrolled in three open, prospective controlled trials. Hp infection was confirmed by Giemsa stain and Rut. In Trial I, 52 cases received 20 mg omeprazole + 2 x 250 mg clarithromycin + 2 x 500 mg tinidazole (OCT), 48 patients were given 20 mg omeprazole, 2 x 1000 mg amoxicillin + 2 x 500 mg metronidazole (OAM) for 7 days; in Trial II, 48 cases received 40 mg pantoprazole + 2 x 1000 mg amoxicillin + 2 x 500 mg clarithromycin (PAC) for 7 days and 5l cases 2 x 400 mg ranitidin bismuth citrate + 2 x 500 mg clarithromycin for 14 days (RBC-C); in Trial III, 60 cases were treated with 2 x 30 mg lansoprazole + 2 x 250 mg clarithromycin + 2 x 500 mg metronidazole and 6l patients received 2 x 400 mg ranitidin bismuth citrate+2 x 250 mg clarithromycin + 2 x 500 mg metronidazole (RBC-CM). The patients were controlled within 4-6 weeks by endoscopy in trials I-II and 13C-urea breath test in trial III. RESULTS: Eradication rates on ITT/PP basis were: OCT: 72.3/80.2% vs OAM 51.2/63.5% (P = 0.02/P = 0.03); PAC: 80.8/88.3% vs RBC-C 80.3/85.4% (P = 0.65/0.67) and LCM 78.3/92.1% vs RBC-CM 78.7/90.5% (P = 0.86/P = 0.93). Side effects occurred in 5.2, 8.6, 9.5, 14.5, 13.5 and 18.3% of the cases. CONCLUSION: Regimens using 2 x l PPI or RBC + 2 antibiotics for l week proved to be the most effective for Hp eradication in duodenal ulcer patients.

[Acute pancreatitis with few symptoms and extensive necrosis]. / Akut pancreatitis tünetszegény, kiterjedt, távoli necrosisokkal.

The authors present a particular case of an acute pancreatitis. The disease developed in a young male patient following cholelithiasis and cholecystectomy. The inflammation affected the outer layers of the pancreas as a mantle and it caused widespread fat necrosis. Necrectomy for septic state was conducted to improve the condition, but the patient died of pulmonary embolism. Unexpectedly big necrotic areas of fat necrosis and abscess were found at autopsy.

Connexin 43 expression in rat aortic smooth muscle after ovariectomy and hormonal replacement.

The purpose of this study was to determine the effects of ovariectomy and long-term combined sexual hormone replacement on the gap junctional protein, connexin 43 (Cx43) of aortic medial smooth muscle cells in rats. Twenty non-pregnant mature Wistar female rats were divided into five groups (four animals in each group). Group A underwent ovariectomy, Group B underwent ovariectomy and received estradiol propionate, Group C underwent ovariectomy and received medroxyprogesterone acetate and Group D underwent ovariectomy and received both hormones. Group E was sham-operated and used as control. After 15 weeks of treatment, thoracic aortas were removed and immunohistochemistry was carried out using a specific fluorescent antibody against Cx43. Tissue sections were examined by confocal laser scanning microscopy and analysed by the Scion Image program. All five different groups had the same distribution and extent of Cx43 in the aorta. Neither the ovariectomy nor the hormone replacement had any effect on the Cx43 expression of aortic smooth muscle cells in rats as compared to control animals. These results indicate that sexual steroids do not influence the gap junctional protein Cx43 of the medial layer of aorta in rats. They may suggest that the beneficial effects of estrogen are not mediated via gap junctions in the human aorta either.

Structural vascular changes in hypertension: role of angiotensin II, dietary sodium supplementation, and sympathetic stimulation, alone and in combination in rats.

Elevated circulating angiotensin (Ang) II levels, dietary sodium, and sympathetic stimulation are recurrent themes of hypertension research, but their in vivo interaction in physiologically meaningful doses has not been adequately investigated. In this study, the interaction of a subpressor dose of Ang II (50 ng. kg(-1). min(-1) SC), 2% NaCl diet, and sympathetic stimulation in the form of overnight cold exposure was investigated in the development of hypertension and of structural vascular changes in male Sprague-Dawley rats. There were 8 experimental groups: sham operation and treatment (control), Ang II, 2% NaCl diet, cold exposure (5 degrees C), Ang II plus 2% NaCl diet, Ang II plus cold exposure, cold exposure plus 2% NaCl diet, and Ang II plus 2% NaCl diet plus cold exposure (triple treatment). For each group, the duration of treatment was 12 weeks. Morphometric measurements of maximally dilated, in situ fixed, second-order (250 to 320 microm OD), intermediate-size (100 to 150 microm OD), and small (50 to 100 microm OD) mesenteric arteries were performed, and wall-to-lumen ratios (W/L) were calculated. During the 12-week study, the blood pressure (BP) load (the area under the systolic BP curve) of rats receiving the combined treatment of Ang II and 2% NaCl diet was increased (P:<0.05), and that of rats receiving the combined treatment of cold exposure and 2% NaCl diet was decreased (P:<0.05); there were no BP changes in the remaining groups of rats. The most pronounced changes among groups occurred in W/L of small resistance arteries. The W/L of small arteries increased in Ang II-treated (P:<0.01) and in cold-stressed rats (P:<0.01). The effect of Ang II was potentiated by the addition of a 2% NaCl diet. In contrast, the addition of 2% NaCl diet to cold stress reduced the W/L of small arteries (P:<0.01). No other positive or negative synergism occurred among groups, including the rats receiving triple treatment. The findings confirm the potentiation of the hypertensinogenic and vascular trophic effects of Ang II by a high-sodium diet but do not provide evidence for synergism between Ang II and sympathetic stimulation. The finding of hypotension and reduced W/L of small resistance arteries in rats receiving the combined treatment of cold stress and high-sodium diet is unique because there are few known nonpharmacological vascular "hypotrophic" stimuli. The ultimate test of the hypertensinogenic potential of pressor stimuli alone or in combination is their long-term administration in physiologically meaningful doses to experimental animals.

[Lansoprazole versus ranitidine bismuth citrate containing triple regimens for Helicobacter pylori eradication in patients with duodenal ulcer]. / Lanzoprazol- vagy ranitidin bizmut citrát-tartalmú hármas kezelés a Helicobacter pylori-fertózés eradikációjában nyombélfekélyes betegekben.

The aim of this study was to compare in an open, controlled and prospective trial the efficacy of one-week regimen using either lansoprazole (2 x 30 mg) + 2 x 500 mg metronidazole + 2 x 250 mg clarithromycin (group I, 60 cases) or ranitidine bismuth citrate (2 x 400 mg) + 2 x 500 mg metronidazole + 2 x 250 mg clarithromycin (group II, 61 cases) on the eradication of Hp infection in duodenal ulcer patients. The diagnosis was stated endoscopically. Hp infection was confirmed from 2 antral + 2 corporeal biopsies by the modified Giemsa stain and rapid urease test. After eradication the patients were given on-demand treatment with 30 mg lansoprazole (group I) or 2 x 150 mg ranitidine (group II). Control 13C-urea breath test was performed 4-6 weeks after eradication. On intention to treat basis, Hp was eradicated in 78.3% (confidence interval, CI: 67.6-89.1%) in group I and 78.7% (CI: 68.1-89.2%) in group II (p > 0.05). Per protocol eradication rates were 92.1% (CI: 84.5-99.7%) in group I and 90.5 (CI: 82.4-98.6%) in group II (p > 0.05). Side effects were recorded in 13.5% in group I and 18.3% of cases in group II. Short term triple therapies using either lansoprazole or ranitidine bismuth citrate + 2 antimicrobials were effective and safe in the eradication of Hp in duodenal ulcer patients.

Different structural vascular changes in angiotensin II-treated and cold-stressed rats.

The role of the renin-angiotensin and sympathetic nervous system in the pathogenesis of structural vascular changes in experimental hypertension was investigated by comparing the effect of angiotensin II (ANG II) administration and of sympathetic stimulation by cold stress on the structure and composition of mesenteric arteries of rats. Adult male Sprague-Dawley rats were administered subcutaneously 100 ng/kg per min ANG II or exposed to 5 degrees C cold overnight for 12 weeks. Sham-operated rats were controls. At the end of treatment, the mesenteric circulation of rats was perfusion-fixed for morphometric measurements by light microscopy and volume density measurements by point counting on electron micrographs. Tail systolic blood pressure of ANG II-treated rats increased by 37 mm Hg at week 2 and remained elevated for the rest of the experiment. The systolic BP of cold-stressed rats measured at room temperature did not change. These findings were confirmed by direct measurement of mean arterial pressure in free-moving rats. Compared to control rats, medial thickening of large and small arteries in ANG II-treated and cold-stressed rats was the main finding of this study. Thickening of the media in the two treated groups of rats appeared to be due to hypertrophy of vascular muscle, as indicated by the increased width of smooth muscle cells. Loose matrix (interstitial fluid compartment) was increased in media of large arteries of ANG II-treated rats, and collagen was increased in the outer media of arteries of cold-stressed rats. Measurements of compositional changes in addition to morphometric changes are needed to detect differences in the pathogenesis of structural vascular changes in the various forms of hypertension.

World Health organization (WHO) and the World Heart Federation (WHF) pathobiological determinants of atherosclerosis in youth study (WHO/WHF PBDAY Study) 1986-1996. Histomorphometry and histochemistry of atherosclerotic lesions in coronary arteries and the aorta in a young population.

BACKGROUND AND AIM: The present work is a chapter in an investigation directed by the World Health Organization on the Pathobiological Determinants of Atherosclerosis In Youth (WHO-PBDAY). Our aim was to study the development of atherosclerotic lesions in a young population. METHODS AND RESULTS: Samples of left anterior descending coronary artery (LDC) and thoracic (TA) and abdominal aorta (AA) from five Collaborating Centres (Budapest/Hungary, Havana/Cuba, Heidelberg/Germany, Mexico City/Mexico, Peradeniya/Sri Lanka) of 214 subjects who died aged 15 and 34 were analysed at the Budapest Reference Centre. Slides stained with haematoxylin-eosin and with stains for extracellular matrix were quantitatively and qualitatively evaluated. Mean intima/media (I/M) ratio and the prevalence of type III-IV lesions (preatheroma; atheroma; calcified and fibrous atheroma) were determined and compared in different risk factor (high blood pressure, smoking) groups. High I/M ratio was found in the LDC and type III-IV lesions were frequently found both in the LDC and in the AA. I/M ratio and the occurrence of type III-IV lesions increased in all arteries by age. Atherosclerotic lesions in men were more severe, particularly in the LDC. Geographic origin had a limited effect on the histologic lesion parameters. Appearance of type III-IV lesions was associated with substantially different extracellular matrix changes. Myoelastic layer formation was found in each artery in both early and type III-IV lesions. Hypertension was associated with higher prevalence of type III-IV lesions in all arteries, in particular, in the TA; smoking showed a significant effect on the AA only. CONCLUSIONS: Atherosclerotic lesions were found in many of these young subjects. The effect of hypertension and smoking on their development suggests that control of risk factors, beginning in early adolescence, could help to prevent cardiovascular diseases.

[Detection of antibodies against pancreatic islet cells in clinical practice]. / Hasnyálmirigy-szigetsejt elleni antitestek vizsgálata a klinikai gyakorlatban.

Development of diabetes mellitus caused by pancreatic beta-cell destruction of autoimmune origin is the result of a long lasting process. The most easily examinable feature of this stage is the occurrence of the islet cell antibodies. The sera which are positive for islet cell cytoplasmic antibodies (ICA), examined by indirect immunofluorescence, contain a mixture of antibodies. The glutamic acid decarbocylase (GAD), the tyrosin phosphatase (IA2), the insulin, and the GM2-1 glycolipid can be the targets of these antibodies. One can routinely examine the ICA, the GADA, the IA2 antibodies. The detection of antibodies against insulin (IAA) and GM-2-1 glycolipid is not invented in the routine laboratory work. The aim of the authors was the evaluation of clinical significance of occurrence of islet cell antibodies: one hundred and eighteen nondiabetic children an adult human being without known diabetic first degree relatives and 366 type 1 diabetic children and adult patients served as controls. The authors evaluated the predictive value of the different islet cell antibodies to the development of type 1 diabetes mellitus in 596 nondiabetic children with type 1 diabetic first degree relatives. The authors looked for markers of beta-cell destruction among sera of 320 diabetics manifested after 30 years of age with at least half a year of non-insulin-dependency and in the sera of 68 females suffered from gestational diabetes after 0-14 years of the index pregnancy. Finally the authors report 7 cases in which the examination of islet cell antibodies helped the diagnosis and classification of diabetes mellitus. Indirect immunofluorescence method was used for the detection of ICA, radioimmunoassay for that of GADA and IA2 antibodies. There was no positive reaction for ICA and GADA in the nondiabetic population without diabetic first degree relatives. Among the freshly diagnosed type 1 diabetic children 39% were positive for only ICA, 44% for only GADA and 80% for any antibodies. Among the freshly manifested type 1 diabetic adults ICA positivity only was observed in 21%, GADA positivity only in 7.1% and 93% for any antibodies. From the 595 nondiabetic children with type 1 diabetic first degree relatives 23 were positive for ICA, from whom 5 became diabetic during a two years observation period. These diabetic children had multiplex autoantibodies besides ICA. One child from this group, who was negative for ICA became diabetic, too. Among type 2 diabetic patients 13% were positive for ICA alone, 17% were positive for GADA alone and 27% were positive for any antibodies. The insulin dependency manifested in a short time was associated with antibody positivity. Among the gestational diabetics 10 were found positive for ICA. From them, 7 were type 1 diabetics, and 3 were type 2 diabetics at the time of the detection of antibodies. The authors suggest the need of determination of islet cell antibodies in the group of nondiabetic first degree relatives of type 1 diabetic patients (ICA, GADA, IA2 and IAA), in the group of non-insulin-dependent diabetics (ICA and GADA) as a screening for later insulin dependency, and in gestational diabetes after delivery (ICA) as screening for type 1 diabetes mellitus.

Structural vascular changes in hypertension: role of angiotensin II, dietary sodium supplementation, blood pressure, and time.

The dose and time dependence of angiotensin II (Ang II) induced hypertension and structural vascular changes and the effect of dietary sodium supplementation on these relationships were investigated. Male Sprague-Dawley rats were treated with 50, 100, or 200 ng . kg-1 . min-1 Ang II subcutaneously for 4 or 12 weeks on normal sodium diet (0.7% NaCl) or with 50 ng . kg-1 . min-1 Ang II SC for 12 weeks on high sodium diet (2% NaCl). Additional rats were sham-operated and fed normal sodium (control rats) or high sodium diet. Plasma Ang II level of rats receiving 100 ng . kg-1 . min-1 Ang II for 4 weeks was 26+/-5 pg/mL (mean+/-SEM, n=7) compared with 11+/-2 pg/mL (n=15) in control rats (P<0.03). Lumen and external diameters of small (50 to 100 microm OD) and intermediate-size (100 to 150 microm OD) resistance arteries were measured in maximally dilated, pump-perfused (55 to 60 mm Hg), in situ fixed mesenteric vascular beds of rats, and wall-to-lumen ratios (W/L) were calculated. Large mesenteric arteries of rats treated with 100 ng . kg-1 . min-1 Ang II for 12 weeks were examined to distinguish hypertrophy from hyperplasia of vascular muscle. Tail systolic blood pressure (BP) and W/L of resistance arteries of Ang II treated rats increased in a dose-dependent manner. Treatment with 50 ng . kg-1 . min-1 Ang II for 12 weeks had no significant effect on BP but produced the same increase in W/L (+10%, n=8, P<0.06) as 100 ng . kg-1 . min-1 Ang II for 4 weeks (+9%, n=18, P<0.05) (time dependence). A 2% NaCl diet for 12 weeks had no significant effect on either BP or W/L, but in combination with 50 ng . kg-1 . min-1 Ang II, it increased systolic BP by 31 mm Hg (P<0.01) and W/L of small resistance arteries by 28% (P<0.01) (synergism). In rats treated with 100 ng . kg-1 . min-1 Ang II for 12 weeks, arterial smooth muscle cell thickness was increased without a change in the number of cell layers (hypertrophy). There was a dissociation between the average BP load (the area under the weekly systolic BP curve) of Ang II treated rats and the W/L of their mesenteric resistance arteries. Ang II induced hypertension and structural vascular changes are dose- and time-dependent and synergistically enhanced by dietary sodium supplementation. Dissociation between BP and vascular structure in Ang II treated rats suggests that a direct trophic effect of Ang II may contribute to the development of structural vascular changes.

The functional and morphological damage of ischemic reperfused skeletal muscle.

Skeletal muscle is frequently damaged by ischemia-reperfusion both caused by direct injury and also by surgery. The purpose of the present experiments was to examine how the different types of skeletal muscles (fast and slow) react functionally and morphologically after 1 and 2 h of ischemia followed by different periods of reperfusion. The fast-twitch (musculus extensor digitorum longus, EDL) and the slow-twitch (musculus soleus, SOL) muscle of Wistar rats were prepared. They were stimulated in vivo, either directly or indirectly at different reperfusion times following tourniquet ischemia, and the contraction force of the muscles was recorded. The morphological changes were examined by light microscopy. At early reperfusion times, the contraction force of the EDL muscle was reduced by 40 and 90% after 1 and 2 h of ischemia, respectively. The contraction force was about 50% at the end of a 2-week reperfusion period in the 1-hour ischemia group and it increased significantly (from 5 to 38%) during the second week if the ischemia lasted for 2 h. Reduction of contraction force in the SOL muscle was over 50 and 90% following 1 and 2 h of ischemia, respectively, and it started to improve from the 2nd week. Morphological changes of the two types of muscle were identical. At early reperfusion times granulocytes were seen in the blood vessels adhering to the endothelium. 24 h later neutrophil granulocytes migrated into the endomysium and thereafter into the perimysium. One week after 1 h of ischemia both muscles showed normal histology. However, the structural regeneration process only started at the end of the 1st week of reperfusion after 2 h of the ischemic damage. The following conclusions can be drawn. (1) There is functional morphological evidence of ischemic and reperfusion injury in both muscles after 24 h and also after 1 week of reperfusion. (2) Functionally, the two types of muscles regenerate differently, i.e. the SOL starts to regenerate earlier than the EDL. (3) Morphologically the two types of muscle show the same reactions. An increase in the time of ischemia from 1 to 2 h delays the regeneration processes.

[Neonatal primary hyperparathyroidism]. / Ujszülöttkori primer hyperparathyreosis *ikeres mútéti megoldása kisdedkorban.

The authors report on a case of severe primary hyperparathyroidism with clinical signs from birth. The boy was admitted because of poor somatomental development, hypotony, hepatosplenomegaly and osseous abnormalities, resembling those of rachitis. Laboratory data showed the typical findings of primary hyperparathyroidism. The authors performed parathyroidectomy with simultaneous heterotopic parathyroid tissue autotransplantation. Histology revealed parathyroid chief cell hyperplasia. Because of the hypercalcaemia and clinical signs persisting after the operation they removed the parathyroid autografts. Since this later was ineffective they performed a left sided neck dissection on the side of the excessive parathormone production. The child became hypocalcaemic necessitating calcium and vitamin D administration. He is now 17 months after the last operation. His somatomental development is accelerated. In connection with the case the authors surveyed the literature of this rare entity.

Ultrastructural study of a black insulinoma.

A case of black insulinoma is reported. The color was due to a cytoplasmic pigment. Immunostaining for neuron-specific enolase and chromogranin was positive in the tumor cells, and the pigment granules themselves reacted with the chromogranin antibody. Numerous beta cell type dense core granules as well as atypical granules were found by electron microscopy. An important finding was that the dense core granules contribute to the lipofuscin pigment formation.

Sequence of morphological alterations in a small intestinal ischaemia/reperfusion model of the anesthetized rat. A light microscopy study.

Previous studies have shown serious mucosal damage and destruction to be associated with intestinal ischaemia/reperfusion. As both destruction and concomitant regeneration can be observed together in this potentially lethal condition we have studied the development and sequence of events by evaluating morphological changes of the small intestine in an ischaemia/reperfusion model in anaesthetized rats. Forty-five minutes of ischaemia was followed by 4 hours of reperfusion. Tissue samples of the small intestine were examined by light microscopy in normal and semithin sections. Samples were collected at the end of ischaemia, at 10 min, and at 1, 2, 3 and 4 hours of reperfusion, respectively. Survival was assessed in a parallel group of anaesthetized rats. The morphological changes were described and they were analysed by a semi-quantitative method using five different markers of histological alteration. The mortality rate of a control survival group was 100%. Mucosal destruction at the end of ischaemia and during reperfusion was diffuse and steadily increased as a function of reperfusion time. At the same time the epithelium showed intensive regenerative growth which covered the denuded mucosal surface by the third hour of reperfusion. A secondary epithelial desquamation followed this process and was accompanied by heavy inflammatory cell infiltration. The infiltration may be the cause of the secondary epithelial injury.

[Pathology of the collagen framework of the myocardium]. / A szívizom rostos vázának pathológiája.

The myocardial collagen matrix was studied in three groups of patients. The first group consisted of nine patients who had an isolated degradating damage of the collagen framework. In the second group the myocardial fibrillary matrix was examined in different cardiopathies. The author concluded that the collagen framework had degradated in the places of necroses and amyloid depositions, and it was bulky corresponding to fibrosis. Three persons who died suddenly in brain damages served as a control group. Integrity of the collagen matrix has an important role in the myocardial function, its desintegration--unrelated to myofiber necrosis--causes cardiac insufficiency.

[Heart damage associated with cerebrovascular accidents]. / Agyi vascularis katasztrófákhoz csatlakozó szívkárosodás.

The authors present a clinico-pathological study on 21 patients who died in acute cerebrovascular diseases. The main myocardial lesions were focal hemorrhages, contraction band necroses and myocarditis. The ECG abnormalities and the pathogenesis of the cardiopathy are discussed on the basis of their investigations and dates of references. Their conclusions is that the heart damages are modulated by catecholamines. The occurrence of this cardiopathy should be prevented by beta-blockers, so the life-expectancy of patients and the number of heart donors could increase.

Myocardial collagen degradation: morphological and biochemical correlation.

An attempt was made to prove the phenomenon of myocardial collagen breakdown in a norepinephrine (NE) induced model of reversible cardiopathy in anesthetized rabbits. NE (0.3 mg/kg in 90 min) was infused to 22 animals. Histologically it was found that immediately and during the first two days after the catecholamine administration the myocardial collagenous network became disrupted and it partly disappeared. Collagenase and peptidase activities were measured from homogenates of the same hearts. A significant increase of these activities was observed and that could be correlated with the intracellular matrix destruction.