Bone marrow cell transplant does not prevent or reverse murine liver cirrhosis.

We tested the effect of bone marrow cell (BMC) transplantation in either preventing or reversing cirrhosis on an experimental model of chronic liver disease. Female Wistar rats were fed a liquid alcohol diet and received intraperitoneal injections of carbon tetrachloride (CCl4) over 15 weeks. Ten animals (cell-treated group) received five injections of BMCs during the cirrhosis induction protocol (on the 4th, 6th, 8th, 10th, and 12th weeks) and four animals received the cells after liver injury was established through tail vein. Nine animals (nontreated group) were submitted to the previously described protocols; however, they received vehicle injections. Analyses were performed to verify whether the infusion of cells was effective in preventing the development of cirrhosis in our model of induction, and if the cells could reverse cirrhosis once it was established. Hepatic architecture and fibrotic septa were analyzed in liver slices stained with hematoxilin & eosin and Sirius red, respectively. Fibrosis quantification was measured by Sirius red histomorphometry. Indirect immunofluorescence was performed to detect the amount of tissue transglutaminase 2. Blood analyses were performed to assess liver injury and function by the assessment of alanine aminotransferase and albumin. Ultrasound was performed to analyze the portal vein caliber and presence of ascitis. Cirrhosis features (regenerative nodules and fibrous septa) were observed in histopathology after 15 weeks of continuous hepatic injury in nontreated and cell-treated groups. Collagen content, immunofluorescence analysis, and biochemical and ultrasound parameters were similar in nontreated and cell-treated groups; however, both groups showed significant differences compared to a normal control group. Cell infusions with bone marrow-derived cells seem to be ineffective in improving morphofunctional parameters of the liver when applied to chronic cases either during or after establishment of the hepatic lesion.

Empty sella turcica in intracranial sarcoidosis. Pituitary insufficiency, primary polydipsia, and changing neuroradiologic findings.

A 37-year-old man with visual loss was found to have hypopituitarism and primary polydipsia associated with sarcoidosis. Neuroradiologic studies demonstrated a dramatic evolution of CNS lesions, including a left thalamic infarct, an enhancing suprasellar mass, and ultimately an empty sella turcica. The patient has been clinically stable in spite of these changes. This case is likely to be the first reported of CNS sarcoidosis with an empty sella turcica documented by computed tomography.

Enhanced prostaglandin I2-formation of human lymphatics during pulsatile perfusion.

Previous studies demonstrate that prostacyclin (prostaglandin I2, PGI2) is the main arachidonic acid product in human lymph vessels. Pulsatile perfusion increases and prolongs PGI2-formation as do leukotrienes (LT) such as LTC4. Thus, physical activity besides local mechanical and biochemical influences on lymph pressure and flow also stimulates local lymphatic PGI2 synthesis, a prime counterbalancing factor in lymphatic constriction induced by other eicosanoids.

Effect of leukotrienes C4 and D4 on prostaglandin I2-liberation from human lymphatics.

Whereas prostaglandin I2 (PGI2), a major metabolite of human lymphatics, does not itself affect lymphatic contractility significantly, it is able to counterbalance the contractile response to thromboxane and leukotrienes. We now demonstrate that leukotrienes C4 and D4 evoke a dose-dependent increased production of PGI2 from human lymphatics. It is likely that leukotrienes either exert a contractile rhythmic effect on human lymphatics or, alternatively, evoke increased PGI2-formation which relaxes human lymphatics. These mechanisms may be of local importance in regulating lymphatic "tone" at sites of inflammation as leukotrienes are liberated from activated white blood cells.

Arachidonic acid metabolites of human lymphatics.

Human lymphatics convert exogenously added 14C-arachidonic acid into PGE2, PGF2 alpha and the main metabolite 6-keto-PGF1 alpha. Thromboxane formation is undetectable either by radiothinlayer-chromatography or by radioimmunology. These data confirm and extend our earlier findings indicating an important PGI2-synthetic mechanism in human lymphatics. Assuming that lymphatic contractility is regulated at least in part by thromboxane A2, we propose that this derivative of arachidonic acid derives from extralymphatic sources.

Regulation of human lymph contractility by prostaglandins and thromboxane.

Thromboxane A2 (TXA2), but not prostacyclin (PGI2), plays an important role in human lymph vessel contraction. Paradoxically, whereas substantial amounts of PGI2 are detectable in human lymphatics, TXA2 is undetectable and probably derives from surrounding tissues.

Prostacyclin synthesis in human lymphatics.

The ability of human lymphatics to generate prostacyclin in important amounts (4.5 +/- 2.1 pg/mg/min) is described. The prostacyclin produced, exhibits the same properties as reported for arterial and venous tissue. No age and sex difference could be observed. The role of prostacyclin in physiology of lymphatics, however, is unknown.

Chylopericardium: a rare cause of pericardial effusion.

A 21 year old man presented with asymptomatic, isolated chylopericardium. Despite echocardiography, radionuclide-angiography, computer tomography, and chemical analysis of the chylous effusion, the etiology remained obscure. After patent blue dye infusion into peripheral soft tissues, the appearance of coloring material in the effusion at 4 hours suggested direct communication of the pericardium with an apparently large thoracic duct. Fifteen months later, cardiomegaly persists in site of medium-chain triglyceride dietary restriction.

[Defects in the prostaglandin system. II. Familial platelet-prostacyclin receptor defect (Wien-Hietzing defect)--pathogenetic significance for (early) development of atherosclerosis?]. / Defekte im Prostaglandinsystem. II. Familiärer Plättchen-Prostacyclin-Rezeptor-Defekt (Defekt Wien-Hietzing)--pathogenetische Bedeutung für (frühzeitige) Entstehung der Atherosklerose?

A case is reported of a 10 year-old girl admitted to hospital because of severe intermittent claudication. Occlusion of the left popliteal artery was diagnosed. Since successful surgical intervention the patient has been symptom-free. No causative factor was detected for this premature occlusion. During intensive laboratory check-up an extreme diminution in sensitivity of the platelets to prostacyclin and a receptor defect were discovered. This defect seems to be genetically determined. The extent to which this as yet unreported platelet defect might have contributed to the development of atherosclerosis at such an early age is discussed.

[Peripheral lymphangiopathies - 15-year follow-up]. / Periphere Lymphangiopathien - 15-Jahre-follow-up

353 patients suffering with peripheral lymphangiopathies were observed. In 276 patients with histological examinations, 201 portrayed obliterative LAP. 85% were females, which indicate a ratio of nearly 1:4. The etiologic factors are unknown. A therapeutic trial with a combination of saluretics and small doses of corticoids, is discussed.

[The natural course of coronary heart disease]. / Zum natürlichen Verlauf der koronaren Herzkrankheit

For a critical evaluation regarding surgical therapy of coronary heart disease, we quote from important publications to the following points: Early mortality due to surgical treatment, by estimating the severity of the disease as determinated by the criterions of the New York Heart Association, or by the number of the diseased coronary vessels, or by important parameters of the function of the left ventricle (0% to 12%). Frequency of acute myocardial infarction, intra-or postoperatively (10% to 15% of the survivers, 50% of the lethal cases). Frequency of occlusion, of an aorto-coronary saphenous vein bypass (up to 30%). Amelioration of ischemic heart pain by surgical treatment (up to 90%). Prevention of the progression of coronary heart disease (not proved). Natural history of patients with coronary heart disease without surgical treatment, by estimating the number of the diseased vessels (2% for one-, 6% for two-, and 10% for three vessel diseases; 30% mortality rate due to stenosis of the left main coronary artery). Comparison of the mortality rates of surgically treated patients against those without surgery for coronary heart disease with equal severity (no difference). We investigated the connection between the severity of coronary heart disease (determinated by coronary angiography), and the mortality rate in our own patient material. A fundamental conformity appeared, with the results as quoted in the literature. Finally we difined the indications for surgical treatment of coronary heart disease due to angina pectoris, which cannot be managed conservatively and which makes a normal live difficult or impossible. Moreover, the function of the left ventricle should be fairly good. An absolute indication is a stenosis of the left main coronary artery.

[Myocardial infarct after gastroscopy. Case report and pathogenetic considerations]. / Myokardinfarkt nach Gastroskopie. Fallberichte und pathogenetische Uberlegungen

Three cases are reported of myocardial infarction and severe myocardial ischemia following gastroscopy in patients with coronary heart disease. These cases demonstrate the high risk of endoscopy in such patients. It is assumed that the main pathogenetic factors are catecholamine-mediated tachycardia and the close vicinity of the lower esophagus to the right coronary artery, with its tendency to coronary spasmus.