[Heterotopic gastric mucosa of the rectum. Case report with literature review]. / Rektale Magenschleimhautheterotopie. Ein Fallbericht in Zusammenschau mit der Literatur.

Heterotopic gastric mucosa is a rare finding in the rectum. Apart from two other hypotheses, a misdifferentiation of entodermal stem cells is the most widely accepted aetiopathogenetic assumption today. Due to acid secretion, the lesions predominantly manifest with hematochezia. Therapeutic options include medicinal therapy and particularly (endoscopic) removal. From the pathologist's point of view a careful evaluation is required also in terms of basically possible dysplastic or malignant changes.

[MR-colonography in hospitalized patients: feasibility and sensitivity]. / MR-Kolonografie bei stationären Patienten: Durchführbarkeit und Sensitivität.

INTRODUCTION: Besides conventional colonoscopy, CT and MR colonography offer alternate virtual imaging modalities of the colon. The sensitivity of CT colonography, which is associated with radiation exposure, has been published in prior, large studies. Regarding MR colonography, in particular dark lumen MR colonography with the rectal administration of a water enema as a contrast agent, only limited published data exist. The goal of this study was to compare MR colonography with conventional colonoscopy in the detection of colorectal polyps. In addition the feasibility and image quality in unselected hospitalised patients were assessed. PATIENTS/METHODS: Included were 103 hospitalised patients who had to undergo colonoscopy for various indications. Immediately prior to conventional colonoscopy, MR colonography with rectal water enema and additional intravenous administration of contrast material was performed. Detection rates for polyps and adenomas were documented with both imaging modalities. Image quality and completion rates (practicability) and other (incidental) findings were also recorded. RESULTS: In 15 of 103 patients the MR examination could not be done or was only partially completed. The detection rate of MR colonography for polyps (adenomas) was 2% (4%) for polyps (adenomas) up to 5 mm in diameter, 38% (56%) for polyps (adenomas) 6-10 mm in diameter and 89% (89%) for polyps (adenomas) up to 11 mm in diameter. One flat carcinoma seen with conventional coloscopy was missed on MR colonography. CONCLUSIONS: MR colonography offers the possibility of imaging the colon without exposure to radiation. Polyps and adenomas are detected, similar to the detection rate of CT colonography, with adequate sensitivity only if they are larger than 10 mm in diameter. Therefore this imaging technique is not (yet) suitable as a screening test. Additional limitations are the necessary cooperation of the patient which can reduce the practicability and image quality in selected patients. Further studies like the just started German multicentre trial are needed to assess the position of MR colonography.

Selective irreversible binding of chloroethylclonidine at alpha 1- and alpha 2-adrenoceptor subtypes.

We have determined the alkylating effects and affinity of chloroethylclonidine at alpha 1- and alpha 2-adrenoceptor subtypes in saturation and competition radioligand binding studies. Treatment with chloroethylclonidine (10 microM, for 30 min at 37 degrees, with subsequent washout) abolished [3H]prazosin binding to alpha 1B-adrenoceptors in rat spleen almost completely and reduced specific binding in rat kidney and cerebral cortex by a percentage comparable to the known alpha 1B-adrenoceptor content of these tissues. Chloroethylclonidine treatment also markedly reduced [3H]rauwolscine binding to human platelet and kidney membranes but did not affect [3H]rauwolscine binding to rat kidney. Similar chloroethylclonidine treatment (10 microM, 20 min at 37 degrees) reduced the number of detectable alpha 2-adrenoceptors in cell lines transfected with the alpha 2-C10 or alpha 2-C4 gene but not in those transfected with alpha 2-C2 adrenoceptors. In concentration-response experiments, higher chloroethylclonidine concentrations were required for inactivation of human platelet alpha 2A-adrenoceptors, compared with rat spleen alpha 1B-adrenoceptors, and a smaller maximal inactivation was achieved. The lack of inactivation of rat alpha 1A- and alpha 2B- and human alpha 2-C2-adrenoceptors was not due to a lack of chloroethylclonidine binding, because the affinity of chloroethylclonidine at these subtypes, as determined in competition binding experiments, was at least as high as the apparent affinity at the alkylated subtypes. alpha 2A-Adrenoceptor alkylation by chloroethylclonidine treatment was functionally relevant, because it significantly reduced alpha 2A-adrenoceptor-mediated Ca2+ elevations in HEL cells. We conclude that chloroethylclonidine binds to all major alpha-adrenoceptor subtypes and irreversibly inactivates not only alpha 1B-adrenoceptors but also alpha 2A- and alpha 2C-adrenoceptors, whereas alpha 1A- and alpha 2B-adrenoceptors are relatively resistant to its alkylating action, although they can bind chloroethylclonidine.

Alpha 1-adrenoceptor subtype affinities of drugs for the treatment of prostatic hypertrophy. Evidence for heterogeneity of chloroethylclonidine-resistant rat renal alpha 1-adrenoceptor.

We have used radioligand binding and inositol phosphate accumulation studies to determine the affinity at mixed alpha 1A- and alpha 1B-adrenoceptors (rat cerebral cortex and kidney), alpha 1A-adrenoceptors (rat cerebral cortex and kidney following inactivation of alpha 1B-adrenoceptors by chloroethylclonidine treatment) and alpha 1B-adrenoceptors (rat spleen) for drugs currently under investigation for the treatment of benign prostatic hypertrophy, alfuzosin, naftopidil and (-)- and (+)-tamsulosin. Alfuzosin and naftopidil had similar affinities in all model systems (approximately 10 nM and 130 nM, respectively) and lacked relevant selectivity for alpha 1-adrenoceptor subtypes. Their potency to inhibit noradrenaline-stimulated inositol phosphate formation in cerebral cortex matched their affinities as determined in the binding studies. Tamsulosin had higher affinity at alpha 1A- than at alpha 1B-adrenoceptors, and was slightly more potent than alfuzosin and naftopidil at alpha 1B- and considerably more potent at alpha 1A-adrenoceptors. However, the interaction of the tamsulosin isomers with chloroethylclonidine-insensitive (alpha 1A-like) adrenoceptors was complex. A detailed analysis of the tamsulosin data and those obtained with other drugs, most notably noradrenaline and oxymetazoline, suggested that chloroethylclonidine-insensitive alpha 1-adrenoceptors may be heterogeneous and that this heterogeneity may differ between cerebral cortex and kidney of the rat.

Rapid progression of septal hypertrophy in an adult with hypertrophic cardiomyopathy and excimer laser-treated coronary artery disease.

We present the case of a 55-year-old man with rapid progression from asymmetrical septal hypertrophy to hypertrophic obstructive cardiomyopathy over a 1-year period leading to persistent anginal symptoms despite adequate treatment of his concomitant coronary artery disease. The potential mutagenic side effects of XeCl excimer laser-radiation that was used to remove the arteriosclerotic plaque from the left anterior descending coronary artery may have contributed to the sudden increase in septal thickness.

Efficacy of nicorandil versus propranolol in mild stable angina pectoris of effort: a long-term, double-blind, randomized study.

Nicorandil is a potent coronary vasodilator. To assess its long-term antianginal effect, we designed a randomized, parallel double-blind trial of 6 weeks' duration comparing nicorandil (10 or 20 mg b.i.d.) with propranolol (40 or 80 mg t.i.d.). The study comprised 77 men with stable angina, no maintenance medication at entry, and an exercise test positive for angina and ST-segment depression. The therapy was started with 10 mg nicorandil b.i.d. or 40 mg propranolol t.i.d. After 3 weeks, the dosage could be doubled according to clinical criteria. Four men receiving nicorandil and one receiving propranolol were withdrawn with side effects; in three cases, the data were not complete. Thus, comparative data were obtained in 69 patients; in 51 of these (26 receiving nicorandil and 25 receiving propranolol), the dosage was increased to the higher level. Blood pressure and heart rate were unaltered by nicorandil and lowered by propranolol. The number of anginal attacks decreased relative to baseline on nicorandil and propranolol (p < 0.002), but total exercise duration was not influenced by either drug. The exercise test performed 2 h after either pill ingestion showed a decrease and a delay in occurrence of myocardial ischemia. The test performed 12 h after medication exhibited reduced ischemia, whereas only propranolol resulted in delayed ST-segment depression. The double product of heart rate and systolic blood pressure was affected only slightly by nicorandil and reduced significantly by propranolol (p < 0.001). Thus, nicorandil medication affords similar improvement as propranolol in patients with angina pectoris, but the mode of action appears to be different.

Post-extra systolic potentiation: influence of calcium and verapamil in rat and rabbit hearts.

The interactions of the inotropic effects of verapamil (0.05-2.0 mumol l-1), calcium (0.33-5.2 mmol l-1) and post extra systolic potentiation (PESP) as induced by paired stimulation were studied in isolated rabbit and rat hearts under isovolumic and isotonic conditions. At low doses of verapamil, contractions were depressed, but those elicited by paired stimulation showed less depression than contractions of the same rate during single stimulation and even exceeded the unpotentiated contractions without verapamil. At high doses of verapamil contractility could not be restored by paired stimulation. Although contractions were restored to control level by an increase in extra-cellular calcium they were still abnormal in the sense that PESP could not be elicited. The excitation-contraction (e-c) uncoupling due to low calcium perfusion could be counteracted by paired stimulation but e-c uncoupling due to high dose verapamil could not be reversed by paired stimulation. Our results support the view that PESP does not only depend on augmented slow channel calcium influx but also on an enhanced calcium shift within the sarcoplasmic reticulum. We are doubtful about the idea that PESP can be used clinically to counteract the negative inotropic effect of high doses of verapamil.