Effects of colostrum feeding and glucocorticoid administration on insulin-dependent glucose metabolism in neonatal calves.

Colostrum feeding and glucocorticoid administration affect glucose metabolism and insulin release in calves. We have tested the hypothesis that dexamethasone as well as colostrum feeding influence insulin-dependent glucose metabolism in neonatal calves using the euglycemic-hyperinsulinemic clamp technique. Newborn calves were fed either colostrum or a milk-based formula (n=14 per group) and in each feeding group, half of the calves were treated with dexamethasone (30 microg/[kg body weight per day]). Preprandial blood samples were taken on days 1, 2, and 4. On day 5, insulin was infused for 3h and plasma glucose concentrations were kept at 5 mmol/L+/-10%. Clamps were combined with [(13)C]-bicarbonate and [6,6-(2)H]-glucose infusions for 5.5h (i.e., from -150 to 180 min, relative to insulin infusion) to determine glucose turnover, glucose appearance rate (Ra), endogenous glucose production (eGP), and gluconeogenesis before and at the end of the clamp. After the clamp liver biopsies were taken to measure mRNA levels of phosphoenolpyruvate carboxykinase (PEPCK) and pyruvate carboxylase (PC). Dexamethasone increased plasma glucose, insulin, and glucagon concentrations in the pre-clamp period thus necessitating a reduction in the rate of glucose infusion to maintain euglycemia during the clamp. Glucose turnover and Ra increased during the clamp and were lower at the end of the clamp in dexamethasone-treated calves. Dexamethasone treatment did not affect basal gluconeogenesis or eGP. At the end of the clamp, dexamethasone reduced eGP and PC mRNA levels, whereas mitochondrial PEPCK mRNA levels increased. In conclusion, insulin increased glucose turnover and dexamethasone impaired insulin-dependent glucose metabolism, and this was independent of different feeding.

[Detection of thrombosis of the left atrium in mitral valve stenosis. Particular value of transesophageal echography]. / Détection des thromboses de l'oreillette gauche du rétrécissement mitral. Intérêt particulier de l'échographie transoesophagienne.

This retrospective study assessed the prevalence of left atrial thrombi in mitral stenosis and evaluated the diagnostic value ot the main means of investigation Five hundred and eighty-one patients underwent open heart surgery over a 10 year period. The prevalence of atrial thrombi was 7%, the majority (60%) being located in the left atrial appendage. The sensitivity of transthoracic echocardiography for detecting thrombi in the left atrial cavity was satisfactory (65%) but was very poor for detecting thrombi in the left atrial appendage (4%). The results of invasive investigations (atrial angiography and coronary angiography) are no better. Without any doubt, transoesophageal echocardiography, performed in 101 patients in this series, has transformed these results (sensitivity 83%, specificity 97%). False negatives in this study mainly concerned small thrombi adherent to the atrial wall. Under these conditions, it would seem reasonable to propose transoesophageal echocardiography to all patients with mitral stenosis complicated by an embolic event or for those for whom percutaneous commissurotomy is suggested.

Diagnosis of left atrial thrombi in mitral stenosis--usefulness of ultrasound techniques compared with other methods.

The purpose of this study was to evaluate various methods of diagnosis of left atrial thrombi (LAT) in patients (pts) with mitral stenosis (MS). From 1980 to 1990, 581 pts with MS have undergone open mitral commissurotomy (n = 169) or valve replacement (n = 412). All pts had transthoracic 2D echocardiography (TTE), 101 transoesophageal echocardiography (TEE), 192 a left atrial angiography (A) (from a left ventricular injection if associated mitral regurgitation grade 3 (n = 154) or from an injection in the pulmonary artery (n = 38) and 229 a coronary angiography (CA). Tomodensitometry (TD), nuclear magnetic resonance (NMR) and 111 Indium platelet imaging (IPI) were performed in some cases, 2, 8 and 5 respectively. All these examinations were carried out in the month before surgery. LAT was found by the surgeon in 43 pts (7%). The site was left atrial appendage in 26 cases (60%) and left atrial cavity in 17 cases. Sensitivity (Se), specificity (Sp) of TTE/TEE/A/CA were the following: TTE, Se% 28, Sp% 99; TEE, Se% 83, Sp% 97; A, Se% 28, Sp% 99; CA, Se% 14, Sp% 100. Specificity was high with all methods but sensitivity was high only with TEE and poor with other methods because of difficulty in detecting thrombi of the left atrial appendage. Specificity and sensitivity of TD, NMR and IPI require more information. False-negative cases are possible with NMR (1 case) and IPI (1 case) in well established LAT. We conclude: TEE is the easiest way to detect LAT, particularly when located in the left atrial appendage. It should be carried out systematically before percutaneous mitral valvuloplasty or surgery.

Effects of (+)-tubocurarine on [3H]acetylcholine release from the rat phrenic nerve at different stimulation frequencies and train lengths.

The effect of (+)-tubocurarine (TC) on the release of [3H]acetylcholine from the rat phrenic nerve-hemidiaphragm preincubated with [3H]choline was investigated at different stimulation frequencies and train lengths. At 0.5 Hz (100 pulses) TC failed to modulate the evoked acetylcholine release. A slight (30%) inhibition was observed at 1 Hz (100 pulses). Release of acetylcholine evoked at 5, 25 and 50 Hz (100 pulses) or 100 Hz (200 pulses) was markedly reduced by TC. The degree of inhibition (60%) was similar between 5 Hz and 100 Hz. A concentration of 1 mumol/l TC was a maximal effective concentration at 5 Hz whilst at all higher stimulation frequencies a 10-fold higher concentration was necessary for the maximal effect. When 300 pulses were continuously applied at 5 Hz or 50 Hz TC caused only a slight inhibition (20%). Additionally, the phrenic nerve was stimulated intermittently. Trains of 15 pulses were repeated 10 times with an interval of 3 s between each train. Under this latter stimulation condition TC failed to reduce acetylcholine release. It is concluded that nicotinic autofacilitation of acetylcholine release from the motor nerve operates at frequencies and stimulation conditions similar to the pattern of nerve activity under in vivo conditions. At least more than 15 pulses are required before the nicotinic autofacilitation becomes apparent. It appears unlikely that the TC induced fading of end-organ responses can only be attributed to a blockade of the presynaptic nicotine receptors.

[3H]acetylcholine release from the phrenic nerve is increased or decreased by activation or desensitization of nicotine receptors.

Nicotinic agonists (nicotine, 1,1-dimethyl-4-phenylpiperazinium (DMPP) increased [3H]acetylcholine release when the pre-exposure time was short (20 s). This effect was antagonized by pretreatment with d-tubocurarine (d-TC), which indicates a receptor-mediated effect. After a longer pre-exposure time (3 min) 10 microM nicotine significantly decreased the evoked [3H]acetylcholine release, probably because desensitization of the nicotine autoreceptors had abolished the nicotinic autofacilitation of transmitter release.

[Porokeratosis plantaris, palmaris et disseminata]. / Porokeratosis plantaris, palmaris et disseminata.

A 74-year-old patient has been affected for about 40 years by hardly discomforting keratotic lesions of the trunk and extremities, especially on the palms and soles. Some of his children and grandchildren have shown similar lesions. Histologically the diagnosis of porokeratosis was established by demonstration of a cornoid lamella. Clinically it appeared to be the rare form of porokeratosis plantaris, palmaris et disseminata, in which mainly the palms and soles are affected by hyperkeratotic papules, but nearly the whole body may be involved. It is discussed how this genodermatosis can be differentiated from other forms of porokeratosis. The family tree of our patient is compatible with autosomal dominant inheritance.

[Contact allergy caused by triethanolamine]. / Kontaktallergie durch Triäthanolamin.

Triethanolamine and its compounds are used as emulsifiers, stabilizers, and saponifying agents in chemical industry. A total of 1,357 patients suspected of having allergic eczematous contact dermatitis were patch-tested with triethanolamine. Positive tests were obtained in 41 of these 1,357 patients. Twenty-nine of them had suffered from venous insufficiency or sports injuries. They had used antiphlogistic local medicaments for some time and were most probably sensitized against triethanolamine by these topical drugs.