[Sensitivity of the antitoxic liver function. Experimental demonstration].
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Biomedical subjects
Publications and source records attributed to R Dietrich.
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A whole-body scan with 99mTc-pyrophosphate and 85Sr-nitrate demonstrates extension of calcinosis in one case of dermatomyositis with cutaneous, subcutaneous, and muscular calcinosis. The authors suggest the potential use of 99mTc-phosphate compounds as an auxiliary instrument in the evaluation of dermatomyositis-polymyositis syndrome.
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A membrane-based visual dipstick enzyme immunoassay for the simultaneous detection of up to five mycotoxins was developed. Multiple dots of the respective antibodies against aflatoxin B1 (AFB1), T-2 toxin (T-2), 3-acetyldeoxynivalenol (3-AcDON), roridin A (RA), and zearalenone (ZEA) were applied onto a dipstick membrane. The competitive immunoreactions were performed by incubation of the dipstick in a test tube containing sample solution and a mixture of the respective toxin-horseradish peroxidase conjugates. After a second incubation in enzyme substrate/chromogen solution, a complete suppression of the (blue) colour development of the respective dot was scored positive. Visual detection limits for AFB1, T-2, 3-AcDON, RA, and ZEA in buffer solution were 2 ng/ml, 5 ng/ml, 50 ng/ml, 30 ng/ml, and 5 ng/ml respectively. Using a simple extraction procedure, the detection limits of the multimycotoxin assay in artificially contaminated wheat samples were 30 ng/g, 100 ng/g, 600 ng/g, 500 ng/g, and 60 ng/g, respectively.
The current status of immunochemical techniques for analysis of paralytic shellfish poisoning (PSP) toxins is summarized. Important aspects regarding production of the biological reagents necessary for immunochemical methods, the characteristics of polyclonal and monoclonal antibodies against saxitoxin and neosaxitoxin, and the importance of test sensitivity and specificity are discussed. Applications of immunochemical techniques for PSP toxins include microtiter plate enzyme immunoasays and enzyme-linked immunofiltration assays for toxin detection, and immunoaffinity chromatography (IAC) for sample extract cleanup. A major advantage of enzyme immunoassay (EIA) is simplicity and rapidity of the test procedure, and higher sensitivity than other methods. However, quantitative agreement between EIA and mouse bioassay is dependent on antibody specificity and the toxin profile in the shellfish; thus, both over- and underestimation of total toxicity may occur. For screening purposes, however, EIAs offer major advantages over the mouse bioassay, which is criticized in Europe because of animal welfare. A major application of antibodies against PSP toxins is their use for extract cleanup by IAC, which gives highly purified extracts, thereby enhancing determination of PSP toxins by conventional physicochemical methods such as liquid chromatography. IAC can also be used to isolate PSP toxins for preparation of analytical standard solutions.
Arginine vasopressin (AVP) and AVP binding sites have been localized in brain areas involved in cardiovascular control. To elucidate the mechanisms by which brain AVP may participate in central blood pressure regulation, we investigated the effects of central AVP receptor stimulation on mean arterial pressure (MAP), heart rate (HR), efferent splanchnic nerve (SpNA), and renal nerve activity (RNA) in conscious chronically instrumented rats. Intracerebroventricular (i.c.v.) injections of AVP (1-100 ng) produced dose-dependent increases in MAP together with marked increases in HR, SpNA, and RNA. The pressor responses were inhibited by peripheral alpha-adrenoceptor blockade with i.v. phentolamine. In contrast, the pressor responses to either i.v. or intracarotid injections of AVP were accompanied by baroreceptor reflex (BRR)-mediated decreases in HR and SpNA. Central (i.c.v.) pretreatment with d(CH2)5AVP, a V1-AVP receptor antagonist, completely abolished the responses to i.c.v. but not to i.v. AVP. The same antagonist had no effect on the responses to i.c.v. angiotensin II. Our results demonstrate that: (a) central AVP overrides the BRR by sympathetic stimulation, whereas blood-borne AVP activates the BRR; (b) specific AVP receptors in the brain probably of the V1-subtype are involved in the central pressor responses to AVP; (c) the central pressor actions of AVP are transmitted to the periphery by stimulation of the sympathetic nervous system. We conclude that brain AVP may contribute to central cardiovascular control by modulating the sympathetic outflow to the periphery.