Measurement of angiotensin II in human plasma: technical modifications and practical experience.

This paper presents our experience in measurement of plasma angiotensin II concentration according to the method described by Düsterdieck, G. and McElwee, G. (1971) Eur. J. Clin. Invest. 2, 32-38. Certain technical modifications of the procedure have been worked out. For each individual plasma sample, the recovery across extraction and elution steps is determined by addition of radio-iodinated angiotensin II. A time-saving recycling elution procedure is described. Evidence for the clinical applicability of the modified method is presented.     

A note on the practical aspects of the assay of N-acetyl-beta-glucosaminidase in human urine.

1. Some practical aspects of the assay of urinary N-acetyl-beta-glucosaminidase activity were studied in patients with renal disease. 2. Centrifugation and dialysis of urine were not necessary prior to assay. 3. When enzyme activity was related to urinary creatinine random urine samples could be used. 4. Since preservatives used to prevent bacterial growth may inhibit enzyme activities, samples should be assayed immediately after collection or stored at 4 degrees C or 20 degrees C. 5. Mild visible haemoglobinuria, eg. derived from lysed red blood cells did not interfere with the enzyme assay.     

Linearity and accuracy of ultraviolet and visible wavelength photometer: an interlaboratory survey.

A survey was made to determine the linearity and accuracy of ultraviolet and visible wavelength photometers used by laboratories in New York State. Two solutions each of high-purity potassium dichromate and cobalt ammonium sulfate were submitted for photometric performance studies. The majority of the participant spectrophotometer results showed good correlation with reference data. Broad half-band width (greater than 10 nm) photometers showed little deviation from linearity. Coefficients of variation for the models surveyed were 5-10%.     

The systemic administration of local anaesthetics produces a selective depression of C-afferent fibre evoked activity in the spinal cord

An electrophysiological analysis of the antinociceptive effects of systemic lidocaine and its longer acting primary amine congener, tocainide, has been performed in the decerebrate-spinal unanaesthetised rat. Neither of these local anaesthetic drugs when administered systemically in doses of up to 10 mg/kg (lidocaine) or 100 mg/kg (tocainide), produced any evidence of a block in the conduction of action potentials in A beta, A delta or C primary afferents. The local anaesthetics also failed to reduce mustard oil induced neurogenic extravasation, a test of cutaneous C-fibre terminal function. Lidocaine produced a transient (1-2 min) depression in monosynaptic reflexes at doses of greater than or equal to 1 mg/kg while tocainide had no effect on this reflex at any dose up to a 100 mg/kg. Both drugs, however, significantly suppressed the C-fibre evoked polysynaptic reflex generated by stimulating the sural nerve. The tocainide effect was longer lasting with less action on the short latency A beta-evoked reflex than lidocaine. The reflex activity in hamstring flexor alpha-motoneurones evoked by pinching the toes of the ipsilateral hind paw was reduced by both drugs but not abolished. Thermal and noxious chemical evoked reflexes were, however, completely suppressed by the local anaesthetic drugs, again with a longer action from tocainide. These results demonstrate that the systemic administration of drugs which increase the inactivation of sodium channels can produce a selective central block of certain types of afferent evoked activity in the spinal cord. There are resemblances between the selective C-fibre suppressing actions of systemically administered local anaesthetic and the pharmacological actions of narcotic opiates which may represent a similar mechanism for the analgesic action of these quite different classes of drugs.     

In vitro assessment of the intra luminal phase of gliadin digestion in coeliac disease: γ-glutamyl transpeptidase-like activity in saliva

γ-Glutamyl transpeptidase (GGTP) is an enzyme of potential relevance to the digestion of dietary gliadin, and hence of possible importance in the development of coeliac disease (CD). We have confirmed that human saliva has GGTP-like activity. Comparison of this activity between treated CD patients in long-term remission, age- and sex-matched normal control subjects, and unaffected relatives of CD patients did not show statistically significant differences. Although our results have not demonstrated a primary abnormality of this particular enzyme activity in CD, the intraluminal phase of gliadin processing is potentially important in the aetiology and pathogenesis of CD and thus deserves further study.     

Pain relief by somatostatin in attacks of cluster headache

The pain relieving effect of somatostatin treatment during 72 attacks of cluster headache in 8 male patients was compared to treatment with ergotamine or placebo in a double-blind study. Infusion of somatostatin (25 micrograms/min for 20 min i.v.) reduced the maximal pain intensity and the duration of pain significantly compared to placebo treatment, and to a degree comparable to ergotamine tartrate treatment (250 micrograms i.m.). The results obtained provide new information concerning the possible mechanism of cluster headache attacks and suggest a new therapeutic approach.     

Representation of the thoracic outlet syndrome as a problem in chronic pain and psychiatric management

The diagnosis of thoracic outlet syndrome depends upon subjective complaints and sometimes rather limited physical findings. There is a tendency to favour other non-specific diagnoses, like ‘soft tissue damage’ or to suspect neurosis, particularly in patients who have had motor vehicle or other injuries for which they claim compensation. We report here 3 patients in whom the diagnosis of thoracic outlet syndrome was overlooked and who responded to surgical treatment with good or excellent results.     

An evaluation of stabilizing agents in competitive protein-binding assay for 25-hydroxyvitamin D

We have recently described a major variation from the normal levels of serum thyroxine-binding globulin in many Australian Aborigines [1]. Subsequently we presented evidence that affected individuals were widely distributed throughout Australia, that “low” values of thyroxine-binding globulin were not caused by environmental or health factors, but were inherited in an autosomal dominant fashion [2]. Refetoff [3] has shown that the cause of genetically determined low thyroxine-binding globulin levels in Caucasians is alteration in synthesis rate without any structural variation of the protein. Since however the “low” thyroxine-binding globulin of Aborigines is vastly more prevalent and genetically distinct from the X-linked type, we investigated the possibility that this may be a structural variant. Evidence suggestive of this includes results from heat inactivation, competitive binding of thyroxine to thyroxine-binding globulin to measure affinity, and use of a radioimmunoassay different from that used in the original work. The “low” thyroxine-binding globulin of Aborigines may be a protein with a structural variation at or near the binding site for thyroxine, resulting in lower affinity for thyroxine and hence “low” results with assay methods which depend upon the thyroxine binding site. Since the Australoid peoples, to whom Australian Aborigines are racially related, are distributed widely throughout the southern hemisphere it is important to establish whether this variant is found outside Australia in order to avoid the likelihood of misdiagnosis of thyroid disease in such subjects.     

Coagglutination for detection and serotyping of bacterial antigens: Usefulness in acute pneumonias

Staphylococcal coagglutination was evaluated for detection of Streptococcus pneumoniae and Haemophilus influenzae antigens in vitro and in the clinical setting of acute pneumonia. Coagglutination testing was performed with Phadebact reagents and with polyvalent and type-specific reagents for pneumococci prepared in the laboratory. Purified capsular antigens of 10 of 14 pneumococcal serotypes (included in the current pneumococcal vaccine formulation) were detected by coagglutination in the range of 0.5-62 ng/ml; serotype 6 was detected at 125 ng/ml, and serotypes 12, 23, and 25 were detected only at 500 ng/ml or more. Haemophilus influenzae type b antigen was detected at 100 ng/ml. Sputum, blood, and urine specimens of 36 consecutive patients admitted with pneumonia were evaluated prospectively by coagglutination. Nonspecific reactions were eliminated by pretreatment with ethylenediaminetetra-acetic acid and heating and with staphylococcal protein A. Eight of nine patients with sputum cultures positive for pneumococci had positive sputum coagglutination (sensitivity of 89%); 24 of 27 patients with cultures negative for pneumococci had negative sputum coagglutination (specificity of 89%). Serum or urine coagglutination was positive in five patients with pneumococcal pneumonia, including the only bacteremic case, the only fatality, and another patient who had a protracted clinical course. In conclusion, coagglutination is a simple, rapid, sensitive, and specific test for antigen detection in patients with acute pneumonia.     

The contribution of alpha1-antitrypsin to the total antitrypsin activity of human serum. A study of two phenotype PI OO individuals.

Comparison of the levels of alpha1-AT, alpha2-M, inter alpha-AT, C1 inactivator and antiplasmin and global antitrypsin activity in a group of normal phenotype PI MM individuals, a group of normal individuals with phenotypes with intermediate alpha1 AT activities and alpha2-AT-deficient persons show that alpha1-AT contributes more than 90 percent of the total antitrypsin activity of normal plasma. AT III and fast reacting antiplasmin are shown to contribute to the remaining activity. It can be assumed that due to test conditions the antitrypsin activity of alpha2-M is not assessed. C1 inactivator and inter alpha1-AT do not contribute to a perceptible extent to the overall antitrypsin activity estimated according to the method of Eriksson (Eriksson, S. (1965) Acta Med. Scand. 177, 1).