Changes of glaucomatous field defects. Degree of accuracy of measurements with the automatic perimeter Octopus.

The analytical programme Delta was used to determine longterm fluctuation and accuracy of measurement of the programme 31 of Octopus when used on glaucoma patients. Programme 31 examines the 30 degrees field. The test locations are arranged in a square grid with 6 degrees resolution. The programme Delta determines and compares 1) the disturbed area in %; 2) the total loss, the total sensitivity being around 2000 dB; 3) the loss in dB per mean number of disturbed points. Thirty-two eyes of 22 patients with established glaucomatous field defects were examined twice within two to six days and two months later again twice. The size of the disturbed area served for classification of our sample into three groups: 1st group: disturbed area 1-33%; 2nd group: disturbed area 34-66%; 3rd group: disturbed area 67-100%. Long-term fluctuations and accuracy of measurement could be determined as respectively follows: 1) Disturbed area between 0.7 +/- 8% in group 3 and 1.7 +/- 13% in group 2. 2) The total loss increases proportionately to the disturbed area and was 4.9 +/- 29.2 dB in group 1 and 31.8 +/- 82.4 dB in group 3. 3) The total loss per mean number of disturbed points was 0.5 +/- 2 dB in group 1 and 0.3 +/- 1.2 dB in group 2. This signifies that if the learning effect is over, changes of more than 2 dB, especially if several adjacent points are affected, are a significant loss. The learning effect, as determined in an earlier study, may go up as high as 2 dB per point.

Automatic (Octopus) and manual (Goldmann) perimetry in glaucoma.

Of 115 patients with chronic open angle glaucoma or suspected glaucoma 115 eyes were subjected to a visual field examination with the manual Goldmann perimeter and the automatic Octopus perimeter. In 84.4 +/- 8.9% the automaton detected more visual field loss, including 27.8 +/- 10.9% of the eyes where no visual field loss was found by the manual perimetry. Since some eyes with normal fields on manual perimetry and abnormal fields detected by automatic perimetry remained abnormal on retesting, it is assumed that scotomas found by automatic perimetry and not shown by manual perimetry constitute false-negative manual fields rather than false-positive automatic fields.

A highly specific 125I-radioimmunoassay for cholic acid conjugates.

Several modifications of the immunization procedure permitted development of a highly specific radioimmunoassay (RIA) for cholic acid conjugates. Antiserum was produced in guinea pigs using cholic acid-thyroglobulin complex as immunogen. 125-I-Cholyglycylhistamine was prepared as radioactive ligand according to a modification of the method of Spenney et al. (Spenney, J.G., Johnson, B.J., Hirschowitz, B.I., Mihas, A.A. and Gibson, R. (1977) Gastroenterology 72, 305--311). The association constant of the antisera to taurocholic acid was 1.8 x 10(7) l/mol, the working range of the assay between 9.5--890 pmol. Cross-reactivities of the antiserum to bile acids other than cholic acid species were less than 3%, which is lower than for any published bile acid RIA. Concentrations of cholic acid conjugates in sera obtained from 17 healthy fasting volunteers ranged from 0.4--1.9/mumul/l.

[Blood pressure and renin activity in essential hypertension under pindolol]. / Blutdruck und Reninaktivität bei essentieller Hypertonie unter Pindolol

20 essential hypertension patients with diastolic blood pressure of 100-140 mm Hg were treated with increasing doses (15-45 mg/day by mouth) of pindolol for 14 weeks after an initial placebo period of 5 weeks. Systolic and diastolic blood pressure decreased significantly with as little as 15 mg of pindolol (p less than 0.001). No further changes in systolic and diastolic blood pressure were observed when the doses of pindolol were increased. Plasma renin activity (PRA) determined by radioimmunoassay did not change under increasing doses of pindolol. The blood pressure changes did not correlate with initial PRA or with individual changes in PRA under increasing doses with individual changes in PRA under increasing doses of pindolol. These results do not afford evidence for a renin-dependent hypotensive effect of pindolol.

[Effect of saralasin on normal blood pressure and on reno-vascular hypertension (author's transl)]. / Angiotensinblockade mit Saralasin. Einfluss auf den normalen Blutdruck und auf den renovaskulären Hochdruck

The angiotensin antagonist saralasin was given intravenously to six normotensive students before and after dietary sodium restriction and to two patients with renovascular hypertension. Both patients responded to the angiotensin antagonist with a decrease of the systolic (32 and 38 mm Hg) and of the diastolic (29 and 16 mm Hg) blood pressure. The small changes in blood pressure observed in the normotensive subjects during the infusion of the angiotensin antagonist indicate that angiotensin II plays no important role in the control of normal blood pressure in recumbent men. The fall in blood pressure induced by saralasin in both patients, however, demonstrates that their hypertension was at least partly angiotensin-dependent. Renal vein renin determination led to the same conclusions. The saralasin infusion test seems to be a simple procedure to diagnose angiotensin-dependent hypertension and will probably help to identify patients with suspected renovascular hypertension.

Plasma renin activity (PRA) and plasma aldosterone (PA) in hypertensive kidney allograft recipients.

Basal and stimulated plasma renin activity (PRA) and plasma aldosterone (PA) were measured in 13 hypertensive and 16 normotensive patients with kidney allografts one to nine years after transplantation. In both groups no significant differences were observed between mean basal and stimulated PRA and PA values. Therefore, we conclude that abnormal renin secretion might not be the main factor causing hypertension in renal allograft recipients. Other mechanisms seem to be involved in the pathogenesis of hypertension in these patients.

Characteristics of aldosterone antisera related to the duration of immunization.

Three antisera specific to aldosterone and elicited with different aldosterone protein conjugates (aldosterone-3-oxine rabbit serum albumin and aldosterone-3-oxime bovine gamma-globulin) were studied by radioimmunological methods at various times subsequent to first-immunization. A considerable variability of the parameters important in radioimmunoassay was observed over the whole experimental period. Titer, sensitivity and specificity of two antisera tended to increase as long as the animals were boosted. In the third they did not change in a uniform way.

In vivo effects of angiotensin antagonists on plasma aldosterone in the dog.

The effects of infusions of equimolar doses of Sar1-Ile8-angiotensin II and of Sar1-Ala8-angiotensin II on plasma aldosterone, plasma renin activity and arterial blood pressure were compared in normal dogs. Plasma aldosterone increased significantly after Sar1-Ile8-angiotensin II whereas it was unaffected by Sar1-Ala8-angiotensin II. Changes in blood pressure and renin activity were small without marked differences between both groups of animals. The experiments demonstrate a clear steroidogenic potency of Sar1-Ile8-angiotensin II. Therefore, Sar1-Ala8-angiotensin II should be preferred as antagonist of the action of angiotensin II in the adrenal gland.

Production and characterisation of antisera to 18-hydroxy-11-deoxycorticosterone.

The production of highly sensitive and specific antisera to 18-hydroxy-11-deoxycorticosterone (18,21-dihydroxy-4-pregnene-3,20-dione) is reported. The antisera were generated in rabbits and guinea pigs with a 3-carboxymethoxime derivative of the steroid coupled to rabbit serum albumin. Antibody characteristics were determined by a radioimmunoassay procedure. Only minor differences between the two animal species were observed. Antibody titers ranged from 10 to 8000. Association constants were in the order of 10(8) to 10(10) 1/mole. A minimal amount of 40 pg unlabeled steroid was necessary to displace 50% of the tritiated steroid. Cross reaction with cortisol was 0.0002% to 0.031%, with aldosterone 0.0007% to 1.09%, with corticosterone 0.0025% to 1%, with 18-hydroxy-corticosterone 0.05% to 1% and with progesterone 0.0048% to 1.5%.

Effect of propranolol and prindolol on renin secretion in normal supine man.

To investigate the effect of propranolol and prindolol on renin secretion plasma renin activity (PRA) was determined overnight at short-time intervals in 10 sodium-restricted normal supine subjects. 4 of them were on a 4-days medication with propranolol, 3 were rreated with prindolol and 3 were used as control group. In normal controls renin was secreted episodically and showed characteristic night-day variations. Both in propranolol and in prindolol-treated subjects secretory episodes in renin secretion either did not occur or were less frequent than in normal controls. With one exception night-day variations in renin secretion were not observed. Mean PRA values were significantly lower than in the control group (p less than 0.001). Our results show that both propranolol and prindolol lower PRA and eliminate or reduce the frequency of secretory episodes. It is concluded that the sympathetic nervous system plays an important role in regulating night-day variations and short-time fluctuations of renin secretion in normal supine man.

Effect of angiotensin II and of an angiotensin II analogue (Sar1-Ile8-angiotensin II) on blood pressure, plasma aldosterone and plasma renin activity in the dog.

1. The effect of infusions of equimolar doses of angiotensin II (AII) and of the angiotensin analogue Sar1-Ile8-angiotensin II on arterial blood pressure, plasma aldosterone and plasma renin activity were compared in normal anaesthetized dexamethasone suppressed dogs. 2. Angiotensin II induced a significant increase of blood pressure and of plasma aldosterone whereas plasma renin activity decreased. The blood pressure was only slightly affected by large doses of the analogue. Plasma aldosterone, however, increased and plasma renin activity decreased. These changes were significant but less pronounced than after the infusions of angiotensin II. Plasma aldosterone remained high and renin activity low for 40 min after the infusions of the analogue. 3. The results suggest a strong agonistic potency of Sar1-Ile8-angiotensin II at the adrenal and renal angiotensin receptors, and that it is almost ineffective at the vascular receptors. The inhibition of renin secretion by angiotensin seems not be related to its vasoconstrictive activity.