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Biomedical subjects

K Kusterer

Publications and source records attributed to K Kusterer.

46 records · Page 3Linked to original sources
PubMed1990

Thyrotoxic crisis in Graves' disease: indication for immediate surgery.

Thyrotoxic crisis (thyroid storm) is a rare complication of hyperthyroidism. It can be observed not only in thyroid autonomy with latent hyperfunction after exposure to iodine, but also in Graves' disease with overt hyperfunction. Adequate management of thyrotoxic crisis is still controversial. We report about four patients (four women, mean age 75 years) with Graves' disease who developed thyrotoxic crisis during therapy with antithyroid drugs so that surgical intervention became necessary. The patients had been admitted to the hospital for nonspecific symptoms such as headache, cachexy, and psychosis. Thyroid hormone levels had reached twice the normal range prior to surgery. All patients showed severe neurological deficits leading to coma. In three cases euthyroidism was achieved within two days after surgery. The neurological symptoms disappeared after an average of four days. The postoperative course did not show severe complications and all patients recovered completely. Especially in the elderly a monosymptomatic or nonspecific course of thyroid storm with neurological symptoms may represent a severe and life-threatening situation. In these cases surgery can become necessary even if euthyroidism has not been achieved preoperatively.

Aged↗
PubMed1989

The role of gastric and duodenal pH in the cysteamine-induced duodenal ulcer in the rat.

Many secretory studies reported an increase in gastric acid secretion by the duodenal ulcerogen cysteamine. A detailed analysis of these experiments, especially the results from rats with chronic gastric fistula suggest that direct stimulation of gastric acid secretion may not be the primary mechanism of the duodenal ulcerogenic action of cysteamine. We used a different approach and measured the pH at the site of ulceration in the proximal duodenum. A duodenal ulcerogenic dose of cysteamine did not change the pH at the anterior or posterior wall of the duodenum during 4 hr. In the same dose and by the same route of administration, cysteamine nevertheless induced duodenal ulcers in 24 hr. These experiments demonstrate that in addition to the effect on gastric acid secretion, other factors are needed to the effect on gastric acid secretion, other factors are needed to explain the early duodenal ulcerogenic action of cysteamine.

Animals↗
PubMed1987

Gastric mucosal protection by acetazolamide derivatives: role of carbonic anhydrase and sulfhydryls.

Acetazolamide, a carbonic anhydrase inhibitor, prevents acute gastric hemorrhagic lesions induced by ethanol. We used acetazolamide and other carbonic anhydrase inhibitors to correlate their gastroprotective effects with the degree of inhibition of carbonic anhydrase. Since acetazolamide is a thiadiazole, we also investigated structurally related thiadiazoles that contain sulfhydryls to test the hypothesis that the protection against ethanol-induced gastric erosions is related to the presence of sulfhydryls. Dose-response studies with acetazolamide revealed that the protection did not correlate with the inhibition of carbonic anhydrase in the rat gastric mucosa. The carbonic anhydrase inhibitors sulfanilamide and ethoxzolamide, did not offer protection. Bismuthiol I, a thiadiazole with two sulfhydryls, was twice as protective as 2-amino-5-mercapto-1,3,4-thiadiazole with only one sulfhydryl group. We conclude that the protection by acetazolamide against ethanol-induced lesions is not related to the inhibition of carbonic anhydrase in the gastric mucosa. The gastroprotective effect of acetazolamide and its derivatives may be related to their content of sulfhydryls in an oxidized or reduced state.

Acetazolamide↗
PubMed1987

Role of lipid peroxidation in gastric mucosal lesions induced by HCl, NaOH, or ischemia.

We investigated whether lipid peroxidation is an important biochemical mechanism in acute gastric mucosal injury induced by acid, base, or postischemic reperfusion. Lipid peroxidation products, i.e., the concentration of conjugated dienes (absorbance at 242 nm), products absorbing at 270 nm, and malondialdehyde were measured in the gastric mucosa of rats killed 30 s or 1, 3, or 6 min after intragastric (ig) administration of 0.6 N HCl or 0.2 N NaOH. No increase in any of the lipid peroxidation products was detected at any of the time intervals. Mucosal lesions, however, were already visible at 30 s. Cumene hydroperoxide (1 ml, 100 mM ig) induced neither mucosal lesions nor lipid peroxidation. In vitro incubation of mucosal homogenates with cumene hydroperoxide (1 or 10 mM) however, rapidly induced elevation of the three parameters of lipid peroxidation. Ischemia induced by clamping the blood vessels of the stomach for 20, 30, and 40 min followed by reperfusion for 10, 30, and 40 min did not induce lipid peroxidation, despite the development of hemorrhagic mucosal lesions. Similarly, in gastric mucosal lesions induced by hemorrhagic shock no lipid peroxidation products were detected. In the small intestine, however, prolonged ischemia (2 h) followed by reperfusion (30 min) resulted in mucosal necrosis and elevation of malondialdehyde levels. These results suggest that lipid peroxidation is not a major pathogenetic mechanism in rapidly developing acute gastric mucosal injury caused by 0.6 N HCl or 0.2 N NaOH, or in the more slowly developing mucosal injury caused by postischemic reperfusion.

Animals↗
PubMed1986

Cytoprotective properties of somatostatins.

Secretion of many hormones is inhibited by regular cyclic somatostatin-14. Since additional cytoprotective properties of this hormone have been described, the question arises of whether analogs of somatostatin with increased endocrine activity may also exert increased cytoprotective activity. It could be shown that the endocrine and the cytoprotective property of somatostatin-14 must have different modes of action. In analogs of somatostatin with increased endocrine activity the cytoprotective effect is also increased. A maximal increase in the cytoprotective effect of certain analogs of somatostatin is accompanied by a loss of endocrine activity.

Amino Acid Sequence↗
PubMed1986

Gastric mucosal protection by somatostatins.

Somatostatin and somatostatin derivatives were tested for their ability to prevent gastric hemorrhagic erosions induced by ethanol. The somatostatin analogues were cyclohexapeptides with the rearranged amino acids 7-14 of somatostatin (S-14): Phe-Thr-Lys(Z)-Trp-Phe-D-Pro(I), Phe-Thr-Lys-Trp-Phe-D-Pro(II), Phe-Thr-Lys-D-Trp-Phe-Tyr(III) and Tyr-Phe-D-Trp-Lys-Thr-Phe(IV). In Spraque-Dawley rats receiving ethanol alone, the lesions involved 18.1 +/- 3.2% of the glandular stomach while after S- 14 (10(-7) mol/rat) the lesioned area was reduced to 6.3 +/- 1.1% (p less than 0.05). Peptide I and peptide II (doses 10(-7) -10(-9) mol/rat) decreased the area of erosions to less than 5%. Peptide III was less active and peptide IV was inactive. In rats with chronic gastric fistula S- 14 and peptide II decreased the cysteamine-stimulated acid secretion without affecting the pepsin output. We also continuously measured the intraluminal pH in the stomach of Wistar rats which develop gastric erosions after subcutaneous injection of cysteamine. The erosions were reduced by S- 14 or SMS while the intraluminal pH did not change under the influence of cysteamine or the combination of cysteamine plus S- 14 or SMS. Thus some of the peptides derived from S- 14 exert prominent gastric mucosal protection without influencing gastric secretion.

Animals↗
PubMed1984

Vasopressor systems during smoking in humans.

In this study we correlated the effects of cigarette smoking on the activity of vasopressor systems in humans with changes in heart rate and blood pressure and compared them with changes observed after physical exercise or graded norepinephrine infusion. No relationship was established between changes in either plasma angiotensin II or vasopressin concentration and the hemodynamic parameters, although there was a small increase in both hormones during smoking. In contrast, heart rate (r = -0.245, p less than 0.01, n = 136) was negatively related to plasma norepinephrine concentration during the smoking of five cigarettes. A comparable, negative correlation, although much closer, was found during graded norepinephrine infusion between heart rate and norepinephrine concentration (r = -0.682, p less than 0.001), whereas both parameters were positively related under conditions of physical exercise (r = 0.866, p less than 0.001). In an attempt to block the assumed nicotine-induced sympathetic stimulation, smoking experiments were carried out after acute beta blockade (200 mg metoprolol orally). There was a parallel shift of heart rate and blood pressure to lower values. However, beta blockade did not abolish the smoking-induced rise in blood pressure and heart rate. At the present time no direct evidence is available for a nicotine-induced increase of norepinephrine concentration at postsynaptic receptors during smoking in humans.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMedDate not supplied

The impact of contralateral cooling on skin capillary blood cell velocity in patients with diabetes mellitus.

In healthy volunteers, cooling of the contralateral hand leads to a rapid decrease in the ipsilateral capillary perfusion via a nerval reflex arc. The aim of this study was to investigate whether this reflex arc after contralateral cooling might be altered in patients with diabetes mellitus with and without peripheral neuropathy. Therefore, 12 patients with diabetic neuropathy (4 IDDM, diabetes duration 17.2 +/- 2.9 (SD) years, age 60.8 +/- 4.0 years, HbA1c 6.5 +/- 0.3%) and 12 patients with diabetes mellitus but without neuropathy (6 IDDM, diabetes duration 15.1 +/- 2.7 years, age 55.9 +/- 4.5 years, HbA1c 5.4 +/- 0.1%) were investigated by nailfold capillaroscopy. Twelve healthy volunteers (age 56.8 +/- 3.1 years, HbA1c 4.8 +/- 0.2%) served as controls. Contralateral skin capillary blood cell velocity was determined at rest and during the following 20 min after cooling of the hand (3 min at 15 degreesC). Blood pressure, heart rate and local skin temperature were examined regularly during the investigation. Resting capillary blood cell velocity did not differ between patients and controls. While contralateral cooling resulted in a decrease in capillary blood cell velocity (CBV) in controls (0.29 +/- 0.05 vs. 0.42 +/- 0.05 mm/s, p < 0.03), CBV remained unchanged or was delayed in patients. These results demonstrate that in diabetic patients nerval reflex arcs are impaired. A long-term follow-up in a larger number of patients is required to evaluate whether these findings might serve as a very early diagnostic tool for the diagnosis of developing diabetic neuropathy.

Blood Cells↗