Diabetic autonomic neuropathy.
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Biomedical subjects
Publications and source records attributed to P Kempler.
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The authors examined the effect of beta-blocker monotherapy (Tobanum tab = 5 mg cloranololum hydrochloricum) and beta-blocker + diuretic (Tobanum + Furosemide) combination therapy on glucose tolerance and insulin secretion in response to oral glucose doses in hypertensive non-diabetic patients. Twenty-six patients were examined (13 men, 13 women). The patients were followed up for 28 weeks after a 2-week drug-free period. The hypotensive dose was adjusted individually within 4 weeks. Oral glucose tolerance test and immuno-reactive insulin determination were performed concurrently before starting hypotensive therapy and on weeks 6, 14, and 28 of therapy. The results of the examinations were evaluated separately in two patient groups. Fifteen patients were given daily 10-20 mg Tobanum (Group I) while 11 patients received daily 10-20 mg Tobanum + 40-80 mg Furosemide (Group II). The glucose area of patients on Tobanum monotherapy did not change, insulin secretion decreased gradually (from 804 to 495 pmol/l). The decrease was significant (p less than 0.05). The glucose area of Tobanum + Furosemide-treated patients increased from 13.2 +/- 3.2 mmol/l to 16.1 + 4.9, the insulin secretion decreased from 1039 + 339 to 706 + 411 pmol/l during therapy (p less than 0.02 and p less than 0.05, resp.). When evaluating the results the decrease of insulin secretion is attributed to Tobanum effect while the deterioration of glucose tolerance may be correlated to the action of Furosemide on extrapancreatic metabolism.
Autonomic neuropathy has been evaluated by various cardiovascular bedside tests in 99 patients with chronic alcoholism (33 alcoholics without liver disease, 33 patients with fatty liver and 33 with cirrhosis), in 10 patients with primary biliary cirrhosis, in 12 patients with cirrhosis of other origin, and in 40 healthy controls. Parasympathetic integrity was evaluated by beat-to-beat variation during deep breathing (6 min), Valsalva manouver and standing up, sympathetic function by blood pressure response to standing up and to sustained handgrip test. Autonomic reflex damage was found in all groups examined. Patients with alcoholic cirrhosis exhibited the most severe alterations. Our results suggest, that chronic hepatopathy itself presents a pathogenetic factor of autonomic neuropathy. Autonomic failure has to be considered as a possible cause of symptoms in liver diseases with all its prognostic consequences.
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Systolic time intervals were studied in 28 young, previously healthy burn patients (TBS 10-90%) on 145 occasions. A NEK 116 type 3 channel recorder of 100 mm/sec paper speed was used. Synchronous ECG recordings in lead II, PCG in the m "1" frequency band, and external carotid pulse tracings were recorded. RR, QS2, S1S2, LVET, PEP, PEP/LVET and QT, QTc, QS2-QT intervals were measured in 5-10 cardiac cycles in each of the examinations. Calculation of the additional parameters ICT, LVET/ICT, DT, EVR, PRP, EF and SV values were correlated to the extent of, and the time elapsed since, burn injury. The derivated parameters and statistical analysis were performed on a Commodore 64 type computer based on a software program. Elongation of QTc (greater than 440 msec) and frequent electrodynamic failure (QT-QS2 greater than 40 msec) especially during the first postinjury week were found characteristic in severe injury. In 53% the PEP/LVET ratio was less than 0.31, mean 0.32 +/- 0.093. In 21 cases of severe hypovolaemia the increase of PEP raised this value beyond 0.41. With the exception of 3 examinations, QS2I was normal or shortened. Calculated EF were normal or increased, SV reduced being interdependent with burn extent and shortening of DT. In patients with severe burns, oxygenization was inadequate (EVR less than 0.8); it showed an inverse correlation to HR. The simultaneously high LVET/ICT ratio and shortened ICT values pointed to an increase in contractility.
An 89-year-old man with chronic glaucoma received hourly pilocarpine eye drops for seven hours, when he developed third-degree atrioventricular block with a slow idioventricular escape rate. After discontinuing the pilocarpine, the atrioventricular block gradually disappeared. The site of pilocarpine-related block was most likely within the His-Purkinje system.
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