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Biomedical subjects

G Menzinger

Publications and source records attributed to G Menzinger.

At least 55 records · Page 3Linked to original sources
PubMed1994

Relationship between autonomic neuropathy, 24-h blood pressure profile, and nephropathy in normotensive IDDM patients.

OBJECTIVE: To evaluate the relationship between autonomic neuropathy, nephropathy, and 24-h blood pressure (BP) pattern in insulin-dependent diabetes mellitus (IDDM). RESEARCH DESIGN AND METHODS: We studied 30 normotensive IDDM patients without overt nephropathy, divided into two groups and matched for age, duration of diabetes, and HbA1, according to the presence of cardiovascular autonomic neuropathy. We simultaneously measured 24-h BP and urinary albumin excretion rate (UAE) on urine collections timed overnight and at 2-h intervals during the day. RESULTS: Mean day and night systolic and diastolic BP values did not significantly differ between the groups. Mean night albuminuria was significantly higher in patients with autonomic neuropathy than in those without (61.4 +/- 104.6 [mean +/- SD] vs. 16 +/- 25.2 micrograms/min, P < 0.04). The percentages day-night changes in systolic BP, diastolic BP, and UAE were significantly lower in neuropathic patients (systolic BP: 2.4 +/- 7.7 vs. 9.6 +/- 4.2%, P < 0.001; diastolic BP: 8.4 +/- 6.9 vs. 15.5 +/- 5.4%, P < 0.002; UAE: -8 +/- 99.4 vs. 49.3 +/- 29.4%, P < 0.02) and were inversely related to autonomic score, index of autonomic neuropathy degree (r = -0.54, P < 0.002; r = -0.58, P < 0.001; and r = -0.53, P < 0.005, respectively). In patients with autonomic neuropathy, 2-h day periods and day and night UAE were more strongly related, respectively, to mean 2-h day periods (r = 0.58, P < 0.0001), day systolic BP (r = 0.67, P < 0.04), and night systolic BP (r = 0.69, P < 0.04) than in patients without autonomic neuropathy (2-h day periods: r = 0.32, P < 0.001; day: r = 0.37, NS; night: r = 0.35, NS). CONCLUSIONS: Autonomic neuropathy in IDDM patients is associated with reduced nocturnal falls in BP and UAE and with a stronger relationship of UAE to systolic BP. We suggest a pathogenetic role of autonomic neuropathy in the development of diabetic nephropathy through changes in nocturnal glomerular function and by enhanced kidney vulnerability to hemodynamic effects of BP.

Adult↗
PubMed1993

Increased left ventricular mass in normotensive diabetic patients with autonomic neuropathy.

The possible relationship between diabetic autonomic neuropathy, circadian blood pressure changes, and echocardiographic parameters was investigated in 27 normotensive diabetic patients (10 with and 17 without autonomic neuropathy) who underwent 24 h noninvasive ambulatory blood pressure monitoring and M-mode echocardiographic recording. The two groups were comparable for age, sex, duration of diabetes, body mass index, and metabolic control. There were no significant differences in 24 h average and diurnal values of systolic, diastolic, or mean blood pressure. The percent changes from day to night of systolic, diastolic, and mean blood pressures were significantly lower in diabetics with neuropathy than in those without (P < .04 or less). Increased left ventricular mass index (LVMI) (135.4 +/- 10.2 v 102.9 +/- 6.3; P < .005), septal wall thickness, and posterior wall width were observed in neuropathic patients. Fractional shortening, peak velocity of early left ventricular filling (E), peak velocity of late ventricular filling (A), and their ratio (E/A) were similar in the two groups. The increased LVMI we observed may represent a possible link between diabetic autonomic neuropathy, nocturnal blood pressure levels, and higher cardiovascular mortality rate.

Adult↗
PubMed1993

Abnormal agonist-stimulated cardiac parasympathetic acetylcholine release in streptozocin-induced diabetes.

We examined the effect of three distinct depolarizing conditions on [3H]ACh release from cardiac postganglionic parasympathetic neurons in age-matched controls and insulin-treated STZ-induced diabetic rats to determine whether alterations in neurotransmitter release were present in the diabetic group. The effect of TTX, which exerts a use- and voltage-dependent block of sodium channels, was examined on the release of ACh stimulated by SRIF14 (preferentially acts at the cell body). We also studied the effect of STZ-induced diabetes on [3H]ACh release by the relatively site-specific depolarizing agent VT (preferentially acts at the axon) and high potassium (non-site-specific). Basal, SRIF14-(10(-7) M), VT-(10(-4) M), and K+ (100 mM)-stimulated [3H]ACh release was similar in control and STZ-induced diabetic animals. However, in STZ-induced diabetic but not control rats, SRIF14-induced [3H]ACh release was resistant to TTX (2 x 10(-7) M). In addition, the response to submaximal K+ (25 mM) stimulation was greater in STZ-induced diabetic compared with control animals. Treatment with insulin corrected these abnormalities. These data indicate that in the acute STZ-induced diabetic rat, SRIF14-, VT-, and high K(+)-evoked release of ACH is not impaired, which suggests that the mechanisms associated with ACh storage and release in postganglionic cardiac parasympathetic neurons are not affected in this model.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1993

Relationship between the circadian rhythms of blood pressure and sympathovagal balance in diabetic autonomic neuropathy.

In diabetic autonomic neuropathy, abnormal circadian patterns of blood pressure and sympathovagal balance with reduced fall of blood pressure and prevalence of sympathetic activity during the night have been described. To correlate the abnormalities of blood pressure to those of sympathovagal balance, we simultaneously performed 24-h noninvasive monitoring of blood pressure and ECG in 25 diabetic patients (45.6 +/- 13.6 yr of age with a 17.6 +/- 9.1 yr duration of diabetes) with various degrees of cardiovascular reflex impairment. Autoregressive power spectrum analysis of RR interval variability was applied to 24-h ECG recordings to obtain for day and night periods the mean power of low- (0.03-0.15 Hz) and high-frequency (0.18-0.40 Hz) components, which are relative markers of sympathetic and vagal activity, respectively, and their ratio (low frequency/high frequency), assumed as index of sympathovagal balance. Diabetic patients showed a lower percentage of day-night change in systolic blood pressure (9 +/- 5.48 vs. 11.6 +/- 4.78%, P < 0.037), a lower day low frequency (5.9 +/- 0.81 vs. 6.62 +/- 0.73 In-ms2, P < 0.001), a lower night high frequency (6.06 +/- 0.71 vs. 6.52 +/- 0.85 In-ms2, P < 0.05), a lower day low frequency:high frequency ratio (1.82 +/- 1.77 vs. 3.05 +/- 1.82, P < 0.01), and a lower percentage of day-night change in low-frequency:high frequency ratio (-13.4 +/- 109.9 vs. 28.7 +/- 29.7%, P < 0.05), when compared with control subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Carbohydrate metabolism in hypertension: influence of treatment.

Epidemiologic studies suggest a close association between hypertension, obesity, and diabetes. It has been demonstrated that essential hypertension, per se, is an insulin-resistant state. However, the pathogenesis of the association between insulin resistance and hypertension is poorly understood. Elevated plasma insulin levels may contribute to the development of hypertension through renal sodium reabsorption, the sympathetic nervous system, the transmembranous cation transport, the renin-angiotensin system, the cardiovascular reactivity, and the atrial natriuretic peptide. Diuretics, beta-blockers, calcium antagonists, angiotensin-converting enzyme (ACE) inhibitors, and alpha 1-antagonists are first-choice drugs in the management of hypertension. Diuretics, except indapamide, impair insulin sensitivity and glucose tolerance. The same negative effects, exerted by beta-blockers, are reduced employing those with selective activity. With few exceptions, calcium antagonists have no adverse influence on carbohydrate metabolism. ACE inhibitors and alpha 1-antagonists do not influence or even improve glucose metabolism.

Adrenergic beta-Antagonists↗
PubMed1991

Regression of microalbuminuria in type II diabetic, hypertensive patients after long-term indapamide treatment.

The influence of hypertension on the progression of persistent microalbuminuria in type II diabetes has not yet been clarified. We have studied the effects of 36 months of indapamide treatment (2.5 mg once daily) on blood pressure (BP), albumin excretion rate (AER), urinary immunoglobulin G4 (IgG4), and glomerular filtration rate (GFR) in 10 patients who were mildly hypertensive and had type II microalbuminuric diabetes (AER greater than 30 mg/24 hours and less than 300 mg/24 hours). BP, AER, and IgG4 significantly decreased after 6 months until the end of the study. Mean GFR was 94.4 +/- 7.5 ml/min/1.73 m2 in the baseline and did not change significantly throughout the course of the antihypertensive therapy. AER and IgG4 were directly related (r = 0.57; p less than 0.004), whereas BP did not relate to GFR, AER, or IgG4. The nephropathy index (45.5 +/- 4 in the baseline) significantly decreased at 12 months (38.7 +/- 2.1), 24 months (35.4 +/- 1.6), and 36 months (36.5 +/- 1.5) (at least p less than 0.01). Long-term indapamide treatment reduced BP and urinary protein loss without affecting GFR. These results indicate a potential role of this drug in the long-term renal protection of patients with type II diabetes, mild hypertension, and microalbuminuria.

Adult↗
PubMed1990

Efficacy of antihypertensive treatment with indapamide in patients with noninsulin-dependent diabetes and persistent microalbuminuria.

In patients with insulin-dependent diabetes, antihypertensive treatment has a beneficial effect on the rate of progression toward uremia of overt diabetic nephropathy (albumin excretion rate [AER] greater than 300 mg/24 hour). The influence of hypertension on the progression of "incipient" nephropathy (AER ranging between 30 and 300 mg/24 hours) is not well defined, particularly in patients with noninsulin-dependent diabetes. In this study, 21 patients with noninsulin-dependent diabetes and hypertension (11 with normoalbuminuria and 10 with microalbuminuria), who were comparable for age, duration of diabetes and hypertension, were treated with indapamide, 2.5 mg once daily, and followed up for 24 months. Blood pressure, glomerular filtration rate (GFR), albumin excretion rate and subclass 4 of urinary immunoglobulin G (IgG4) were indicated. In normoalbuminuric patients, blood pressure was significantly reduced, whereas AER, IgG4 and GFR did not show any variation throughout the study. In microalbuminuric patients, blood pressure, AER and IgG4 were significantly reduced, and GFR remained unchanged. In patients with noninsulin-dependent diabetes, antihypertensive treatment, which is begun during incipient diabetic nephropathy, may have a beneficial effect on the progression of the disease, although a long-term follow-up study is needed to confirm this.

Adult↗
PubMed1990

Autonomic neuropathy and secondary hyperparathyroidism in uremia.

To evaluate the relationship between autonomic neuropathy, and biochemical and radiological parameters of secondary hyperparathyroidism, we examined 19 predialysis and 24 hemodialysis non-diabetic uremic patients. Autonomic neuropathy was assessed using four cardiovascular tests. Ten predialysis and 15 hemodialysis patients showed abnormalities in one or more autonomic tests. Ca, Ca2+, P, alkaline phosphatase, immunoreactive parathyroid hormone and osteocalcin did not significantly differ in uremic patients with and without abnormal autonomic test results. Radiological markers of hyperparathyroidism such as acro-osteolysis (score A) and subperiosteal resorption (score B) were more common in patients with abnormalities in autonomic tests than in patients without. When predialysis and hemodialysis patients were considered separately, the correlation between score A, score B and autonomic neuropathy was confirmed only in hemodialysis patients. In conclusion, autonomic neuropathy is not related to biochemical parameters of hyperparathyroidism, while it appears correlated with radiological signs of osteodystrophy, suggesting a possible pathogenetic link between autonomic neuropathy and secondary hyperparathyroidism.

Adult↗
PubMed1990

Autonomic neuropathy and secondary hyperparathyroidism in uraemia.

To evaluate the relationship between autonomic neuropathy, and biochemical and X-ray parameters of secondary hyperparathyroidism, we examined 19 predialysis and 24 haemodialysis non-diabetic uraemic patients. Autonomic neuropathy was assessed using four tests: deep breathing, Valsalva manoeuvre, lying to standing, and postural hypotension. Serum Ca, Ca2+, P, Mg, alkaline phosphatase, iPTH, and osteocalcin were assayed. Hand X-ray was obtained to evaluate acro-osteolysis (score A) and subperiosteal resorption (score B). Ten predialysis patients (52%) and 15 haemodialysis patients (62%) showed one or more abnormal autonomic tests. Age, dialysis duration, and biochemical parameters of secondary hyperparathyroidism did not differ significantly in uraemic patients with and without abnormal autonomic tests. Furthermore, there was no significant relation between autonomic tests and iPTH or osteocalcin. Score A and score B was significantly greater in patients with abnormal tests than in patients without (P less than 0.009 and P less than 0.025). When predialysis and haemodialysis patients were considered separately the correlation between score A, score B, and autonomic neuropathy was confirmed only in haemodialysis patients. In conclusion, autonomic neuropathy does not seem to be related to the biochemical parameters of secondary hyperparathyroidism, while it appears significantly associated with the radiological signs of osteodystrophy, suggesting a possible pathogenetic linkage between autonomic neuropathy and secondary hyperparathyroidism.

Adult↗
PubMed1989

Intravenous dexamethasone and subsequent ACTH test in comparison with dexamethasone oral test in the diagnosis of Cushing's syndrome: a report of 20 cases.

Dexamethasone inhibits ACTH secretion in the pituitary corticotropic cells of normal subjects; this ability is variously affected in Cushing's syndrome. The iv infusion of dexamethasone is not time consuming, nor it is influenced by the variability of intestinal absorption or hepatic metabolism, as occurs with oral administration. Iv dexamethasone (1.5 mg/h) over 7 h and an ACTH bolus at the 6th h were administered to 17 patients with Cushing's disease, 3 patients with Cushing's syndrome (2 with adrenal adenoma, 1 with ectopic ACTH secretion) and 13 normal subjects. After 4 days the 20 patients were also given the standard oral low-dose and high-dose dexamethasone test. Two h after starting the drug infusion, cortisol concentrations were inhibited by more than 50% in each control subject. In contrast, in all but one patient they remained higher than 50% over the baseline. At the 6th heach control subject and 15 of the 17 patients with Cushing's disease showed an inhibition of plasma cortisol concentration which was greater than 50%. Inhibition was less than 50% in 2 patients with Cushing's disease and in the 3 patients with non-pituitary dependent Cushing's syndrome. The sensitivity and specificity of this test are comparable with those of the dexamethasone oral test. Although statistically significant, results obtained from ACTH bolus were not sufficiently discriminating. If studies conducted on a larger population confirm these preliminary data, the rapidity and reliability of the dexamethasone infusion test could make it an important new tool in diagnosing Cushing's syndrome.

Administration, Oral↗
PubMed1986

Pancreatic polypeptide response to a protein-rich meal in diabetic patients with and without neuropathy.

A protein-rich meal and insulin-induced hypoglycemia (ITT) are two of the most important stimuli on pancreatic polypeptide (PP) secretion in diabetic patients. Previous studies have shown a reduced PP response to ITT in diabetic patients with autonomic neuropathy (AN). Twelve patients without AN (mean age 44 +/- 10.8 yr, mean duration of diabetes 11 +/- 5.6 yr), 9 with AN (51.4 +/- 6 yr, 15.8 +/- 6.9 yr) and 9 controls (N) were studied. AN was assessed by the evaluation of the beat-to-beat variation of the heart rate during deep breathing. PP secretion was stimulated by a protein-rich meal (200 g meat, 150 g milk). All insulin-dependent diabetic (IDD) patients lacked circulating PP antibodies. All diabetic patients showed a significant reduction in the early vagal phase compared to controls. This behavior was more evident in diabetic patients with AN and the secondary phase of these two groups overlapped with the response of controls. These data may be explained by the initial alterations of vagal functions not detectable by current methods.

Adult↗
PubMed1983

Influence of glucoregulation with continuous subcutaneous insulin infusion on nerve conduction velocity and beat to beat variation in diabetics.

Limited and contrasting data are available on the relationship between metabolic control and diabetic neuropathy. In eight type I diabetics peripheral and autonomic neuropathy were studied, first in conditions of poor metabolic control and then after one and three months during which an improved control of glycemic levels had been obtained by continuous subcutaneous insulin infusion. Autonomic neuropathy was investigated by evaluating beat to beat variation during deep breathing; peripheral neuropathy by measuring maximum motor conduction velocity of peroneal and median nerves and sensory conduction velocity of median nerve. Our data showed significant improvement of motor conduction velocity in both nerves studied, whilst sensory conduction velocity did not show any significant variation. The changes observed in beat to beat variation in five subjects with initially abnormal scores might reflect an improvement in autonomic nervous function, even if long-term studies are needed.

Adult↗
PubMed1981

Exaggerated glucagon secretion in diabetic and non-diabetic subjects with surgical porto-caval anastomosis.

Pancreatic glucagon (IRG) levels in the postabsorptive (fasting) state and in response to arginine test (ATT), have been investigated in 17 subjects with porto-caval anastomosis (PCA). Out of these, seven subjects were insulin-treated diabetics, 5 were untreated diabetics, and 5 had no evidence of clinical diabetes. Basal and stimulated IRG values in the overall group of PCA subjects were significantly increased in comparison to 14 normal controls. No significant difference was found between the three groups of patients in respect to IRG values. The mean fasting IRG levels, grouped in relation to the age of shunt, were significantly raised six months after surgery. In addition no significant difference in IRG values (fasting or stimulated) was observed in relation to the entity of the liver disease (child degree) or to the type of surgical shunt. Finally, when PCA patients with or without encephalopathy were considered, fasting and peak IRG values were significantly increased in those patients with encephalopathy.

Arginine↗
PubMed1980

Inhibition of allogeneic lymphocyte E-rosettes induced by sera from newly diagnosed type I diabetics.

Sera from 64 juvenile onset insulin-dependent diabetics (Type I diabetics) and 30 normal subjects were tested for their ability to inhibit sheep red blood cell rosette formation (E-rosette) by normal allogeneic lymphocytes. Inhibition of E-rosette formation by greater than 20% was found with 16 (66%) sera from newly diagnosed patients, 3 (16%) sera from patients with duration of disease between 2 and 12 months and with 4 (18%) sera from diabetics with duration of disease between 1 and 7 years. On the other hand, only 2 (6%) control sera showed inhibitory effect. No relationship between E-rosette inhibition and islet-cell antibodies presence, anti-lymphocyte antibodies occurrence, anti-HLA activity, blood glucose levels, respectively, was found. Investigation of the properties of this inhibitory factor suggests that it is different from other substances that reportedly inhibit E-rosette formation.

Adolescent↗
PubMed1978

Glucagon and growth hormone secretion in insulin-treated diabetics: effects of added sulfonylureas.

Eleven insulin-dependent ketosis-prone diabetics were given glibenclamide (5 mg/day) in addition to their usual insulin treatment for a period of 1 or 6 mo. There was significant reduction in arginine-induced IRG and hGH secretion and no change in blood glucose levels after either 1 or 6 mo of treatment. During that time no change in weight or insulin requirement was observed. The importance of the duration of treatment and the fact that in this type of patient the effects on IRG and hGH secretion could not be mediated by the influence on insulin secretion are stressed.

Adult↗