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Biomedical subjects

K D Palitzsch

Publications and source records attributed to K D Palitzsch.

At least 55 records · Page 3Linked to original sources
PubMed1996

Atrial natriuretic factor and digoxin-like immunoreactive factor in diabetic patients: their interrelation and the influence of the autonomic nervous system.

In diabetic patients, several factors contribute to volume expansion and have to be counteracted by humoral and neuronal feedback control systems. We investigated N-terminal proatrial natriuretic factor (ANF1-98) and digoxin-like immunoreactive factor (DLIF), which are two counteracting hormones, and their interrelationship, with additional consideration given to autonomic nervous function in diabetic patients. ANF1-98 and DLIF were measured in 64 diabetic patients. Autonomic nervous function was assessed using nine autonomic nervous function tests. The patients were subdivided into two groups, one with four or more (group 1) and one with less than four abnormal results in autonomic function tests (group 2). Compared with group 2, group 1 demonstrated detectable DLIF levels less often (17.2 vs. 45.7, P = 0.0195) and increased levels of ANF1-98 (mean +/- SEM: 850.0 +/- 108.8 vs. 554.8 +/- 45.9 pmol/L, P = 0.0099). However, the groups did not differ in blood pressure, daily sodium, and daily potassium excretion. The number of abnormal autonomic function tests correlated significantly with ANF1-98 (P = 0.0002). In patients with detectable DLIF, DLIF correlated with ANF1-98 (P = 0.0080). These results demonstrate close interactions between the autonomic nervous system and the two natriuretic hormones. In patients with autonomic nervous dysfunction, higher levels of ANF may possibly compensate for the lack of the natriuretic DLIF to counteract hypertension and chronic volume expansion.

Adult↗
PubMed1996

Impact of disease duration on cardiovascular and pupillary autonomic nervous function in IDDM and NIDDM patients.

OBJECTIVE: To determine the age-independent impact of disease duration on autonomic nervous function in diabetic patients and to compare it with other disease-related complications. RESEARCH DESIGN AND METHODS: Of the patients with diabetes, 166 (66 IDDM, 100 NIDDM) were investigated using standardized cardiovascular and pupillary test procedures, which provide 10 age-independent percentile values for each patient. Sensorimotor neuropathy was assessed using a standardized clinical examination, retinopathy by fundoscopy, and nephropathy using daily urinary protein excretion and creatinine clearance. RESULTS: The duration of the disease did not correlate with the results of any one of six standard cardiovascular tests (P > 0.15). Pupillary parameters showed a weak negative correlation with disease duration (P < 0.04). Prevalence of cardiovascular autonomic dysfunction was not different in five different subgroups subdivided according to disease duration (0-6, 7-12, 13-18, 19-24, and > or = 25 years), whereas prevalence of pupillary dysfunction changed significantly with disease duration (P = 0.016). In contrast, the prevalence of sensorimotor neuropathy (P = 0.006), retinopathy (P < 0.001), and proteinuria (P = 0.010) was significantly higher in patients with long-standing disease. Disease duration was not significantly different in patients without overall cardiovascular dysfunction, as compared with patients with dysfunction (15.6 +/- 1.0 vs. 16.5 +/- 1.5 years, P = 0.626). This was also found when considering overall pupillary dysfunction (14.5 +/- 1.4 vs. 17.2 +/- 1.0 years, P = 0.125). CONCLUSIONS: Disease duration was not correlated with cardiovascular autonomic nervous function, whereas a correlation was observed with pupillary autonomic nervous function, sensorimotor neuropathy, retinopathy, and proteinuria. This may indicate that cardiovascular autonomic nervous function does not markedly change during the course of the disease. The question arises whether cardiovascular autonomic neuropathy may be more a functional abnormality than a structural lesion of the autonomic nervous system, which may be already present at the beginning, or even before, the manifestation of diabetes.

Adolescent↗
PubMed1995

Leucocyte-endothelial cell adhesion in a model of intestinal inflammation.

Leucocyte-endothelial cell adhesion is modulated by a variety of adhesion glycoprotein expressed on the surface of leucocytes and endothelial cells. Although in vitro studies show that these adhesion molecules mediate the decrease in leucocyte rolling velocity and the increase in leucocyte adherence and emigration associated with inflammation, there are few in vivo data to support this hypothesis. The aim of this study was to assess the role of leucocyte (CD11b/CD18) and endothelial cell (P- and E-selectin) adhesion molecules in mediating the leucocyte-endothelial cell adhesion elicited in rat mesenteric venules during a model of longlasting intestinal inflammation. Indomethacin was injected 48 and 24 hours before the experiment. The mesenteric microcirculation was observed by intravital microscopy in animals treated with monoclonal antibodies (MAb) directed against either P-selectin, E-selectin, or CD11b/CD18. Leucocyte rolling velocity, and the number of adherent and emigrated leucocytes as well as vessel diameter and erythrocyte velocity were monitored in roughly 30 micron diameter postcapillary venules. Indomethacin treatment resulted in mucosal ulceration and granulocyte infiltration, and a corresponding inflammatory response in the mesentery, which was characterised by an increase in the number of adherent (eightfold) and emigrated (sixfold) leucocytes and a reduction (80%) in leucocyte rolling velocity. The indomethacin induced leucocyte-endothelial cell adhesion in mesenteric venules was significantly reduced by treatment with MAbs against either CD11b/CD18 or E-selectin, but not by the P-selectin MAb. These results suggest that both leukocyte (CD11b/CD18) and endothelial cell (E-selectin) adhesion molecules contribute to the granulocyte accumulation in a chronic model of intestinal inflammation.

Animals↗
PubMed1995

Lung damage aggravates gastric mucosal lesions induced by ethanol in the rat.

The hypothesis that severe lung damage generated by acid aspiration or a 50-hour exposure to 100% oxygen aggravates ethanol-induced hemorrhagic mucosal lesions in the stomach was examined in the rat. Animals were either given intratracheally with pyrogen-free saline or HCl (pH 1.75) or exposed for 50 h to 100% oxygen before the intragastric application of 1 ml of 50 or 75% ethanol. All rats receiving 50% ethanol were also given 3% monastral blue, 3 min before ethanol administration as a vascular tracer. Lung acid damage and inflammation as assessed by bronchopulmonary lavage were severe. We observed a significant increase in extracellular lactate dehydrogenase beta-glucosaminidase, albumin and the number of polymorphonuclear leukocytes in the lavage fluid. The number of resident macrophages decreased significantly. Blood gas analysis was not influenced. Hemorrhagic gastric mucosal lesions after 50 or 75% ethanol increased from 4.4 or 8.2% to 9.8 or 13.1% after HCl and from 6.7 or 18.2% to 10.6 or 21.6% of the glandular stomach following oxygen exposure. The area of mucosal vascular damage caused by 50% ethanol as revealed by monastral blue labelling was 3.3 and 2.6 times larger in rats with lung damage induced by HCl or hyperoxia, respectively. Thus, severe lung damage predisposes to microvascular damage and aggravates chemically induced hemorrhagic mucosal lesions.

Animals↗
PubMed1995

Effect of histamine on haemorrhagic mucosal lesions is related to vascular permeability in rats: studies with histamine, H1-, H2- and H3-agonists and bradykinin.

OBJECTIVE: To test the hypothesis that an early increase in vascular permeability is correlated with later gastric mucosal protection in the rat. METHODS: Histamine, its agonists (H1, H2, H3) and bradykinin, were either given subcutaneously or intragastrically before the intragastric administration of ethanol. The extravasation of intravenously injected 99mTc-glucoheptonate into the gastric wall and into the gastric contents was used as an indicator of increased permeability. Gastric haemorrhagic lesions where measured by computerized planimetry and ethanol absorption was determined by an ACA Clinical Analyzer. RESULTS: Histamine and bradykinin increased vascular permeability in the glandular stomach and provided significant gastroprotection, similar to H1-, H2- and H3-agonists, against ethanol-induced gastric haemorrhagic lesions. This gastroprotection was accompanied by low blood levels of ethanol, probably indicating decreased ethanol absorption and the creation of a histodilutional barrier in the stomach by histamine. CONCLUSIONS: These data indicate that an increase in vascular permeability dissipates the concentration, and may delay the absorption, of ethanol in gastric mucosa by creating a perivascular histodilutional barrier. Vascular injury, which is an early pathogenetic factor in the development of ethanol-induced gastric haemorrhagic erosions, may thus be prevented.

Absorption↗
PubMed1994

Valid parameters for investigation of the pupillary light reflex in normal and diabetic subjects shown by factor analysis and partial correlation.

Pupillary test data of 103 normal and 119 diabetic subjects (47 IDDM, 72 NIDDM) were evaluated by factor analysis. From a total of nine pupillary parameters three factors were extracted in the analysis. Factor 1 represents maximal pupillary area, contraction velocity at 1 s, dilation velocity at 6 s and minimal pupillary area--static and simple dynamic parameters; factor 2 amplitude of pupillary unrest, area under the detrended curve of pupillary unrest and period of pupillary unrest--parameters of pupillary unrest; factor 3 fusion frequency of pupillary response following flicker stimuli and latency time of pupillary light reflex--second order dynamic parameters. Factor analysis was then applied to investigate diabetic patients with a high percentage of autonomic neuropathic participants (about 39% had pupillary and about 35% had cardiorespiratory function disorders), which revealed the same three factors as those identified in normal subjects. Furthermore, an age-related database of parameters of pupillary unrest is given. It demonstrates that normal subjects and diabetic patients did not differ in the period of pupillary unrest (normal vs diabetic (mean +/- SEM): 1550 +/- 29 vs 1536 +/- 27 ms; 2p > 0.5). The difference in amplitude (47.8 +/- 2.8 vs 41.0 +/- 2.6% percentile; 2p = 0.071) and area under the detrended curve of pupillary unrest (47.9 +/- 2.8 vs 40.8 +/- 2.6% percentile, 2p = 0.062) seems to show a trend but was not significant. In conclusion, factor analysis revealed three different pupillary test factors.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1994

Metronidazole inhibits leukocyte-endothelial cell adhesion in rat mesenteric venules.

BACKGROUND/AIMS: The beneficial effects of metronidazole in intestinal inflammation are generally attributed to the drug's antimicrobial actions. The objective of this study was to determine whether metronidazole exerts an anti-inflammatory action by inhibiting leukocyte-endothelial cell adhesion in postcapillary venules. METHODS: Short-term (leukotriene B4 superfusion) and long-term (subcutaneous indomethacin injections) inflammatory responses were elicited in rat mesentery). The number of adherent and emigrated leukocytes, leukocyte rolling velocity, erythrocyte velocity, blood flow, and shear rate were monitored in normal and inflamed postcapillary venules. RESULTS: Eightfold and 2.7-fold increases in leukocyte adherence and comparable increments in leukocyte emigration were observed 48 hours and 14 days after indomethacin treatment, respectively. Metronidazole, but not its vehicle (methylcellulose), reversed the leukocyte adherence and emigration responses elicited by indomethacin. The antibiotic was equally effective in preventing the reduction in leukocyte rolling velocity and increased leukocyte adherence/emigration elicited by acutely exposing venules to leukotriene B4. CONCLUSIONS: These results indicate that some of the beneficial effects of metronidazole in intestinal inflammation may be related to its influence on leukocyte-endothelial cell adhesion.

Animals↗
PubMed1994

Influence of digoxin-like immunoreactive factor on late complications in patients with diabetes mellitus.

The aim of this study was to compare the intensity of typical late complications in diabetic patients (n = 65, 28 type I, 37 type II) who were not on glycoside drugs with low vs. high serum levels of digoxin-like immunoreactive factor (DLIF: group I, n = 42, DLIF < or = the detection limit of 0.2 ng ml-1; and group II, n = 23, mean +/- SEM: 1.17 +/- 0.31 [0.25-4.96] ng ml-1). For detection of nephropathy, urinary albumin excretion (24 h) and creatinine clearance tests were used. For coronary heart disease a questionnaire and standard ECG; for peripheral occlusive vascular disease a questionnaire; for eye disease a fundoscopy; for neuropathy a neurological score system; and for autonomic neuropathy a standardized test battery was employed. Patients with high DLIF levels showed better test results in vibratory perception (95.7 +/- 1.5 vs. 82.8 +/- 3.8%, normal finding = 100%, 2p = 0.016), had better percentile localizations concerning maximal pupillary area in darkness (28.4 +/- 6.6 vs. 8.1 +/- 1.8%, 2p = 0.0004), contraction velocity at 1 s (21.5 +/- 5.8 vs. 8.0 +/- 2.2%, 2p = 0.012), and dilation velocity at 6 s (23.0 +/- 6.8 vs. 10.5 +/- 2.5%, 2p = 0.041), had less retinopathy (with retinopathy: 26.1% vs. 64.3%, 2p = 0.0028), and better percentile localizations in the respiratory sinus arrhythmia test (68.4 +/- 7.3 vs. 44.1 +/- 4.9%, 2p = 0.0064). There was no difference concerning nephropathy, blood pressure, coronary heart disease and peripheral vascular disease. Separate analysis according to the type of diabetes confirmed the results in each group.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1994

The role of drug treatment in variceal bleeding.

Pharmacological management of acute variceal hemorrhage appears to be effective in patients with liver cirrhosis. Somatostatin and presumably its longer-acting analog, octreotide, are more efficient and safer than other vasoconstrictors like vasopressin, terlipressin or their combination with nitroglycerin. Drug treatment, however, usually represents only a valuable adjunct to other measures to stop bleeding such as endoscopic variceal sclerotherapy. Prophylaxis of first bleeding by beta-blockade appears justified in patients at a high risk of bleeding which still has to be defined more precisely. Prevention of recurrent hemorrhage can be effective in some but not in all of the patients with liver cirrhosis and a first bleeding episode. Treatment of patients with good liver function under direct control of the wedged hepatic vein pressure gradient presumably will reduce the failure rate of prophylaxis with beta-blockade.

Esophageal and Gastric Varices↗
PubMed1994

Impact of obesity on neuropathic late complications in NIDDM.

OBJECTIVE: This cross-sectional study was aimed to investigate the isolated influence of obesity on peripheral sensorimotor and autonomic neuropathy in patients with long-term non-insulin-dependent diabetes mellitus (NIDDM). RESEARCH DESIGN AND METHODS: Ninety-one long-term NIDDM patients with a mean duration of 13.6 +/- 1.0 years and a mean age of 60.4 +/- 1.0 years were divided into two groups according to their body mass index (BMI) (lean with a BMI < 26.5: n = 41, age = 58.6 +/- 1.7 years, BMI = 23.7 +/- 0.3 kg/m2; and obese with a BMI > or = 26.5: n = 50, age = 61.9 +/- 1.2 years, BMI = 30.5 +/- 0.5 kg/m2). The two groups were not different in age, duration, gender, current parameters of glycemic control, number of smokers, cholesterol, triglycerides, and systolic and diastolic blood pressure. Neuropathic late complications were scrutinized by a standardized clinical examination that delivers a neuropathy score, pupillary autonomic neuropathy assessed by pupillometry, and cardiovascular autonomic neuropathy using a standardized test battery. RESULTS: One-way analysis of variance revealed that obese patients had poor results in the clinical neuropathy test (overall score in obese vs. lean: 71.1 +/- 2.9 vs. 80.6 +/- 3.0 points, 2P = 0.0266; 100 points were absolutely normal). This was particularly true for the discrimination perception (obese vs. lean: 67.0 +/- 4.0 vs. 81.7 +/- 3.3 points, 2P = 0.0073) and the reflex status (obese vs. lean: 57.4 +/- 4.0 vs. 71.8 +/- 4.3 points, 2P = 0.0164). Furthermore, obese patients had a poor result in the respiratory sinus arrhythmia (RSA) test, one of six autonomic function tests (RSA: obese vs. lean in average RSA percentile: 36.9 +/- 4.9 vs. 54.0 +/- 5.9%, 2P = 0.0264). CONCLUSIONS: Obesity influences sensorimotor and autonomic neuropathic late complications. The poor result in RSA in obesity may indicate an interrelation between pathogenesis of obesity and disorders of the respiratory and heart rhythm-generating control centers in the brain stem. Moreover, it could be due to intrathoracic fat deposits that alter lung mobility. Body mass control may be an important approach to reduce neuropathic complications. Beyond that, it seems necessary to control for body mass when comparing neuropathy in two groups of patients with NIDDM.

Adult↗
PubMed1994

Effect of 1-year treatment with nitrendipine versus enalapril on urinary albumin and alpha 1-microglobulin excretion in microalbuminuric patients with type 1 diabetes mellitus. A randomized, single-blind comparative study.

In order to compare the long-term effects of nitrendipine (CAS 39562-70-4) and enalapril (CAS 75847-73-3) on variables of glomerular and tubular function in type 1 diabetes mellitus, a single-blind, randomised comparative 1-year study was carried out in microalbuminuric patients (6 women, 14 men, age, 30-58 years, duration of diabetes, 3-41 years, HbA1 sigma 5.5-10%). 10 patients were treated with 20 mg/d nitrendipine, 10 patients were treated with 10 mg/d enalapril. On the average, urinary albumin excretion was decreased by 38 +/- 4% by nitrendipine (p < 0.01 vs. before treatment) and by 21 +/- 8% by enalapril (p < 0.05 vs. before treatment). The excretion of alpha 1-microglobulin decreased by 35 +/- 10% and by 39 +/- 9%, respectively (p < 0.05 vs. before treatment). Creatine clearance rose by 20 +/- 30% during nitrendipine treatment (p < 0.05 vs. before treatment) but was unchanged during enalapril treatment. Total kidney volume decreased by 23 +/- 4% (p < 0.01) and by 14 +/- 6% (p < 0.05), respectively. Blood pressure fell by 8 +/- 1% systolic and by 13 +/- 1% (diastolic) in nitrendipine-treated patients (both p < 0.01) and by 10 +/- 1% and 13 +/- 1% in enalapril-treated patients (both p < 0.01). Thus, nitrendipine long-term treatment of microalbuminuric type 1 diabetic appeared to be as effective as the treatment with enalapril in preventing or postponing the progression of diabetic nephropathy.

Adult↗
PubMed1994

Free radicals in inflammatory bowel diseases pathophysiology and therapeutic implications.

Inflammatory bowel diseases are characterized by the accumulation of granulocytes and monocytes/macrophages at the site of inflammation. Activation of these cells leads to the release of degradative enzymes, e.g., proteinases and glycosidases, and the production of reactive oxygen metabolites. This has been shown both in animal models of experimental intestinal injury, and in human inflammatory bowel disease. Scavenging of oxygen radicals protected tissue from damage in experimental inflammation models. Human studies with specific oxygen radical scavengers are rare, preliminary results appear promising. The fact that the aminosalicylates used in the treatment of inflammatory bowel disease are potent antioxidants underscores the important role of reactive oxygen metabolites in this setting.

Aminosalicylic Acids↗
PubMed1993

[MODY diabetes].

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Chromosomes, Human, Pair 20↗
PubMed1993

[Patients with type-II diabetes mellitus and neuropathy have no deficiency of vitamins A, E, beta-carotene, B1, B2, B6, B12 and folic acid].

The present study was aimed to determine the vitamin status of vitamins A, E, beta-carotene, B1, B2, B6, B12 and folate in plasma using HPLC and vitamins B1, B2 and B6 in erythrocytes using the apoenzyme stimulation test with the Cobas-Bio analyzer in 29 elderly type II diabetic women with (G1: n = 17, age: 68.6 +/- 3.2 years) and without (G2: n = 12, age: 71.8 +/- 2.7 years) diabetic polyneuropathy. The basic parameters as age, hemoglobin A1c, fructosamine and duration of the disease did not differ in both groups. Furthermore, retinopathy was assessed with fundoscopy and nephropathy with creatinine clearance. The creatinine clearance (G1: 50.6 +/- 3.4 vs. G2: 63.6 +/- 3.7 ml/min, 2p < 0.025) and the percentage of retinopathy (G1: 76.5% vs. G2: 16.7%, 2p = 0.002) were different indicating that G1 had significantly more severe late complications than G2. Current plasma levels of all measured vitamins (A, E, beta-carotene, B1, B2, B6, B12 and folate) and the status of B1, B2 and B6 in erythrocytes did not vary between the two groups (2p > 0.1). In summary, we found a lack of association between the actual vitamin condition in plasma and erythrocytes and diabetic neuropathy.

Aged↗
PubMed1993

Rat liver injury induced by hypoxic ischemia and reperfusion: protective action by somatostatin and two derivatives.

Natural somatostatin and two synthetic derivatives (octreotide, 008) were tested for their ability to prevent hypoxic ischemic cell injury of the isolated perfused rat liver. The cyclic octapeptide octreotide is known to have endocrine and cytoprotective activities, whereas the cyclic hexapeptide 008 exerts protective actions without any endocrine effects. In isolated perfused rat livers flow rate was reduced and oxygen supply interrupted for 180 min. Then the livers were normoxically reperfused for 30 min. LDH and GLDH activity as well as Ca2+ concentration was determined in the effluent. Hypoxic ischemia led to a substantial enzyme release from the liver and to a strong Ca2+ influx. Pretreatment with somatostatin, octreotide and 008 significantly reduced LDH and GLDH release (P < 0.001). The somatostatins significantly increased the Ca(2+)-influx into the hypoxic, ischemic perfused rat liver (P < 0.001). Ca(2+)-influx is known to be an essential factor in the final common pathway of cell death induced by hypoxic ischemia. Even though the administration of the somatostatins was associated with an enhanced Ca(2+)-influx, the somatostatins reduced hypoxic ischemic liver injury.

Amino Acid Sequence↗
PubMed1993

Human atrial natriuretic peptide in patients with type 1 diabetes mellitus: is it related to the development of diabetic nephropathy?

There is controversy as to whether increased plasma levels of human atrial natriuretic peptide (hANP) in patients with type 1 diabetes mellitus may contribute to the development of diabetic nephropathy. Therefore, we decided to conduct two studies to examine the relationship of hANP levels to urinary albumin excretion and blood pressure. In a cross-sectional study, 83 randomly selected type 1 diabetic patients were investigated. 19 of the patients had increased urinary albumin excretion. 45 healthy volunteers served as controls. In a longitudinal study, 19 type 1 diabetic patients were examined for one year at monthly intervals. An increased risk of eventually developing diabetic nephropathy was identified in 7 out of these patients by repeatedly revealing increased urinary albumin excretion. On the average, hANP levels were increased in type 1 diabetic patients in comparison to controls (P < 0.001). In both studies, hANP levels were positively related (P < 0.05) to mean arterial blood pressure. There was no correlation between hANP levels and metabolic control. hANP levels lay within normal range irrespective of normal or elevated urinary albumin excretion provided that mean arterial blood pressure was normal. In the longitudinal study, increased urinary albumin and alpha-1-microglobulin excretion preceded the increase in both hANP levels and mean arterial blood pressure. Although hANP levels were evidently not related to the disease mechanisms of early diabetic nephropathy, it is tempting to speculate that hANP may contribute to the vicious circle connecting diabetic kidney disease to hypertension once that its levels are increased by elevated blood pressure.

Adolescent↗