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Biomedical subjects

K Engels

Publications and source records attributed to K Engels.

17 recordsLinked to original sources
PubMed1995

[Immunohistochemical detection of epidermal growth factor receptor (EGF-R) in paraffin sections of breast carcinoma tissue: correlation and clinical significance].

Analyses of the level of expression of the epidermal growth factor receptor (EGF-R) of breast cancer tumours may add independent information about the prognosis for individual patients. Furthermore, the use of monoclonal antibodies directed against EGF-R as therapeutic tools (e.g., Mab 425) requires a reliable evaluation of the individual EGF-R content. Various analytical methods have been published, including (1) biochemical detectonn of EGF-R by a radiolabelled physiological ligand, (125I)EGF, (2) enzymatic analyses of EGF-R content (IEMA), (3) immunological analyses of EGF-R content with a monoclonal antibody (ELISA), and (4) immunohistochemical EGF-R detection. Studies with immunohistochemical analyses of EGF-R overexpression in formalin-fixed, paraffin-embedded tumour samples are rare. In a retrospective study, we examined the clinical data from 142 patients and the EGF-R expression in their formalin-fixed, paraffin-embedded tumour samples. The average follow-up was 69 months. EGF-R expression was compared to oestrogen (ER) and progesterone (PgR) receptor expression, histological grade, tumour size, lymph node metastases and menopause. 52 of 142 tumours were EGF-R positive. EGF-R overexpression correlated with high tumour grade, large tumours and elevated numbers of lymph node metastases. There was no significant correlation between ER or PgR and EGF-R expression. Determination of EGF-R overexpression revealed no significant difference in disease-free interval (DFI) or overall survival (OS). In this study, the determination of EGF-R in formalin-fixed, paraffin-embedded tumour samples proved feasible. Unfortunately, this did not add any additional information concerning DFI or OS.

Adult↗
PubMed1995

Renal effects of acute amino acid infusion in hypertension induced by chronic nitric oxide blockade.

L-Arginine is the physiological substrate of nitric oxide, a vasodilator that controls blood pressure and renal hemodynamics in the basal state. In the present studies, we produced chronic nitric oxide blockade by oral administration of the L-arginine analogue NG-nitro-L-arginine methyl ester, which produced sustained hypertension and increased renal vascular resistance in conscious rats. Acute excess L-arginine had little effect on blood pressure but completely normalized renal vascular resistance and increased renal plasma flow in chronically nitric oxide-blocked hypertensive rats. In contrast to L-arginine, D-arginine had no renal hemodynamic effects in either normal or chronically nitric oxide-blocked rats. Acutely administered glycine was ineffective in vasodilating the chronically nitric oxide-blocked rat kidney, in a dose that produced renal vasodilation in normal rats. These findings indicate the following: (1) Hypertension induced by chronic nitric oxide blockade due to substituted L-arginine analogue cannot be acutely reversed with excess L-arginine, suggesting that the maintenance of the hypertension is not solely caused by competitive inhibition of nitric oxide production; (2) in contrast, the kidney remains responsive to L-arginine whereas the renal vasodilator response to glycine is abolished in this model of hypertension.

Animals↗
PubMed1995

Blood pressure (BP) and renal vasoconstrictor responses to acute blockade of nitric oxide: persistence of renal vasoconstriction despite normalization of BP with either verapamil or sodium nitroprusside.

We have previously reported that acute systemic nitric oxide (NO) blockade in the conscious rat leads to increases in blood pressure and a profound renal vasoconstriction. In the present studies, we investigated the effect on renal vascular resistance of normalization of blood pressure (BP) during acute, i.v. NO blockade with nitro-L-arginine methyl ester (NAME). We found that two separate pharmacologic maneuvers which normalized BP after a transient period of hypertension, namely the NO donor sodium nitroprusside (SNP) or the calcium entry blocker verapamil (VER), did not reverse the increased renal vascular resistance (RVR) produced by acute NAME. In further studies, we prevented the transient increase in BP with the same combination of NAME and VER but with simultaneous administration of the drugs and in this situation, where the kidney was never exposed to a transient rise in renal perfusion pressure, RVR was unchanged compared to control. When we used angiotensin II (AII) as an alternative method of producing acute increases in BP and RVR, we found that VER reversed both the hypertension and the renal vasoconstriction, despite exposure of the kidney to a transient increase in BP. These data suggest that acute, transient exposure of the kidney to an increased BP during NO inhibition produces a sustained increase in RVR that is not reversible with either SNP or VER. The urinary data suggest that the combination of NAME and VER have a synergistic effection the renal tubule to produce a massive natriuretic and diuretic response.

Angiotensin II↗
PubMed1994

Acute nitric oxide blockade amplifies the renal vasoconstrictor actions of angiotension II.

The tone in the renal vasculature is determined by the balance between vasoconstrictor and vasodilator agents. In this study, the effect on renal function was investigated when the acute blockade of the endogenous nitric oxide system was superimposed on a state of high circulating angiotensin II. Studies were conducted in the conscious, unstressed rat measuring renal function before and during acute systemic nitric oxide blockade with nitro-L-arginine methyl ester and with or without concomitant angiotensin II infusion. Nitric oxide blockade alone, in the presence of normal, unstimulated levels of endogenous angiotensin II, caused a large rise in blood pressure and a doubling of renal vascular resistance. The infusion of angiotensin II alone produced a mild rise in systemic blood pressure and a small (30%) rise in renal vascular resistance. When nitric oxide blockade was combined with angiotensin II infusion, the rise in blood pressure was similar to that produced by nitric oxide blockade alone but the increase in renal vascular resistance was much greater (350%), leading to marked declines in renal function. These studies demonstrate that when angiotensin II levels are acutely elevated and are controlling renal vascular tone, nitric oxide is essential for the maintenance of adequate renal perfusion and function.

Angiotensin II↗
PubMed1991

Piracetam in elderly motorists.

101 elderly motorists with reduced reaction capacity were examined under real traffic conditions with regard to their driving ability. They were given a daily dose of 4.8 g piracetam or placebo over a six-week period in a randomised double-blind study. The percentage of correctly solved sign-observance items, which reflects orientation and perception in real traffic conditions, increased in the placebo-treated test-group from 79.86% in the pretest to 80.07% in the retest, whereas the test subjects of the piracetam-treated group improved their performance from 77.08% to 84.16%. After being treated with piracetam for 6 weeks, the drivers showed a significantly better performance than the placebo-group. Of particular interest is the finding that the test-subjects who had scored less than 80% in the pretest improved without exception in the retest after treatment with piracetam.

Aged↗
PubMed1991

Short term natriuretic responses in the conscious Zucker obese rat.

Renal clearance studies were conducted in conscious, chronically catheterized obese and lean Zucker rats to investigate the natriuretic responses to i) acute IV infusion of isotonic NaCl = 5% of total body weight and ii) IV infusion of alpha rat atrial natriuretic peptide (ANP) in a dose of 300 ng/kg/min. In the baseline state, arterial blood pressure (BP) was significantly higher in obese vs lean rats. Absolute values of GFR and sodium excretion were similar but lower in obese vs lean rats when factored for body weight. In the 2 h period during and after NaCl infusion, obese rats showed a greater natriuresis vs lean while BP rose significantly and similarly. ANP infusion was natriuretic in obese rats but had no effect on lean rats. ANP lowered BP in both groups but BP remained higher in obese vs lean rats at all times. These studies show that in the chronic, unstressed preparation the 6-8 month old, female Zucker obese rat has a higher BP vs the 6-8 month old lean Zucker. The short term natriuretic response to either a NaCl load or ANP infusion is greater in obese vs lean Zuckers and the depressor response to ANP is intact in obese Zuckers. Thus the higher BP in this model of obesity is unlikely to be due to either a defective response to ANP or to a defect in the renal response to acute sodium challenge.

Animals↗
PubMed1990

Renal effects of moderate hemorrhage in the conscious pregnant rat.

Studies were performed in conscious, chronically catheterized virgin, 8- to 9-day-pregnant, and 15- to 16-day-pregnant Sprague-Dawley rats in baseline state and after removal of 7.5% total blood volume. Measurements were made of glomerular filtration rate (GFR), renal plasma flow (RPF), renal vascular resistance (RVR), arterial blood pressure (AP), and urinary electrolyte excretion. In baseline state, GFR and RPF were elevated at days 8-9 and days 15-16 of pregnancy (vs. virgins) due to a gestational renal vasodilation. The fall in hematocrit indicates substantial plasma volume expansion by days 15-16 of pregnancy. After removal of 7.5% total blood volume, little change occurred in AP in any group. However, the renal vasculature provided a sensitive response to moderate hemorrhage, since RPF fell and RVR increased similarly in virgin, 8- to 9-day- and 15- to 16-day-pregnant rats. GFR was protected in virgin and 8- to 9-day-pregnant rats but fell significantly in late pregnancy. Urinary electrolyte excretion tended to fall but was not significantly reduced by hemorrhage in any group. These studies indicate that renal vascular response to moderate hemorrhage is similar in virgin, early, and late pregnancy. Thus effector mechanisms that sense volume and regulate RVR must be continually reset to respond to progressive plasma volume expansion of pregnancy as normal.

Animals↗
PubMed1990

Endothelial derived relaxing factor controls renal hemodynamics in the normal rat kidney.

These studies were conducted in the conscious, chronically catheterized rat to determine whether the endothelial derived relaxing factor (EDRF) controls renal function in the normal state. Administration of the EDRF synthesis inhibitors N-monomethyl-L-arginine (NMA; 100 mg/kg body weight) or N-nitro-L-arginine methylester (NAME; 10 mg/kg body wt) led to a large, sustained rise in blood pressure, a large rise in renal vascular resistance, a fall in renal plasma flow, a relatively slight reduction in glomerular filtration rate, and a consequent rise in filtration fraction. In addition, a marked natriuresis occurred because of a reduction in the fractional reabsorption of sodium. In separate studies, a continuous infusion of excess L-arginine (300 mg/kg body wt bolus followed by 50 mg/kg body wt per min) attenuated the NMA- or NAME-induced rise in blood pressure and reversed the renal hemodynamic effects such that a significant rise in renal plasma flow was seen. L-Arginine alone produced a selective renal vasodilation and large increases in sodium excretion. These observations support earlier suggestions that tonic release of EDRF controls the basal blood pressure and also show that renal function in the normal unstressed rat is markedly influenced by EDRF. These studies suggest that, in addition to controlling renal plasma flow, EDRF may have other, complex actions at the glomerulus. The natriuresis seen after acute inhibition of EDRF with NMA or NAME was probably the result of a pressure natriuretic response to the abrupt rise in blood pressure and also, perhaps, reflects removal of an EDRF influence to directly enhance sodium reabsorption somewhere in the nephron.

Animals↗
PubMed1990

[Anesthesiologic implications in the Shy-Drager syndrome--a case report].

Based on a case report with vaginal hysterectomy, the anaesthetic implications are discussed in a patient with Shy-Drager syndrome, which is a degenerative disease in middle-aged to elderly patients, resulting in autonomic dysfunction. The syndrome is reviewed and the anaesthetic management is described. Adequate cardiovascular monitoring and maintenance of haemodynamic stability are important. The response to sympathomimetic drugs is unpredictable and may be extreme due to denervation hypersensitivity. In the postoperative period, signs of postural hypotension may be severe and require training by elevation of the upper part of the body, fluid therapy, sympathomimetics and fludrocortisone.

Anesthesia↗
PubMed1983

[Clinical studies on the effect of various drugs on cardiocirculatory behavior during the induction phase of intubation anesthesia].

In a randomized study on 150 patients (ASA 1) undergoing induction of anaesthesia, the effects of Fentanyl (0.1 mg), the combination of Fentanyl (0.1 mg) and Droperidol (5 mg) (Innovar, Thalamonal) and Atropine (0.01 mg/kg b.w.) alone on cardiocirculatory parameters were studied. Induction and intubation were carried out with Thiopentone and Succinylcholine. All patients were aged between 18 and 50 years. In addition to continuous ECG recording of standard leads I-III, blood pressure measurements (Riva-Rocci), capillary blood gases and serum potassium were estimated at regular intervals. Prior to intubation Atropine caused arrhythmias in 10% and during intubation in 40%, half of which occurred repeatedly. In comparison, the control group showed arrhythmias in only 28% at intubation time. The median value of the rate pressure products rose before intubation time to levels of almost 20,000 units whereas the control group reached the same high product only during intubation. Cardiac rhythm proved most stable using Fentanyl, the systolic, diastolic and mean blood pressure changes were significantly lower than in those groups without an additional analgesic. With Fentanyl and Atropine the increase of all haemodynamic parameters was less pronounced than in the control group given Atropine only. Comparison of the Fentanyl groups showed only a significantly lower arterial mean pressure when Atropine was given, the other parameters were similar. Using Innovar alone, 4 cases of severe and 1 of mild rhythm disturbances appeared, while with Innovar plus Atropine only 2 cases of mild and 1 of repeated extrasystoles occurred. In the Atropine-free groups, the addition of Innovar only caused a lesser increase in the heart rate, while the remaining parameters did not differ.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1982

[Reaction time].

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Automobile Driving↗
PubMed1980

[Driving behavior of cardiovascular patients as affected by beta receptor blockers].

18 male patients under betablocker therapy adapted to their individual stage of hypersympathicotonic circulatory regulation disturbances were tested in a motor-vehicle simulator to find out possible changes of their driving ability. Besides observing driving-style and reactions, the following parameters were controlled: blood pressure, time of pulse waves, heart rate. Speeds of deviation angles (= deviation from straight line per time unit) decreased significantly. No differences between tests under betablocker medication and without it could be demonstrated, neither in simple-reaction times nor in the more complex multiple-reaction times, which can be compared with realistic traffic situations. Blood pressure and heart rate showed more significant decreases after medication than in tests without previous betablocker treatment. The results prove that the betablocking agent Bupranolol does not influence the ability of car-driving, not even in case of semichronical application.

Attention↗