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Biomedical subjects

K Schafferhans

Publications and source records attributed to K Schafferhans.

18 recordsLinked to original sources
PubMed1990

Atrial natriuretic peptide reverses experimental acute renal failure induced by arginine vasopressin.

Recently, it has been reported that atrial natriuretic peptide (ANP) reverses or prevents acute renal failure induced by norepinephrine in rats. Therefore, we tested the hypothesis that vasoconstrictor doses of arginine vasopressin (VP) can induce renal ischemia and that consequent renal dysfunction is reversed by ANP infusion or bolus injections in rats. Intrarenally infused VP produced a significant decrease of glomerular filtration rate (GFR) and an increase of urinary volume and sodium excretion rate. Systemic blood pressure increased significantly during VP administration. In a second experimental period, ANP was also given intrarenally, control rats received isotonic saline solution. ANP infusion revealed a highly significant increment of GFR, urinary volume and sodium excretion. Blood pressure fell down below values of the preperiod. After cessation of ANP infusion, renal function was reduced again. These results indicate that VP induces a nonoliguric acute renal failure which is reversed by ANP infusion but only at the time of its administration.

Acute Kidney Injury↗
PubMed1988

Atrial natriuretic peptide counteracts angiotensin-II-induced impairment of renal function.

The present study was designed to investigate the effect of atrial natriuretic peptide (ANP) on angiotensin II (AT II)-induced impairment of renal function. Female Sprague Dawley were used in this study. After anesthesia and surgical procedure, animals were infused with AT II at two different doses (group I, 15 micrograms/kg BW/min and group II, 15 ng/kg BW/min) into the left renal artery. Subsequently, alpha-ANP was infused intrarenally (left kidney, LK) at 2 micrograms/kg BW/min. Controls received isotonic saline only. In all cases the right and noninfused kidney (RK) served as control organ. In all animals, AT II led to a dose-dependent compromise of kidney function of the LK. Glomerular filtration rate (GFR) had decreased to 0.16 +/- 0.06 ml/min and 0.41 +/- 0.12 ml/min in group I and II, respectively. Subsequent ANP infusion induced a significant increase of GFR to 0.83 +/- 0.23 (p less than 0.01) and 0.99 +/- 0.20 (p less than 0.05) ml/min in group I and II, respectively. Urinary volume (V) exhibited a slight but not significant increase following AT II infusion. ANP infusion led to a highly significant increase of V in both groups. A less pronounced, but significant increase of absolute sodium excretion of the LK was observed in both groups after AT II infusion. Absolute potassium excretion did not change in this phase of the experiment. ANP infusion induced a significant increase in both parameters. Isotonic saline had no effect on all parameters measured. Mean arterial pressure (MAP) had increased dose dependent following AT II infusion. After ANP infusion, a significant diminution of MAP to basal values was obtained from both groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMed1986

Diminished parathyroid gland responsiveness to hypocalcemia in diabetic patients with uremia.

The parathyroid gland responsiveness to hypocalcemia induced by short-term calcium-free hemodialysis in patients with insulin-dependent diabetes mellitus was investigated in comparison with 10 nondiabetic uremic patients and compared with test results from the autonomic nervous system. Diabetic patients had lower C-terminal parathyroid hormone (cPTH) levels before hemodialysis than uremic control patients and showed a significantly smaller increase in cPTH during hypocalcemia. The neurological tests revealed severe disturbances of the autonomic functions in the diabetic group. In conclusion, the disturbances observed in the parathyroid secretory pattern are probably caused by gland dysfunction; it is hypothesized that the defective autonomic nervous system has an additional effect on the development of this hormonal dysfunction.

Adult↗
PubMed1986

Norepinephrine-induced acute renal failure: beneficial effects of atrial natriuretic factor.

The effect of the atrial natriuretic factor (ANF) on early norepinephrine-induced acute renal failure (ARF) was investigated. In anaesthetized female Sprague-Dawley rats, weighing 247 +/- 36 g, ARF of the left kidneys was induced by 40-min intrarenal arterial infusion of norepinephrine (NE; 0.75 micrograms/kg body weight). In each case the right kidney served as a control organ. Inulin clearance was used as an estimate of glomerular filtration rate (GFR). Urine volume (V), GFR and fractional excretion rates of sodium, potassium and chloride were studies in both kidneys. Immediately after NE-induced ARF one group received ANF (alpha-hANaP) and the other groups 5% glucose or isotonic saline; all infusions were administered intrarenally. In the experimental kidney NE-infusion induced anuria. ANF infusion was able to induce complete reversal of the NE effect, and GFR and diuresis improved markedly in the experimental kidney. In addition, a tremendous rise in fractional excretion rates of sodium and potassium after administration of ANF was observed. In the control kidney an additional increase of GFR and diuresis was seen. Following 5% glucose or isotonic sodium chloride infusion, no profound effects were obtained in both kidneys. The results of the present study demonstrate that ANF provides beneficial effects on the functional damage of NE-induced ARF. We conclude that the NE-antagonistic effect of ANF and the consecutive amelioration of GFR may play an important role in the recovery of impaired renal function.

Acute Kidney Injury↗
PubMed1986

Human atrial natriuretic factor prevents against norepinephrine-induced acute renal failure in the rat.

The aim of the present study was to investigate the potential protective effect of atrial natriuretic factor (ANF) on the norepinephrine (NE)-induced acute renal failure (ARF). After determination of basal renal function, ANF at different doses induced a dose dependent increase of glomerular filtration rate (GFR), diuresis (V), sodium (UNaV) and potassium (UKV) excretion. Unilateral intrarenal norepinephrine infusion induced acute renal failure in an isotonic saline pretreated rat group. The experimental kidney in this group was anuric, and no measurable GFR and electrolyte excretion was observed. ANF pretreatment prevented the norepinephrine-induced ARF. In the experimental kidney, GFR, V, UNa V and UK V were subnormal or even elevated during NE-infusion as compared to the basal clearance period. During the 60 min control period after the norepinephrine infusion in the isotonic saline pretreated rat group, anuria persisted. In the ANF pretreated groups, normal or significantly increased levels of GFR, V, UNa V and UK V were obtained.

Acute Kidney Injury↗
PubMed1986

Toxic renal failure in the rat: beneficial effects of atrial natriuretic factor.

Acute renal failure was induced in rats by intramuscular injection of glycerol. Experiments consisted of three periods: a basal infusion period for all animals, an infusion period of atrial natriuretic factor (5 micrograms or 10 micrograms/250 g body weight) in experimental rats, control rats received isotonic glucose solution, and a post-period with isotonic saline infusion in all animals. According to the severity of acute renal failure three subgroups were formed: mild, moderate, and severe acute renal failure. In all experimental rats, atrial natriuretic factor was capable of ameliorating impaired renal function, leading to increased glomerular filtration rate, diuresis and natriuresis. The effects of atrial natriuretic factor were less pronounced in severe forms of acute renal failure.

Acute Kidney Injury↗
PubMed1985

Autonomic neuropathy in chronic renal insufficiency. Comparative analysis of diabetic and nondiabetic patients.

Disturbances of peripheral and autonomic nervous system function were evaluated in 37 normal subjects, in 52 patients with non diabetic chronic renal insufficiency (25 predialysis patients, 27 dialysis patients), and in 21 patients with diabetic chronic renal failure (10 predialysis patients, 11 dialysis patients). In nondiabetic patients, the predialysis group showed abnormal test results indicating parasympathetic lesions, in dialysis patients these derangements were nearly normalized. In predialysis diabetic patients, the autonomic alterations were much more extensive, corresponding to alterations of electroneurographical findings; in addition to parasympathetic lesions, sympathetic disturbances were seen. In contrast to the nondiabetic groups, in dialysis patients a deterioration of autonomic lesions was observed. In conclusion, these data indicate that deranged autonomic functions are common in uremia; they improve in dialysis patients with nondiabetic renal failure in contrast to diabetic patients; in this group the autonomic functions worsen in dialysis patients as a function of duration of diabetes and hemodialysis.

Adult↗
PubMed1985

Disturbances of peripheral and autonomic nervous system in chronic renal failure: effects of hemodialysis and transplantation.

Investigations of peripheral and autonomic nervous system functions were performed in 37 healthy persons, 66 patients with chronic renal failure (31 undialyzed patients, 35 dialyzed patients) and in 18 transplanted patients. The study resulted in disturbances of nerve conduction velocity and pallesthesia in predialysis and hemodialysis patients. After the transplantation, an amelioration of peripheral nerve function was observed. A set of autonomic tests demonstrated vagally mediated disorders in the predialysis group. The sympathetic function was hardly affected. In dialysis group as well as in transplanted patients a significant improvement of parasympathetic dysfunction was observed. We conclude that disorders to the autonomic nervous system in chronic renal failure are characterized by reversible vagal changes, while disorders of peripheral nervous system are resistant to hemodialysis therapy.

Adult↗
PubMed1984

Psychomental stress in tetraplegic man: dissociation in autonomic variables and emotional responsiveness.

Tetraplegic patients with physiologically complete cervical spinal cord transsection are classic ablation models of sympathetic denervation. Therefore this study was conducted to investigate the hemodynamic response (blood pressure, cardiac rate) and the plasma catecholamine (adrenaline, noradrenaline) release induced by a standardized psychomental stress model (sonic confuser). Attention was focussed on subjective evaluation of stress experience in spinal man. During psychomental stress, typical pressure reaction was not observed, cardiac rate was elevated insignificantly, and catecholamine release was diminished. The subjective estimates of stress experience, however, did not differ from those of the control group. It appears that psychomental stress in sympathectomized man is not extinguished despite abolished peripheral autonomic feedback modifying the state of the central nervous system. Cognitive processes and cortical arousal seem to be the initial and important steps of emotional experience and they are independent from peripheral autonomic processes. These results lend support to the centralistic view of emotions and the importance of cognitive factors in emotional responsiveness.

Adult↗
PubMed1983

[Hypocalcemia in malignant diseases].

Hypercalcemia accompanies often malignant diseases. The majority of cases of malignancy complicated by hypercalcemia is induced by metastases involving bone, hypercalcemia may also accompany localised tumors. Various hormones have been implicated in the genesis of malignant hypercalcemia: ectopic secretion of parathyroid hormone by tumor or orthotopic secretion by concomitant primary hyperparathyroidism, prostaglandin activating osteoclasts, production of hypercalcemic factor other than these hormones. This review summarizes current knowledge about endocrine-mediated mechanisms which produce hypercalcemia and about its frequency and mechanism in different types of tumors.

Adrenal Gland Neoplasms↗
PubMed1983

Effect of diuretics and calcium antagonists on circulatory parameters and plasma catecholamines during mental stress.

In a model of mental stress the influence of nifedipine and hydrochlorothiazide on stress-induced changes in blood pressure, heart rate, and plasma catecholamines was studied in normal persons. The drugs were used to investigate whether substances with antihypertensive but no particular sympatholytic properties were capable of suppressing emotionally induced stress reactions. In all subjects blood pressure and heart rate increased significantly during mental stress, and this effect was not inhibited either by nifedipine or hydrochlorothiazide. In the hydrochlorothiazide group plasma noradrenaline levels were significantly higher than in controls in the resting state and during the stress reaction, whereas in the nifedipine group no difference was observed. It is concluded that nifedipine or hydrochlorothiazide do not inhibit emotional stress reactions in normotensive persons.

Adult↗