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Biomedical subjects

H J Kramer

Publications and source records attributed to H J Kramer.

At least 163 records · Page 9Linked to original sources
PubMed1978

Comparative evaluation of metrizamide and meglumine ioxithalamate in angiography of the vessels of the head and neck.

Metrizamide, a non-ionic contrast medium of low osmolality was compared with meglumine ioxithalamate, the ionic angiographic contrast medium currently in use in our department in a double-blind study. Criteria upon which the comparison was based were: 1) the pain reaction of the patient upon intra-arterial contrast injection, 2) bradycardial reactions upon common carotid injection and 3) the quality of the contrast image. Metrizamide induced significantly less painful sensations than meglumine ioxithalamate in those vessels in which injections of contrast medium are frequently painful (external carotid artery, vertebral artery). No significant difference in the degree of bradycardia was caused by the two contrast media. The degree of bradycardia was also found to be poorly reproducible upon successive injections of the same contrast medium in the same patient, thus raising questions as to the suitability of this method for determining the toxicity of the contrast medium. The quality of the angiograms obtained did not differ significantly with the two media. Spasm, when it occurred during selective external carotid injections, was found to be independent of the contrast agent used, being correlated instead with the depth of distal advance of the catheter tip into the external carotid. Of the 51 patients included in the study, two patients suffered transient neurological deficit after angiography with metrizamide, and one patient suffered a permanent hemiplegia after angiography with meglumine ioxithalamate.

Aorta, Thoracic↗
PubMed1978

Effects of inhibition of prostaglandin-synthesis on renal electrolyte excretion and concentrating ability in healthy man.

In five healthy subjects inhibition of prostaglandin (PG)-synthesis with indomethacin did not significantly alter glomerular filtration, urinary flow rate or sodium and potassium excretion during control urine collection periods or i.v. hypertonic saline infusion. Saline administration was accompanied by a fall in urinary PGEI-excretion from 0.58 +/- 0.14 to 0.26 +/- 0.09 ng/min (p less than 0.05). While indomethacin had no effect on basal urinary osmolality (Uosm), renal concentrating ability following hypertonic saline or i.v. administration of 100 mU lysine-vasopressin significantly increased in the presence of indomethacin with Uosm rising from 805 +/- 25 to 970 +/- 53 mosm/L (p less than 0.01) and from 839 +/- 47 to 996 +/- 62 mosm/L (p less than 0.01), resp. Since this was not accompanied by respective changes in urinary excretion of cyclic adenosine monophosphate (cAMP) mechanisms other than PG-antagonism of vasopressin, such as decreased medullary washout of solute, may contribute to enhanced renal concentrating ability following inhibition of PG-synthesis with indomethacin.

Adult↗
PubMed1978

Third factor and edema formation.

Urine extracts as well as plasma and urine fractions from normal persons during extracellular volume expansion and from patients with edema of different origin were tested for natriuretic (rat bioassay) and antinatriferetic (frog skin) activity. Whereas the extracts and fractions from normal persons with extracellular volume expansion proved to have a distinct natriuretic and antinatriferetic effect, no such effect was observed with urine and plasma preparations from patients with sodium retention and edema. Whether or not edema formation is mediated by a loss of natriuretic activity remains still to be clarified.

Adult↗
PubMed1977

[Triamterene in the treatment of hypertension with hydrochlorothiazide and propranolol (author's transl)].

In 36 patients with essential hypertension the action and side effects of hydrochlorothiazide (25 mg/d), hydrochlorothiazide-triamterene (25 and 50 mg/d) and propranolol (160 mg/d) were investigated. Hydrochlorothiazide and hydrochlorothiazide-triamterene led to an average decrease of the systolic blood pressure by 21 and 30 mm Hg and of the diastolic pressure by 11 and 18 mm Hg. Propranolol alone decreased the systolic pressure by 35 mm Hg on average in 8 out of 16 patients. The diastolic pressure was lowered by 20 mm Hg. In the remaining 8 patients the systolic pressure, when propranolol was used alone, decreased by 21.3 mm Hg, the diastolic pressure by 11.3 mm Hg. Addition of hydrochlorothiazide-triamterene lowered pressures by a further 22.5 (systolic) and 10.6 (diastolic) mm Hg. No disturbances of the potassium or acid-base balance were observed using hydrochlorothiazide-triamterene.

Acid-Base Equilibrium↗
PubMed1977

Circulating inhibitor of sodium-potassium-activated adenosine triphosphatase after expansion of extracellular fluid volume in rats.

1. Serum was collected from normal rats and from rats volume-expanded with isotonic sodium chloride solution. 2. The serum was fractionated by gel filtration on Sephadex G-25 and each fraction was tested for inhibitory activity against sodium-potassium-activated adenosine triphosphatase prepared from rat kidney homogenate. 3. A single low-molecular-weight fraction, eluting after the salts and after exogenously added lysine-vasopressin, had significantly greater enzyme inhibitory activity when obtained from serum of volume-expanded animals than from control serum. 4. As this fraction has been shown in previous independent studies to contain a natriuretic factor, it may be concluded that one property of this factor is the ability to inhibit sodium-potassium-activated adenosine triphosphatase.

Adenosine Triphosphatases↗
PubMed1977

The role of prostaglandins in the natriuresis of acutely salt-loaded rats.

Mechanisms determining the natriuresis in ECV expansion are not yet completely known. The present study was therefore performed to investigate (1) the extent to which prostaglandins (PG) are involved in the natriuresis of ECV expansion and (2) by which mechanisms PG may affect renal Na absorption. In nonexpanded rats the prostaglandin synthetase inhibitor indomethacin (INDO) had no effect on renal function. In 16 Sprague-Dawley rats EVC expansion with isotonic saline corresponding to an increase in body weight of 10% was induced and maintained for 60 min. Ten animals received an oral dose of 10 mg/kg BW of INDO prior to ECV expansion. Six animals served as controls (C). Blood pressure (INDO: 132 +/- 4 (SE); C: 130 +/- 3 mm Hg), GFR (INDO: 12.5 +/- 1.0; C: 10.5 +/- 0.9 ml/min/kg BW), fractional K excretion (INDO: 32.1 +/- 2.6; C: 43.4 +/- 4.8%), CH2O and Na-k-ATPase activities in renal cortex, medulla and papilla did not significantly differ in either group. Significant differences were observed in urinary flow rate (INDO: 0.82 +/- 0.8; C: 1.82 +/- 0.23 ml/min/kg KG) and fractional Na absorption (INDO: 91.9 +/- 1.1; C: 81.7 +/- 1.2%). The results indicate that PG are involved in the natriuresis following acute expansion of the ECV and suggest that PG may inhibit the intrinsic tubular capacity for Na absorption in the rat.

Adenosine Triphosphate↗
PubMed1977

Effects of prostaglandin inhibition on intrarenal hemodynamics in acutely saline-loaded rats.

We studied the effect of inhibition of the prostaglandin (PG)-synthesizing enzyme system in female Sprague-Dawley rats following acute expansion of the extracellular fluid volume (ECV). In 57 conscious rats expansion of the ECV with isotonic saline corresponding to an increase in body weight of 10% was induced. Prior to ECV expansion 31 rats received indomethacin (10 mg/kg of body wt) by stomach tube. In six non-ECV-expanded rats indomethacin had no effect on glomerular filtration rate (GFR) and renal plasma flow (RPF). In ECV-expanded rats pretreated with indomethacin, GFR was unaltered but 125I-hippuran clearance decreased, and filtration fraction significantly increased. Intrarenal 86Rb distribution was similar in control and ECV-expanded rats. Indomethacin caused a slight increase in relative cortical 86 RB activity in non-ECV-expanded rats, but had no effect on intrarenal 86Rb distribution in ECV-expanded rats. No difference in intracortical glomerular perfusion was noted between control and ECV-expanded rats. In indomethacin-treated ECV-expanded rats an increase in relative inner cortical perfusion was observed. Absolute perfusion remained unaltered. Thus the decrease in total RPF was entirely due to decreased perfusion of outer cortical nephrons. Renal prostaglandins therefore may play a permissive role for physical factors to promote renal sodium excretion in acute ECV expansion via changes in intrarenal hemodynamics.

Animals↗
PubMed1976

Prostaglandins and renal function in acute extracellular volume expansion.

Mechanisms determining the natriuresis in ECV-expansion are not yet completely understood. The present study was therefore undertaken to investigate if prostaglandins (PG) are involved in the natriuresis of acute ECV-expansion and by which mechanisms PG may affect renal Na-absorption. In non-expanded rats the PG synthetase inhibitor indomethacin (INDO) had no effect on renal function. In 37 Sprague-Dawley rats ECV-expansion with isotonic saline corresponding to an increase in b.wt. of 10% was induced. Twenty-one animals received an oral dose of 10 mg/kg b.wt. of INDO prior to ECV-expansion. Sixteen animals served as ECV-expanded controls (C). GFR (INDO: 12.5 +/- 1.0; C: 10.5 +/- 0.9 ml/min/kg b.wt.) did not significantly differ in both groups. However, total renal plasma flow (RPF) (INDO: 22.9 +/- 1.8; C: 30.1 +/- 2.7 ml/min/kg b.wt.), urinary flow rate (INDO: 1.11 +/- 0.20; C: 1.93 +/- 0.21 ml/min/kg b.wt.) and urinary excretion of sodium (INDO: 141 +/- 26; C: 267 +/- 46 muEq/min/kg b.wt.) and potassium (INDO: 13.0 +/- 0.9; C: 19.8 +/- 1.7 muEq/min/kg b.wt.) markedly decreased in animals pretreated with INDO. The results indicate that PG are involved in the natriuresis of acute ECV-expansion and suggest, that PG may inhibit the intrinsic capacity for Na-absorption in more proximal parts of the nephron possibly via intrarenal physical factors.

Animals↗
PubMed1976

Effects of bumetanide on sodium transport of the isolated frog skin and on renal Na-K-ATPase.

The effects of bumetanide, a new potent diuretic, on net sodium transport of the isolated frog skin and on rat renal Na-K-ATPase were studied. A dose-related decrease in short-circuit current and potential difference with increased electrical resistance was observed when bumetanide was added to the corial side of the skin. Addition to the epithelial side resulted in enhanced net sodium transport with decreased electrical resistance. When applied to the corial side it abolished vasopressin- and aldosterone-stimulated transport. Present in the epithelial bath ouabain-inhibited transport was unaffected by this drug, while triamterene-induced inhibition of sodium transport was completely abolished. In vitro, no significant effects on Na-K-ATPase were noted. It is concluded that bumetanide shares properties of both furosemide and ethacrynic acid and excerts its effects on epithelial sodium transport by altering membrane permeability and possibly by inhibition of some step in the active transport mechanism for sodium.

Adenosine Triphosphatases↗
PubMed1976

Functional and metabolic studies on red blood cell sodium transport in chronic uremia.

Red blood cells from 7 out of 13 patients with chronic uremia were found to have increased intracellular concentrations of sodium associated with a reversible inhibition of ouabain-sensitive Na efflux when incubated in control plasma. Although mean Na-K-ATPase activity of RBC hemolysates was only moderately decreased (21.8 +/- 1.5 vs. 26.5 +/- 1.8 nmol Pi/mg protein/h), enzyme kinetics revealed a significant increase in KmATP values for this enzyme in uremic RBCs (1.01 +/- 0.1 vs. 0.58 +/- 0.03; p less than 0.001) which was closely correlated to serum creatinine concentration (r = 0.9034). While aerobic glycolysis was unaltered, an increase in glucose-6-phosphate dehydrogenase activity was observed, i.e. the enzyme initiating the pentose-phosphate cycle. In addition, intracellular ATP concentrations of uremic RBCs were significantly higher than ATP concentrations of control RBCs (2.13 +/- 0.22 vs. 1.32 +/- 0.06 mmol/l RBC; p less than 0.01). These data suggest that high intracellular concentrations of Na and ATP in uremic RBCs partially result from a competitive reversible inhibition of the transport ATPase by uremic toxins.

Adenosine Triphosphatases↗
PubMed1976

Plasma natriuretic activity in oedematous states.

Accumulating evidence suggests that extracellular volume (ECV) may be governed in part by a natriuretic hormone. To study its possible role in oedema formation plasma fractions IV from patients with the nephrotic syndrome, with cirrhosis of the liver, and with idiopathic oedema were studied for their effects on frog skin Na-transport and on rat renal Na-excretion. Plasma fractions IV from ECV-expanded healthy subjects and patients with aldosteronoma significantly inhibited PD and SCC and in the rat increased urinary flow, CH29, and UNaV. Neither antinatriferic nor natriuretic activities were observed in patients with the nephrotic syndrome or liver cirrhosis. In patients with idiopathic oedema recurrent episodes of fluid retention up to 9 percent of b.wt. followed by spontaneous natriuresis were well correlated with antinatriferic plasma activity. The results suggest that ECV in healthy subjects may be governed in part by a natriuretic hormone which is absent in ECV-expansion due to oedema. However, this mechanism may operate appropriately, though at an elevated threshold, in patients with idiopathic oedema.

Animals↗