[Therapy of the hepatorenal syndrome].
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Combined Modality Therapy↗
Biomedical subjects
H J Kramer
Publications and source records attributed to H J Kramer.
Treatment strategy in depression. I. Non-tricyclic and selective reuptake inhibitors in resistant depression: a double-blind partial crossover study on the effects of oxaprotiline and fluvoxamine.
Antidepressants are ineffective in about 30% of patients with major depression. Some authors then advise treatment of non-responders with (non-tricyclic) more selective reuptake inhibitors. In a double-blind, partial crossover study, 71 patients were selected for treatment during 4 weeks with oxaprotiline and/or fluvoxamine, two non-tricyclic antidepressants that are selective reuptake inhibitors or noradrenaline and serotonin respectively. All patients had failed to respond to earlier treatment with cyclic antidepressants during the current episode. Only 13% of the patients responded, with 27% of them responding to oxaprotiline and none to fluvoxamine. Moreover, a low response of 27% was also obtained in the crossover phase, which included all non-responders to the first treatment, oxaprotiline being effective in 39% and fluvoxamine in 10% of the patients. The results indicate that selective reuptake inhibitors are not an effective alternative for non-responders to other cyclic antidepressants and that non-responders to "noradrenergic" antidepressants do not appear to have much chance of responding to "serotonergic" antidepressants and vice versa.
Adult↗
Treatment strategy in depression. II. MAO inhibitors in depression resistant to cyclic antidepressants: two controlled crossover studies with tranylcypromine versus L-5-hydroxytryptophan and nomifensine.
Antidepressants are ineffective in about 30% of the patients with major depression. Besides electroconvulsive therapy (ECT) and lithium, MAO inhibitors have been suggested as an alternative in such patients. In 2 controlled, partial crossover studies involving 47 patients with major depression who had already been treated unsuccessfully with at least 2 cyclic antidepressants, the effect of the MAO inhibitor tranylcypromine was studied. The first study was an open comparison with L-5-hydroxytryptophan (L-5HTP), the second study a double-blind comparison with nomifensine. Neither the patients treated with L-5HTP nor the patients treated with nomifensine, except one, improved. In contrast, tranylcypromine was effective in 50% of the patients. The depressions of the responders to tranylcypromine appeared to be more endogenous (according Newcastle Scale II) and of shorter duration than those of the non-responders. It is concluded that MAO inhibitors such as tranylcypromine are an effective alternative to ECT and lithium in patients with major depression who have failed to respond to cyclic antidepressants.
5-Hydroxytryptophan↗
[Elevated plasma levels and heterogeneity of human atrial natriuretic peptide in patients with progressive chronic renal failure].
The role of human atrial natriuretic peptide (alpha-hANP) in chronic blood pressure (BP) and extracellular fluid volume (ECFV) regulation remains elusive. Hence, the role of alpha-hANP in chronic renal failure is of particular interest since in this pathological condition: (1) increased sodium and water retention plays a major pathogenetic role in the development of hypertension and (2) altered secretion and/or metabolism of alpha-hANP may contribute to fluid volume and BP regulation. To evaluate the relationship between the degree of renal insufficiency, BP and circulating alpha-hANP, we determined plasma alpha-hANP concentrations by radioimmunoassay in 16 nondialyzed patients with progressive chronic renal failure (CRF) of various degrees; subsequently analysis of potential molecular heterogeneity of immunoreactive (ir) ANP was performed by means of gel permeation of plasma extracts from patients with CRF without concomitant hypertension. Serum creatinine concentrations ranged from 127 to 1187 (435 +/- 76) mumol/l, systolic BP from 135 to 200 (158 +/- 4) and diastolic BP from 80 to 110 (94 +/- 2) mmHg, respectively. Plasma alpha-hANP concentrations ranged from 5 to 75 (23 +/- 4) pmol/l which was thus significantly higher as compared to 9 +/- 2 pmol/l found in healthy volunteers (p less than 0.05). A highly significant linear correlation between plasma alpha-hANP and serum creatinine concentrations (r = 0.92; p less than 0.01) was observed; a weaker correlation was found between mean arterial pressure and alpha-hANP (r = 0.66) and serum creatinine concentration (r = 0.59), respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
[Inhibition of the angiotensin-converting enzyme--effect on kidney function and electrolyte balance].
Inhibition of the angiotensin converting enzyme (ACE) is associated with a decrease in renal vascular resistance, an increase in renal blood flow and a redistribution of intrarenal blood flow toward juxtamedullary nephrons. In general, ACE-inhibition does not affect normal glomerular filtration rate (GFR) but may increase GFR in patients on a low sodium intake prior to treatment. Since the rise in GFR is smaller than the rise in renal blood flow, in most instances a decrease in filtration fraction will result. In contrast to other vasodilator drugs, the decrease in blood pressure induced by ACE-inhibition is not accompanied by sodium retention, but rather by an initial natriuresis. ACE-inhibition also prevents secondary aldosteronism and thereby avoids renal potassium loss. The initial positive potassium balance after ACE-inhibition may protect patients with heart disease from potentially hazardous arrhythmias. Redistribution of intrarenal blood flow with increased medullary flow, in addition, will antagonize the hydrosmotic effect of vasopressin and thus result in a rise in free-water clearance. Finally, based on experimental evidence, long-term treatment with ACE-inhibitors may have a protective effect on renal function by reducing glomerular filtration pressure.
Angiotensin-Converting Enzyme Inhibitors↗
[Obstructive nephropathy; kidney function and renal excretion of prostaglandin (E)2 and Thromboxane B(2) following percutaneous decompression nephropyelostomy].
In patients with chronic urinary obstruction the excretion of prostaglandin E(2) (PGE2) and thromboxane B(2) (TXB2) was measured. During obstruction signs of an increased vasoconstrictor (TXB2)- and a decreased vasodilator (PGE2) activity were found. After percutaneous nephropyelostomy a reverse pattern with decrease of the initially high (TXB2) excretion and increase of the PGE(2)excretion was observed. It is suggested that these changes of the arachidonic acid metabolism previously found in animals also take part in the pathophysiological changes in humans after relief of urinary obstruction having significant effect of renal blood flow, glomerular filtration rate and tubular function in obstructive nephropathy in humans.
Adult↗
[The role of the kidney in the pathogenesis of hypertension].
Neither a temporary increase in salt intake nor the activation of endogenous vasoconstrictor hormones alone will cause a rise in blood pressure in healthy subjects. High blood pressure rather results from an augmented product of cardiac output and peripheral vascular resistance, which also requires defective baroreceptor function. Experimental and clinical evidence from renal transplantation suggests that high blood pressure may be transmitted by the kidney. Morphological or functional inability of the kidney to adequately eliminate excessive salt, as in renoparenchymal hypertension, or with enhanced renal adrenergic activity in the presence of high salt intake, may induce initially salt- and volume-dependent hypertension with increased cardiac output and normal peripheral vascular resistance. In the case of reduced nephron population, this first stage was shown to be followed by a normalization of cardiac output, but a simultaneous rise in peripheral vascular resistance, including decreased compliance of the venous capacitance vessels. What are the underlying mechanisms which convert volume-dependent hypertension into high resistance hypertension without necessarily reducing central blood volume? Increased central blood volume, which may stimulate the secretion of an endogenous Na-K-ATPase inhibitor or other endogenous factors, may cause decreased transmembranous sodium transport, resulting in elevated intracellular concentrations of sodium and calcium with enhanced responsiveness of the vascular smooth muscle cell to vasoconstrictor hormones. Since increased central blood volume also decreases baroreceptor sensitivity, the disturbed interplay of cardiac output and peripheral vascular resistance will result in high blood pressure.
Humans↗
[Severe periodic hypokalemic paralysis. Prevention using beta-receptor blockade].
For ten years, severe physical exercise in a 24 year old male patient had been an almost constant trigger of frequent attacks of pareses which were mostly accompanied by complete tetraplegia and once by the occurrence of cardiac arrest with atrial fibrillation. During the attack, the serum potassium concentration fell to 1.2 mmol/l, whereas the intraleukocytic potassium concentration rose from 136 mmol/l to 149 mmol/l. The catecholamine excretion in the urine was raised during the first 24 hours after admission as an emergency (189 micrograms noradrenalin and 54 micrograms adrenalin). After intravenous adrenalin infusion (0.01-0.1 microgram/kg X min) during the symptom-free interval, there was a major fall of the serum potassium concentration from 3.9 mmol/l to 3.1 mmol/l. This was not accompanied by a raised insulin excretion and could be prevented by prior administration of the nonselective beta blocker propranolol. On the basis of these results, the patient was treated prophylactically with three times 40 mg/d p.o. propranolol. Pareses requiring treatment no longer occurred under this therapy.
Adrenergic beta-Antagonists↗
[Periodic hypokalemic paralysis caused by high endogenous catecholamine activity?].
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Adrenergic beta-Antagonists↗
Baroreflex setting and sensitivity in normal subjects: effects of pharmacologic inhibition of the angiotensin I converting enzyme.
Arterial blood pressure, heart rate and the response of these hemodynamic parameters to exogenous norepinephrine were investigated in healthy volunteers (daily sodium intake of 150 mmol) during a control period and after a single oral dose of 5 mg of the angiotensin I converting enzyme (ACE) inhibitor ramipril (HOE 498). Norepinephrine was infused at doses of 0.1, 0.2 and 0.3 micrograms kg-1 min-1, each for 10 minutes, during control and 3 hours after ramipril administration. Exogenous norepinephrine induced a dose-dependent increase in mean arterial blood pressure from 76.4 +/- 0.9 mm Hg during control to 85.6 +/- 1.5, 92.2 +/- 1.8 and 98.4 +/- 2.4 mm Hg, respectively. Ramipril significantly affected the baroreceptor set point with a decrease in mean blood pressure (72.1 +/- 1.7 vs 76.4 +/- 0.9 mm Hg, p less than 0.01) in the presence of unchanged heart rate (71.7 +/- 0.9 vs 73.6 +/- 1.5 min-1). Baroreceptor sensitivity, estimated by the slope of the delta blood pressure versus delta heart rate relation, was not affected by ACE inhibition. Also, the pressor effect of exogenous norepinephrine was unchanged by converting enzyme inhibition. The present results show that ACE inhibition with ramipril in sodium-replete healthy volunteers induces a decrease in blood pressure that is not accompanied by changes in heart rate, pressor sensitivity to exogenous norepinephrine or baroreceptor sensitivity.
Adult↗
Combined treatment of severe essential hypertension with the new angiotensin converting enzyme inhibitor ramipril.
Ramipril is a newly synthesized angiotensin converting enzyme inhibitor without a sulfhydryl group in the molecule but with a prolonged duration of action. Efficacy, tolerance and safety of this drug were evaluated in 10 patients with severe essential hypertension. After a treatment period of at least 4 weeks with the conventional antihypertensive drug combination of a diuretic and a beta-blocking agent with the vasodilator dihydralazine, their systolic and diastolic blood pressures averaged 161 +/- 6 and 111 +/- 2 mm Hg, respectively. Because diastolic blood pressure during this drug regimen was still greater than 105 mm Hg in all patients, the patients received ramipril initially at single daily doses of 5 mg in addition to their previous medication. The first dose of 5 mg ramipril resulted in a moderate but significant decrease in systolic and diastolic blood pressure in 9 of the 10 patients to 142 +/- 5 and 104 +/- 4 mm Hg (p less than 0.01), respectively, between 3 and 6 hours after drug administration. In 1 patient blood pressure was unresponsive to ramipril and 1 patient complained of nausea and vomiting within the first week of treatment with ramipril. Within the following 8-week treatment period with a once-daily intake of 5 or, if necessary, 10 mg of ramipril, diastolic blood pressure normalized in the remaining 8 patients to less than 90 mm Hg. Systolic and diastolic blood pressure averaged 130 +/- 5 and 83 +/- 2 mm Hg, respectively, at the end of the 8-week treatment period with ramipril. Severe hypotension and reflex tachycardia were not observed.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
The role of renal prostaglandins in the regulation of renal sodium excretion.
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Adult↗
The kidney and cardiovascular system in obstructive jaundice: functional and metabolic studies in conscious rats.
1. The effects of jaundice on renal and circulatory function were investigated in chronic bile duct ligated (CBDL) rats 6 days after surgery. Sham operated (SO) animals served as controls. 2. Body weight was significantly reduced, whereas blood pressure remained unaltered, 6 days after bile duct ligation when serum bilirubin had risen to 169 +/- 18 (SEM) as compared with 2.8 +/- 0.3 mumol/l in SO rats. When compared with control values before surgery, urinary volume had significantly increased and absolute excretion of sodium, potassium, chloride and phosphate had decreased on day 6 after CBDL. Endogenous creatinine clearance was markedly depressed when compared with SO rats. Whereas fractional excretion of potassium remained unaltered, fractional excretion of sodium and of phosphate was significantly increased. 3. Except for a significant increase in urinary thromboxane B2 (TXB2) excretion in CBDL rats, no significant changes were observed in urinary excretion of prostaglandin (PG) E2, in the synthesis of PGE2, 6-keto-PGF1 alpha and TXB2 by isolated aortic tissue in vitro, nor in renal and cardiac adenosine triphosphatase activities or renal cortical mitochondrial function. 4. The adenosine triphosphate content of kidney cortex and cardiac mitochondrial function were significantly depressed in CBDL rats. 5. The results demonstrate that jaundice in CBDL rats is associated with functional and metabolic disturbances of the kidney and cardiac muscle, which may contribute to the renal and haemodynamic characteristics observed in jaundiced animals and humans.
Adenosine Triphosphate↗
Sodium balance as a determinant of prostacyclin production by isolated rat aorta.
The present study investigates whether the synthesis of prostacyclin (PGI2) in isolated rat aorta is dependent on the state of sodium balance of the animals. Three groups of ten rats each were included into the study. Two of them were fed a diet low in NaCl for 10 days with group I receiving 0.9% saline and group II distilled water as drinking fluid. Group III received a regular rat chow containing approximately 0.8 mmol day-1 of sodium, also for 10 days. At the end of the dietary protocol, systolic arterial blood pressure was significantly higher in group I (109.9 +/- 2.4 mmHg) as compared to group II (101.0 +/- 2.4 mm Hg; P less than 0.05) and group III animals (102.2 +/- 1.6 mm Hg; P less than 0.05). Generation of PGI2-like activity was determined in portions of the animals' isolated aorta using a platelet aggregation bioassay following incubation in 0.05 M Tris buffer (pH 9.3) for 12, 15, and 30 min, respectively. During these incubation times, generation of PGI2-like activity averaged 48.6 +/- 3.5, 57.8 +/- 4.3 and 68.3 +/- 3.2 pmol mg-1 in group III animals, which had received the regular rat chow, with similar values in the low salt group II (50.2 +/- 2.5, 57.7 +/- 2.7 and 72.9 +/- 3.7 pmol mg-1). Aortic generation of PGI2-like material was significantly suppressed in the high salt group I (37.5 +/- 2.8, 46.2 +/- 3.2 and 61.3 +/- 4.0 pmol mg-1; P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
Acid-Base Equilibrium↗
Relationship of plasma concentrations of human atrial natriuretic peptide to renal function and blood pressure in patients with progressive chronic renal failure.
Recent experimental and clinical findings indicate that immunoreactive human Atrial Natriuretic Peptide (alpha-hANP) is involved in the regulation of blood volume and arterial blood pressure (BP). Whereas the potential regulatory role of alpha-hANP in acute changes of extracellular fluid volume (ECFV) and in the modulation of BP has been demonstrated in various studies, their involvement in the chronic maintenance of sodium and water homeostasis is still equivocal. Moreover the role of alpha-hANP is of particular interest in chronic renal failure, since in this pathological condition increased sodium and water retention plays a major pathogenetic role in the development of hypertension and altered secretion and/or metabolism of alpha-hANP may contribute to fluid volume and BP regulation. To evaluate the relationship between the degree of renal insufficiency, BP and circulating alpha hANP we determined plasma alpha-hANP concentrations in 16 nondialyzed patients with progressive chronic renal failure (CRF) of various degree. Serum creatinine concentrations ranged from 127 to 1187 (435 +/- 76) mumol/l, systolic BP from 135 to 200 (158 +/- 4) and diastolic BP from 80 to 110 (94 +/- 2) mm Hg respectively. Plasma alpha-hANP concentrations ranged from 49 to 753 with a mean of 228 +/- 42 pg/ml which was thus significantly higher as compared to 90.0 +/- 16.2 pg/ml found in healthy volunteers (p less than 0.05). A highly significant linear correlation between plasma alpha-hANP and serum creatinine concentrations (r = 0.92) was observed; a weaker correlation was found between mean arterial pressure and alpha-hANP (r = 0.66) and serum creatinine concentration (r = 0.59), respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
Acute Kidney Injury↗
Prostacyclin biosynthesis by human arterial tissue in vitro: dependence on oxygen tension.
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6-Ketoprostaglandin F1 alpha↗
[Hemodynamic studies on the action kinetics of phenoxybenzamine in healthy persons and hypertensive patients].
The hemodynamic profile of the pre- and postsynaptic alpha-receptor blocker phenoxybenzamine (POB) was investigated by a non-invasive technique in healthy subjects and in patients with essential hypertension. At a dose of 0.03 mg POB/kg body weight no hemodynamic changes were detected. POB at a dose of 0.07 mg/kg resulted in an initial transient rise in systemic vascular resistance and mean arterial pressure and a fall in heart rate without changes in stroke volume or cardiac index. 6 h after administration of 0.13 mg POB/kg a transient fall in peripheral vascular resistance and mean arterial pressure with an increase in heart rate and cardiac index was observed. A rise of orthostatic index, however, occurred within 1 h after administration of POB and reached its maximum after 4 h. 8 h after POB no hemodynamic changes were detectable. In patients with essential hypertension a similar fall in systemic vascular resistance and mean arterial pressure was observed after 0.13 mg POB/kg body weight. No change in heart rate occurred and the hemodynamic effects were significant already 3 h after administration of POB and persisted up to 8 h after POB administration. In contrast to healthy subjects, patients with essential hypertension showed no significant changes in the orthostatic index after POB. These hemodynamic findings point to a previously unexpected rapidly reversible functional alpha-receptor blockade by POB.
Adult↗