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Biomedical subjects

M D Lifschitz

Publications and source records attributed to M D Lifschitz.

At least 37 records · Page 2Linked to original sources
PubMed1982

Gastrointestinal blood loss in patients with chronic renal failure.

In the management of patients with chronic failure one of the persistent medical problems is that of anemia. Since iron deficiency can be an important component of this anemia, this study was designed to evaluate the possible contribution of gastrointestinal blood loss to their anemia. Blood loss was quantitated by 51 chromium labeling red cells in normals and in patients with chronic renal failure both before and during chronic hemodialysis. Four normal volunteers had a gastrointestinal blood loss of 0.83 ml/day, six azotemic patients not yet on hemodialysis had significantly greater gastrointestinal blood loss of 3.15 ml/day (p less than 0.05). Ten patients on chronic regular hemodialysis had a daily gastrointestinal blood loss of 6.27 ml/day which was significantly greater than both the normals (p less than 0.01) and the predialysis azotemic patients (p less than 0.05). Complete gastrointestinal tract evaluation in the chronic dialysis patients revealed several upper gastrointestinal tract mucosal abnormalities although discrete bleeding sites were not identified. In conclusion, azotemic patients both before and after chronic hemodialysis have increased gastrointestinal blood loss. This increased blood loss contributes to the increased iron loss in this patient population.

Adult↗
PubMed1982

Studies on the mechanism of sodium excretion during drug-induced vasodilatation in the dog.

The administration of vasodilating agents such as bradykinin and acetylcholine cause an increase in urinary sodium excretion. Yet the mechanisms involved in this natriuretic effect are not clear. Recent studies with another renal vasodilator, secretin have shown this drug also causes a profound increase in renal blood flow but without major changes in sodium excretion. To attempt to delineate the basis of this difference in sodium excretion with these drugs, the renal functional effects of secretin and bradykinin were compared at an equivalent vasodilating dose. Bradykinin increased renal blood flow from 222 to 342 ml/min, urine volume from 0.2 to 1.2 ml/min, and urine sodium excretion from 28 to 115 mueq/min. Urine osmolality fell from 1,230 to 401 mosmol/kg. Secretin caused a comparable increase in renal blood flow (216 to 325 ml/min) while changes in urine flow, sodium excretion, and urine osmolality were significantly less. In further studies papillary plasma flow was estimated using the albumin accumulation technique. Control papillary plasma flow was 29 ml/min per 100 g. Bradykinin increased urinary sodium excretion 108 mueq/min and decreased urinary osmolality from 1,254 to 516 mosmol/kg in association with a rise in papillary plasma flow to 62 ml/min per 100 g. Urine sodium excretion, urinary osmolality, and urine flow rate, as well as papillary plasma flow rate (32 ml/min per 100 g) were unchanged from control when secretin was administered. Studies with acetylcholine were qualitatively similar to those of bradykinin. Renal blood flow increased from 150 to 248 ml/min, urinary sodium excretion increased from 20 to 243 mueq/min, urinary osmolality decreased from 1,237 to 411 mosmol/kg and papillary plasma flow increased from 39 to 52 ml/min per 100 g. It is suggested that the natriuretic effect of some vasodilators is due, at least in part, to alterations in medullary hemodynamics, as evidenced by the increase in papillary plasma flow seen with bradykinin and acetylcholine, but not secretin.

Acetylcholine↗
PubMed1981

High urine flow rate increase prostaglandin E excretion in the conscious dog.

Although previous studies from this and other laboratories have shown that urinary prostaglandin E excretion (UPGEV) can very independent of urine flow rate, recent studies during water diuresis in the conscious dog have suggested that high urine flow rate per se may increase UPGEV. To examine the effect of urine flow rate on UPGEV we administered either mannitol, chlorothiazide or Ringer's solution to mongrel dogs and measured UPGEV. During anesthesia neither mannitol or chlorothiazide increased UPGEV. There was, however, a consistent increase with all three agents in awake animals. This increase in UPGEV was independent of alterations in glomerular filtration rate. There was a consistent increase in urinary sodium excretion and decrease in urinary osmolality with all three agents. The changes in PGE, however, were similar to those found during water diuresis when no increase in sodium excretion was found. It is not presently clear whether these findings reflect a true increase in renal PGE synthesis due to some changes in flow or pressure within the renal medulla or rather represent unchanged PGE synthesis by renal tubular cells, the high tubule fluid flow rate causing increased entry into the tubular lumen in contrast to the renal interstitium.

Anesthesia↗
PubMed1980

Dissociation of renin--aldosterone and renal prostaglandin E during volume expansion induced by immersion in normal man.

The relationship of the renin--angiotensin--aldosterone axis with renal prostaglandin E is complex. Although studies have suggested that these two hormonal systems respond to experimental manipulations in a parallel manner, their interdependence has not been assessed fully during volume expansion. Since studies have demonstrated that in normal man the central hypervolaemia induced by water immersion to the neck produces a prompt and profound suppression of plasma renin activity and plasma aldosterone concentration without concomitant alteration of plasma composition, immersion afforded a unique opportunity to assess simultaneously the effects of central hypervolaemia on plasma renin activity, plasma aldosterone concentration and prostaglandin E excretion. 2. Seven normal subjects were studied twice while in balance on a diet containing 10 mmol of sodium/day, 100 mmol of potassium/day: with indomethacin administration (50 mg given every 6 h for five doses) and without indomethacin. Urinary prostaglandin E excretion was measured hourly and plasma renin activity and plasma aldosterone concentration at 30 min intervals. 3. Immersion was associated with a marked suppression of plasma renin activity (59 +/- 7%) and plasma aldosterone concentration (55 +/- 3%) with a return to pre-study values during the recovery hour. Concomitantly, urinary prostaglandin E excretion increased from 4.7 to a peak of 10.9 ng/min. Although administration of indomethacin lowered the basal rate of urinary prostaglandin E excretion and plasma renin activity, it did not prevent the subsequent augmentation of urinary prostaglandin E or the suppression of plasma renin activity and plasma aldosterone during the subsequent 4 h of immersion. 4. These results demonstrate a dissociation of renin--aldosterone and prostaglandin E during hypervolaemia and suggest that whereas prostaglandin E may constitute one of the major determinants of renin release clinically and experimentally, these two hormonal systems can be dissociated from each other in response to central volume expansion in man.

Adult↗
PubMed1980

Role of the autonomic nervous system in the pressor response to calcium in conscious dogs.

The effects of acute hypercalcaemia on arterial pressure and vascular tone have been poorly understood. We analysed the effect of a bolus of calcium chloride (15 mg . kg-1 iv) on arterial pressure, total peripheral resistance, and left ventricular function in 25 conscious dogs studied with or without pharmacological autonomic blockade. Without autonomic blocking drugs, the maximum response to calcium included increases of +139.4 kPa . s-1 (+1046 mmHg . s-1) in maximum rate of change of left ventricular pressure, +2.2 cm3 in stroke volume, +2.6 kPa (+ 19.2 mmHg) in aortic systolic pressure, and +0.6 kPa (+4.4 mmHg) in mean aortic pressure, but total peripheral resistance was unchanged. During beta-adrenergic blockade with propranolol, calcium again increased maximum rate of change of pressure and stroke volume, increased mean aortic pressure (2.2 kPa [+16.5 mmHg]), and increased resistance by 35%. When calcium was given during alpha-adrenergic blockade with phenoxybenzamine or phentolamine, mean aortic pressure did not rise, and resistance fell by 19%. The calcium-induced rise in resistance during beta-adrenergic blockade was abolished by surgical adrenalectomy. We conclude that excess extracellular calcium ion may influence vascular resistance by increasing autonomic nervous system excitation of alpha- and beta-adrenergic vascular receptors. A major mechanism by which the sympathetic nervous system effects occur is through increased release of catecholamines from the adrenal medulla.

Adrenalectomy↗
PubMed1980

Sequential studies on the pathophysiology of glycerol-induced acute renal failure.

The role of volume depletion and renal ischemia in the development of renal functional impairment in glycerol-induced ARF is not clear. This study was designed to evaluate the role of volume depletion in this model by determining the hemodynamic and functional alterations which occur between 3 and 18 hr after glycerol administration and the reversibility of these changes in response to Ringer loading. Three hours after glycerol, Cln and RBF, measured by flowmeter, were reduced 70% and 52%, respectively, in comparison with control values. FeNa was 0.04%. Ringer loading increased Clkn to 103% and RBF to 93% of control values. Qualitatively similar results were found 6 hr after glycerol. At 18 hr, Cln and RBF were 47% of control values. After Ringer loading, RBF rose to 100% of control. The response of Cln, however, was a function of the baseline FeNa. Cln incrased substantijally in rats with low FeNa but changed only slightly in animals in which this parameter was increased. These studies indicate that the early reduction in the Cln is dependent upon the fall in RBF. At 12 and 18 hr, however, the fall in Cln is not blood flow-dependent, and a second mechanism must be operative. FeNa seems to be a reliable index of the functional status of a given animal.

Acute Kidney Injury↗
PubMed1979

Study of factors which modify the development of norepinephrine-induced acute renal failure in the dog.

Previous studies have demonstrated that the fall in inulin clearance which occurs 3 hours after the intrarenal administration of norepinephrine can be markedly attenuated by the prior administration of intrarenal prostaglandin E2 (PGE). Since in the previous studies PGE led to a marked increase in both renal blood flow and solute excretion, we designed the present series of experiments to investigate whether an increase in renal blood flow, solute excretion, or other factors were responsible for the protective effect in the norepinephrine model. Two renal vasodilators, bradykinin and secretin, were evaluated initially. Bradykinin administration prior to norepinephrine administration had a protective effect similar to that previously found with PGE, whereas secretin did not. Both of these vasocilators increased renal blood flow to the same degree, but only bradykinin increased urine flow and solute excretion. The fall in inulin clearance 3 hours after the administration of norepinephrine was also attenuated by two diuretics (mannitol and furosemide) which tended to increase renal blood flow. In contrast, two natriuretic agents, which are also renal vasoconstrictors (chlorothiazide and benzolamide), had no protective effect. Further, chlorothiazide and benzolamide obviated the protective effect of bradykinin. These studies demonstrate that there are several types of pharmacologic agents which can modify the magnitude of renal functional impairment resulting from extreme renal ischemia. Although the mechanism of the protective effects remain unclear, the findings are compatible with the view that the protective effect noted with PGE, bradykinin, mannitol, and furosemide may be related to an increase in osmolar excretion which occurred with administration of each of these agents. This potentially salutory effect (increased osmolar excretion), however, could be overcome by an agent (e.g., chlorothiazide or benzolamide) which also increased renal resistance prior to the administration of norepinephrine.

Acute Kidney Injury↗
PubMed1979

Alport's syndrome associated with macrothrombopathic thrombocytopenia.

The combined occurrence of hereditary nephritis with nerve deafness (Alport's syndrome) and macrothrombocytopathic thrombocytopenia is very rare. The authors have had the opportunity to study such a case in a 20-year-old man who had been followed since birth. The clinical history, renal biopsy, platelet studies, and autopsy findings are presented. The renal pathologic findings are well defined; however, the hemostatic abnormalities and the hearing loss are not well characterized. In this paper, an attept is made to clarify the diverse platelet functional and morphologic abnormalties.

Adult↗
PubMed1978

Urinary prostaglandin E excretion: effect of chronic alterations in sodium intake and inhibition of prostaglandin synthesis in the rabbit.

On the basis of acute experiments in animals, a role for prostaglandin E (PGE) in the regulation of urinary sodium excretion has been suggested. Limited information is available, however, concerning the possible role of PGE in chronic adjustments to sodium intake. These studies were designed to determine whether chronic changes in sodium balance would modify renal PGE excretion and whether partial inhibition of prostaglandin synthesis would alter the ability of the kidney to adjust to an alteration in sodium intake. Thus, we measured sodium and PGE excretion in rabbits on chronic high and low salt diets before and after inhibition of prostaglandin synthesis with indomethacin or meclofenamate. Although the alterations in salt intake resulted in large changes in sodium excretion there was no significant change in urinary PGE excretion. After administration of either indomethacin or meclofenamate for several days there was a significant fall in PGE excretion, but no significant change in sodium excretion. These results suggest that in the rabbit 1) chronic changes in sodium excretion can occur without modifying PGE excretion (and presumably renal PGE synthesis) and 2) inhibition of PGE synthesis does not impair the kidney's ability to adjust to a chronic high or low sodium intake.

Animals↗
PubMed1978

Current concepts on the pathophysiology of acute renal failure.

In the pase decade, several experimental models of acute renal failure (ARF) have been evaluated with micropuncture and hemodynamic techniques. Five of these models have been most extensively studied: glycerol injection, renal artery clamping, intrarenal norepinephrine infusion, uranyl nitrate, and mercuric chloride administration. In the first three models, renal ischemia is the initiating insult, whereas in the two nephrotoxic models a direct effect of the agent on cellular integrity is also seemingly operative. In all of these models, renal blood flow 24--48 h after the initial insult either spontaneously returns to normal or can be elevated to this level with volume expansion but without restoration of the glomerular filtration rate. Therefore, the maintenance of ARF in these various models is due to other factors, which include tubular obstruction, leakage of filtrate across damaged tubular epithelium, and a decrease in the glomerular capillary ultrafiltration coefficient. In a given model, one or all three of these alterations may be present. Although these various models may not be completely analogous to the clinical setting, they have provided powerful tools for the study of ARF and their use has greatly increased our knowledge in this field.

Acute Kidney Injury↗
PubMed1978

Organic acid secretory pathway and urinary excretion of prostaglandin E in the dog.

Urinary prostaglandin E (PGE) has been utilized as an index of renal PGE production. Recent studies, however, have suggested that the organic acid secretory pathway is a major determinant of endogenous UPGEV (urinary excretion of PGE). The following experiments were designed to quantitatively test this latter view. In clearance studies the administration of para-aminohippurate (PAH) or probenecid (25 mg/kg) failed to alter endogenous UPGEV although PAH clearance fell with probenecid. Comparison of the excretion patterns of exogenously administered [3H]PGE and [14C]inulin after intra-arterial injection into the dog renal artery (Chinard technique) demonstrated both glomerular filtration and secretion of [3H]PGE. Blockade of the organic acid pathway by probenecid (25 mg/kg) abolished [3H]PGE secretion. Indomethacin (1 mg/kg) did not alter the secretion pattern of [3H]PGE, but decreased endogenous UPGEV by over 80%. Because this low dose of indomethacin did not decrease [3H]PGE secretion, it probably decreased endogenous UPGEV by inhibiting synthesis. Thus, these tracer studies do indeed confirm the suggestion that PGE may be excreted by the organic acid pathway. However, the failure of total endogenous UPGEV to fall after blockade of the organic acid pathway would suggest that the component of UPGEV due to this mechanism is quantitatively insignificant.

Animals↗
PubMed1978

Acute renal failure: clinical aspects and pathophysiology.

Acute renal failure may be caused by multiple conditions including those which are due to some direct hemodynamic or nephrotoxic insult. In considering the pathophysiology of these entities, it seems appropriate to differentiate between the initiating and the maintenance phase of the disorder. In the former, renal ischemia and/or a direct effect of a given nephrotoxic agent seems to be the basis for the underlying renal damage. In the maintenance phase, renal functional impairment is maintained by a number of factors which include persistent renal vasoconstriction, tubular obstruction, a leakage of filtrate across damaged tubular epithelium, and a reduction in glomerular capillary permeability. The therapy and possible preventive aspects of these entities are discussed.

Acute Kidney Injury↗