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Biomedical subjects

L Hernando

Publications and source records attributed to L Hernando.

At least 55 records · Page 3Linked to original sources
PubMed1987

Role of the natriuretic hormone in the specific natriuresis induced by intraportal infusion of hypertonic saline in dogs.

Previous experiments from our laboratory demonstrated that the infusion of a small amount of hypertonic saline into the portal vein induced higher diuresis and natriuresis than those induced by the infusion of the same amount of saline into a cubital vein. The purpose of the present experiment was to study the role of the so-called natriuretic hormone in this phenomenon. For this purpose, two groups of 5 dogs each were infused with 855 mM NaCl (0.05 ml X min-1 for 20 min), one group through the portal vein and the other through the cubital vein. Samples of peripheral, arterial and suprahepatic blood and urine were obtained, and the fraction described to contain the natriuretic hormone was purified by gel filtration chromatography. Its natriuretic activity was assayed by measuring the natriuresis induced by its infusion in conscious, unilaterally nephrectomized rats. The urine taken from the dogs infused with hypertonic saline into the porta showed higher natriuretic activity than that obtained before infusion or from the dogs infused into the cubital vein. Also, natriuretic activity was observed in the suprahepatic and arterial plasma samples obtained after portal infusion but not in those obtained before the infusion. There were no differences in natriuretic activity between suprahepatic and arterial samples. These results suggest that the natriuretic hormone plays an important role in the natriuresis induced by portal hypertonic saline infusion, and they do not support the hepatic origin of this substance.

Animals↗
PubMed1986

Lack of a direct regulatory effect of atrial natriuretic factor on prostaglandins and renin release by isolated rat glomeruli.

We have tested the direct regulatory effect of synthetic Atrial Natriuretic Peptide (ANP, 8-33aa) on prostaglandins and renin release by isolated rat glomeruli. Variable incubation times and doses of ANP did not modify the rate of PGE2, PGF2a and TXB2 production. Similar results were obtained for renin release. These data do not support a role for ANP in the regulation of prostaglandins and renin release by rat glomeruli.

6-Ketoprostaglandin F1 alpha↗
PubMed1986

Systemic and regional haemodynamic effects of a synthetic atrial natriuretic peptide in conscious rats.

The effect of the intravenous injection of synthetic atrial natriuretic peptide (ANP, 2 micrograms) on systemic haemodynamics and blood flow to several organs has been studied in conscious rats by the radioactive microsphere technique. ANP induced a 540% increase in sodium excretion and a 310% increase in urine flow. Mean arterial pressure decreased by 21 mmHg and the peripheral resistances decreased by 26%, without significant changes in cardiac output. Renal blood flow increased by 37.7% and small intestine and portal blood flow increased by 39% and by 28% respectively. No other alterations in organ blood flows were observed. From these data it can be concluded that atrial natriuretic peptide shows acute vascular relaxant properties, which seem to be specific for renal and mesenteric territories.

Animals↗
PubMed1986

Molecular heterogeneity of circulating prolactin in chronic uremic men and renal transplant recipients.

Serum PRL levels and its molecular heterogeneity were analyzed, basally and after 500 micrograms TRH given acutely, in four groups of men: normal (C, n = 12), chronic renal failure (CRF, n = 11), hemodialysis (HD, n = 12), and transplant recipients (T, n = 11). The mean basal PRL level was higher in group CRF than in group C and even higher in group HD. The basal hyperprolactinemia was due to increased concentrations of little PRL. The absolute levels of total and little PRL 20 min after TRH were comparable in the four groups. The disappearance index (DI = PRL20-PRL120/PRL20) for total and little PRL was lower in CRF than in C and even lower in HD. A positive correlation was found between the DIs of total and little PRL and creatinine clearance in group CRF. Group T had basal and 20 min serum PRL levels and a pattern of molecular distribution similar to those of group C but total and little PRL DI was lower. These results demonstrate that uremic hyperprolactinemia is due to increases in little PRL without major changes in big and big-big forms of PRL. The reduction of glomerular filtration rate seems to be one of the most important mechanisms responsible for little PRL accumulation.

Adult↗
PubMed1985

Synthesis of PAF-acether and blood volume changes in gram-negative sepsis.

Gram-negative sepsis was induced in rats by intraperitoneal injection of Escherichia coli. The development of bacterial peritonitis and septicemia was monitored by counting the number of peritoneal cells and by performing cultures of blood samples. Mortality reached a 50% rate when rats were injected with 2 X 10(8) colony-forming units. Rats injected with the doses of bacteria which induced mortality showed a time- and dose-dependent increase of vascular permeability as judged by the presence of abundant peritoneal exudate and by the depletion of the circulating volume. In order to know whether the generation of PAF-acether could be involved in the development of the permeability changes, the formation of this mediator was measured in the peritoneal cells and spleen of animals at different times and in response to different doses of E. coli. Significant amounts of PAF-acether could be obtained preceding the development of blood volume depletion in response to the injection of doses of E. coli which induced both mortality and the development of permeability. These data suggest that PAF-acether might be one of the inflammatory mediators involved in the pathogenesis of the hemodynamic changes observed in endotoxemia.

Animals↗
PubMed1985

Lack of effect of indomethacin on systemic and splanchnic haemodynamics in portal hypertensive rats.

Portal hypertension was produced experimentally in rats by partial constriction of the portal vein. Twelve rats were injected daily with indomethacin, 4 mg/kg body weight, and 12 with the vehicle (80% ethanol, 0.5 ml/day). There were no differences in portal-systemic shunts nor systemic or splanchnic haemodynamics between indomethacin-treated and untreated rats. These results suggest that cyclo-oxygenase products do not play a significative role in haemodynamic alterations shown by portal-ligated rats.

6-Ketoprostaglandin F1 alpha↗
PubMed1985

Systemic and splanchnic hemodynamic disturbances in conscious rats with experimental liver cirrhosis without ascites.

Rats with CCl4-induced cirrhosis of the liver show histological and clinical features that closely resemble those of the disease in humans. Metabolic cages were used and hemodynamic studies (15-micrograms radioactive microspheres) were performed on 10 conscious, nonascitic, cirrhotic rats and in 10 control rats. Compared with control animals, cirrhotic rats showed lower sodium excretion (0.80 +/- 0.07 vs. 1.01 +/- 0.07 meq/day), total solute excretion (12.52 +/- 0.79 vs. 19.38 +/- 3.7 mosmol/day), and increased aldosterone excretion. No differences were observed in urinary epinephrine and norepinephrine excretion. Cirrhotic rats showed also slight hypotension, increased cardiac output (48.97 +/- 3.94 vs. 26.97 +/- 2.3 ml X min-1 X 100 g-1) without tachycardia, and decreased total peripheral resistance, which was mainly attributed to reduced renal and skeletal muscle resistances with increased blood flow throughout these areas. Cirrhotic rats showed increased hepatic vascular resistances by both portal and arterial inputs with portal hypertension (16.15 +/- 1.01 vs. 9.60 +/- 0.77 cmH2O) but without differences in total hepatic blood flow or portal-systemic shunt rate with respect to control rats. Plasma renin content was not significantly different between the groups of rats. From these data it can be concluded that nonascitic, cirrhotic rats show a hyperdynamic circulatory state, which seems to be caused by a peripheral vasodilation of unknown mechanism; portal-systemic shunting does not seem to be a necessary condition for the hyperdynamic status at this early stage of the hemodynamic disturbances.

Animals↗
PubMed1985

Immunological abnormalities in healthy relatives of patients with IgA nephropathy.

Patients with IgA nephropathy have elevated serum levels of polymeric IgA, probably due to an increase in their synthesis by peripheral blood mononuclear cells, and specific abnormalities in the immunoregulation of IgA. The existence of familial cases of IgA nephropathy, as well as the published association of this nephropathy with some antigens of the HLA system, decided us to test the hypothesis that some of these alterations might be genetically controlled. For this reason we studied some of these immunological assays in 25 first-degree relatives of 7 patients with IgA nephropathy and 22 control subjects matched for age and sex. An abnormal immunological assay was found in at least 1 relative of all families examined. Thus, 16 of 25 relatives had a significant increase in the percentage of polymeric IgA-producing cells after 7 days of culture in the presence of pokeweed mitogen. Some derangement in the concanavalin A generation of specific IgA suppressor cells was found in 11 out of 25 relatives. These results are, though in lower frequency, similar to those seen in patients and suggest that the IgA-immunological abnormalities observed are genetic markers, even if they cannot by themselves explain the pathogenesis of the IgA nephropathy. The absence of IgA immune complexes seen in relatives as well as their high prevalence in patients suggest that in predisposed subjects other factors (genetic or not) are required for the development of IgA nephropathy.

Adolescent↗
PubMed1985

Effect of chronic and progressive increase of portal venous pressure on renal handling of water and electrolytes in rats.

Systemic and splanchnic hemodynamics and the changes in renal function induced by saline infusion (3% body weight) were studied in rats with a chronic and progressive model of portal hypertension (CPH) and in a control group. CPH rats showed a hyperdynamic circulatory status with increased cardiac output, decreased total peripheral resistances, and decreased portal inflow. Portal hypertension was accompanied by intrahepatic hypertension. Clearance studies revealed that in basal conditions CPH rats showed lower glomerular filtration rate (GFR), renal plasma flow (RPF), urinary flow, and potassium excretion than control rats, while the difference in Na and Cl excretion was not statistically significant. After saline infusion (3% body weight, 15 ml/h), differences in GFR and RPF became nonsignificant, but CPH rats showed lower Na, Cl and osmolar excretion and urinary flow than control rats. In basal conditions, plasma renin content was higher in CPH than in control rats, and decreased in both groups after volume expansion, the difference then being not statistically significant. These results demonstrate that chronic portal hypertension results in impairment of GFR, RPF and renal handling of water and electrolytes and suggest the involvement of a hepatorenal sympathetic reflex in these alterations. This reflex could be stimulated by the increase in intrahepatic pressure rather than by portal hypertension per se.

Animals↗
PubMed1985

Vaccination against hepatitis B in renal dialysis units: short or normal vaccination schedule?

Three I.M. injections of hepatitis B vaccine (Merck Sharp & Dohme) were administered, according to the recommended schedule (0, 1, 6 mos), to seronegative individuals of one renal dialysis unit (33 patients, 58 health care personnel) and, according to a shorter regimen (0, 1, 3 mos), in another unit of similar characteristics (30 patients, 53 health care personnel). Staff members and renal patients received, respectively, 20 y 40 mcg of vaccine per injection. In the early vaccination phase, the two regimens did not lead to a difference in seroconversion rates nor in anti-HBs titers. After a 9-month surveillance, lower seroconversion rates, although not significant, were observed with the accelerated regimen among staff members (84.2%) and renal patients (79.2%) as compared with 93% and 87.5%, respectively, following the normal schedule. At the same time, anti-HBs titers were significantly lower (p less than 0.001) in the staff (316 RIA U) and patients (93 U) vaccinated according to the short regimen than in their respective counterparts (4196 and 1047 U) assigned to the normal schedule. A fourth dose of vaccine given to subjects with low and no anti-HBs titers significantly increased seroconversion and anti-HBs levels, although with little success among the former non-responders.

Adult↗
PubMed1984

Immunoreactive pancreatic polypeptide components in plasma from normal subjects and patients with chronic renal failure in basal and postprandial conditions.

Gel filtration of plasma from normal subjects and patients with chronic renal failure (CRF) yielded four immunoreactive human pancreatic polypeptide (IRhPP) peaks of approximately greater than 20,000, 10,000, 4200, and 2000 daltons. In normal subjects, the basal plasma distribution was 36 +/- 2%, 16 +/- 3%, 25 +/- 1% and 23 +/- 2%, respectively. In the CRF patients, the total plasma IRhPP was close to ten times higher than in the normal group. This difference was due to an increase in IRhPP10000 and IRhPP4200 plasma levels. After a standard breakfast, plasma IRhPP10000 and IRhPP4200 levels increased in the normal subjects and in the CRF patients, while the levels of the other two plasma components were not affected by the meal. In a patient with multiple endocrine adenomatosis type 1, the basal plasma levels of IRhPP10000 and IRhPP4200 were, respectively, 41 and 44 times higher than the mean value in the normal subjects; these fractions appeared to be further increased after breakfast. In trying to characterize the IRhPP10000, it was found that treatment with urea, guanadium hydrochloride, and acetic acid (pH 2.2) did not alter its molecular size, whereas limited trypsin treatment was able to destroy part of the immunoreactivity and to produce greater than 20,000-dalton and 4200-dalton immunoreactive materials. Plasma IRhPP10000 seems to be a co-secretory product of the PP cell, and the kidney plays a role in its catabolism as well as in that of the IRhPP4200 component. The IRhPP10000 component may correspond to a PP precursor.

Adult↗
PubMed1984

The role of IgA and IgG immune complexes in IgA nephropathy.

The presence of circulating immune complexes in 54 patients with IgA nephropathy has been studied by two different techniques. 64% of the patients had IgG immune complexes and 37% had IgA immune complexes, both determined with the Raji cell assay, and 48% of patients had IgA immune complexes with the anti-IgA inhibition binding assay (anti-IgA Inh BA). In sequential sera from individual patients, immune complexes remained persistently positive or negative in more than 50% of the cases being intermittently in the rest. The immune complexes detected by the Raji cell assay were mostly of 7-13S in size, while those detected by anti-IgA Inh BA were bigger. There was a good correlation between the serum levels of polymeric IgA and the presence of IgA complexes (Raji cell assay). A certain correlation (p less than 0.05) was found between these IgA immune complexes and the clinical activity assessed by the hematuria. A similar correlation (p less than 0.05) was found with specific polymeric IgA immune complexes studied by a method recently described. No relationship was observed between the presence of any HLA antigens and the existence of circulating immune complexes. These results support the contention that IgA immune complexes, especially those composed of polymeric IgA, may have a role in the pathogenesis of IgA nephropathy. Moreover, the high serum levels of polymeric IgA observed in these patients could contribute to the slow clearance and long persistence in the circulation of IgA immune complexes with their subsequent deposition at the glomerular mesangium.

Adolescent↗
PubMed1984

Phenytoin in IgA nephropathy: a long-term controlled trial.

The final report of a long-term nonrandomized controlled trial of phenytoin therapy in patients with IgA nephropathy is presented. The mean time period of follow-up was 17 months (range 6-48) in the treated group (41 patients) and 14 months (range 6-36) in the nontreated group (32 patients). Both groups were comparable in age, sex, onset of the nephropathy, blood pressure and renal function. The number of episodes per year of macroscopic hematuria decreased in both groups, but was significantly lower at each time period in the treated group than in the control one. The diminution of microhematuria only occurred in the treated group. 1 patient in each group developed advanced renal failure. The mean serum IgA concentration diminished significantly in the treated group, as early as 6 months, but not in the nontreated group. There was a certain association between the presence of the HLAA2 and BW 35 antigens and the lowering of serum IgA. A normalization of the high serum levels of polymeric IgA occurred in the treated patients. A marked diminution of the Raji IgA immune complexes, well correlated with hematuria, was only observed in the treated group. However, despite the diminution of the serum IgA levels, the disappearance of the potential pathogenic IgA immune complexes and the hematuria in a number of treated patients, a progression in the percentage of global or focal glomerular sclerosis and/or vasculointerstitial lesions was seen in some of them. It is concluded that phenytoin decreases the clinical activity and corrects some of the immunological alterations of a certain number of patients with IgA nephropathy but has no valuable effects on the renal lesions. The overall results of this trial do not suggest the employment of this drug in patients with IgA nephropathy and normal renal function. Our data also suggest that a nonimmunological mechanism may be of importance in the progression of chronic renal damage in this disease.

Adolescent↗
PubMed1984

Prolactin plasma levels and its size heterogeneity in acutely uremic rats.

The size distribution pattern of circulating rPRL was studied in intact control (C) rats and in three uremic models, namely urine autoinfusion (UA), bilateral ureteral ligation (BUL), and bilateral nephrectomy (BNx). Plasmas were chromatographed by gel filtration in Sephadex G-100. Rat PRL was measured by RIA. The rPRL levels as well as the size distribution pattern of UA were similar to that of C. BUL and BNx showed a similar degree of hyperprolactinemia which corresponded to an increase in little rPRL. The results suggest that acute uremic hyperprolactinemia seems to be the result of accumulation of little rPRL. Acute uremia by itself does not increase rPRL plasma levels nor does it seem to affect the size distribution pattern of circulating rPRL.

Animals↗
PubMed1984

Splanchnic and systemic hemodynamic alterations in chronic, progressive portal hypertensive rats.

Systemic and splanchnic hemodynamics were studied by using the radioactive microsphere technique, in rats in which a chronic and progressive portal or intrahepatic hypertension was produced by the placement of a nonconstricting, well fitted ligature around the portal or suprahepatic vein when the rat weighted about 100 g. The hemodynamic measurements were performed 80-90 days after ligature placement. Suprahepatic ligated rats presented portal and intrahepatic hypertension, but nonportal-systemic shunts (PSS). The only hemodynamic disturbance observed was a decrease in renal blood flow. Portal ligated rats showed a wide range of PSS and were divided in two subgroups. The subgroups with high PSS rate (greater than 10%) showed increased cardiac output and plasma renin content, as well as decreased splanchnic blood flow, portal venous inflow, hepatic blood flow and renal blood flow. Low portal-systemic shunts subgroups showed decreased cardiac output while its distribution was similar to the control rats. There was no correlation between portal pressure and shunt rate. Low shunt groups, furthermore, showed increased levels of plasma renin concentration.

Animals↗
PubMed1983

Presence in normal human urine of a hypotensive and platelet-activating phospholipid.

Urine from normotensive volunteers and patients with systemic lupus erythematosus glomerulonephropathy was sequentially concentrated by negative-pressure ultrafiltration, dialyzed against distilled water, and extracted into the chloroform phase of a mixture of organic solvents(chloroform:methanol:water, 1:1:0.9 vol/vol). The lipid fraction was further purified by thin-layer chromatography on silica gel plates using neutral, acidic, and basic mixtures of organic solvents and it was then tested for its ability to induce the release of [3H]serotonin from rabbit platelets. All of the samples contained a platelet-activating moiety similar to a synthetic platelet-activating factor (PAF-acether) on the basis of its chromatographic behavior, resistance to the pretreatment of platelets by 10(-6) M indomethacin, and loss of activity by alkaline methanolysis or treatment by phospholipases A2, C, and D. Cross-densensitization experiments between synthetic PAF-acether and the urine factor showed that both compounds act on platelets through the activation of the same putative receptor. Further, the urine factor induced hypotension when intra-arterially injected in normotensive rats, and this activity was also abrogated by alkaline methanolysis. In summary, these data provide evidence of the presence in normal human urine and, probably, of the release by the kidney of a lipid factor with platelet-activating and hypotensive activity whose general structure seems to be alkyl-acyl-glyceryl-phosphorylcholine and, therefore, is similar to the structure of the inflammatory mediator PAF-acether and the antihypertensive polar renomedullary lipid.

Animals↗