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Biomedical subjects

J Quiroga

Publications and source records attributed to J Quiroga.

At least 91 records · Page 5Linked to original sources
PubMed1990

Family history of ischemic heart disease with respect to mean twin-pair cholesterol and subsequent ischemic heart disease in the NHLBI twin study.

This study examines the independent and interactive effects of family history scores (FHxS) for the prevalence of ischemic heart disease with plasma lipids and subsequent morbidity and mortality from ischemic heart disease. FHxS were calculated for 514 sets of middle aged male twins who participated in the entry examination of the NHLBI Veteran twin study in 1969-1973. Comparison of the FHxS with the level of plasma total cholesterol and HDL cholesterol (HDLc) paralleled earlier reported findings in young adults; individuals with high total cholesterol in two exams 8-12 years apart had significantly (P less than .01) higher FHxS. The same relationship was noted when using the mean twin-pair cholesterol level at the initial exam when the twins were in their 40s. Using the pair means over two exams as the cotwins aged into their 50s, the association of FHxS with total cholesterol declined and pairs with HDLc persistently in the highest quintile at both exams had significantly (P less than .01) lower FHxS. The changes in the pattern of association of lipid fractions with FHxS with age parallel the reported age decline of total cholesterol as a risk factor for heart disease. Assessment of ischemic heart disease events up to January 1988 revealed a highly significant association (P less than .0001) of later ischemic heart disease events with FHxS. At each level of lipid categorization pairs who later had events had higher FHxS than those without any subsequent heart disease; these differences were significant in all but the low risk lipid groups (low total cholesterol, high HDLc, and low total cholesterol/HDLc ratio). We conclude that FHxS is related to total cholesterol and HDLc but also is an independent predictor of subsequent ischemic heart disease after 14-18 years of follow-up.

Adult↗
PubMed1989

Systemic and regional hemodynamics in patients with liver cirrhosis and ascites with and without functional renal failure.

Systemic, femoral, and renal hemodynamics were evaluated in 7 control subjects and 20 cirrhotic patients with ascites, 14 of them without (group A) and 6 with (group B) functional renal failure. Hyperdynamic systemic circulation, increased plasma volume, and hyperreninism were present in groups A and B. These changes were more severe in group B, which showed, as compared with group A, lower total vascular resistances and mean arterial pressure together with increased cardiac index and plasma renin activity. Significant differences in regional hemodynamics were also observed between groups. In group A, femoral and renal fractions of cardiac output were respectively increased and reduced as compared with controls. By contrast, in group B, both fractions of cardiac output were reduced when compared either with controls or with group A. In the entire patient group there was a close direct correlation between femoral and renal fractions of cardiac output (r = 0.88; p less than 0.001) and both of them correlated independently with total vascular resistances (r = 0.79; p less than 0.001 in both cases). These results indicate that, in nonazotemic cirrhotics with ascites, vasodilatation in extrasplanchnic areas contributes to the genesis of the hyperdynamic circulation. The presence in group B of a reduced flow to extrasplanchnic territories, in association with an increase of the hyperdynamic circulatory status, suggests that exacerbation of splanchnic vasodilatation is involved in the development of the hepatorenal syndrome. Finally, in cirrhosis, the changes that occur in systemic hemodynamics appear to influence renal function and renal blood flow.

Aldosterone↗
PubMed1989

Renal hemodynamics and the renin-angiotensin system in cirrhosis.

The interrelationship between renal hemodynamics and the renin-angiotensin-aldosterone system in 28 nonazotemic cirrhotic patients has been studied. Patients were divided into three groups: A) Patients without ascites nor edema; B) Patients with ascites and a relatively high sodium excretion (41.9 +/- 12.9 mmol/day); and C) Patients with ascites and very low sodium excretion (4.8 +/- 0.6 mmol/day). Renin and aldosterone levels significantly increased in group C. A significant correlation was observed between plasma aldosterone concentration and urinary sodium excretion, and between plasma renin activity and aldosterone levels. There were no significant differences in urine flow, glomerular filtration rate, effective renal plasma flow, or renal blood flow between the three groups of patients, in spite of marked differences in renin and aldosterone levels. Renal perfusion was not related to plasma renin activity either in the overall sample of patients or in the individual groups. These results show that factors other than total renal perfusion are involved in renin secretion in cirrhosis.

Adult↗
PubMed1986

Determination of 2,3-dinor-6-ketoprostaglandin F1 alpha in urine samples by liquid chromatography and radioimmunoassay.

A method for 2,3-dinor-6-ketoprostaglandin F1 alpha quantification based on high-performance liquid chromatography-radioimmunoassay is described. Samples are acidified to pH 3 and processed through C18 disposable cartridges. The prostanoids are eluted with methyl formate and further separated on a reversed-phase column using acetonitrile-acetic acid-triethylamine buffer (32:68). Studies of the effect of eluent pH were performed in order to optimize resolution and separation of 2,3-dinor-6-keto-PGF1 alpha from other prostanoids. Eluates were collected and assayed by radioimmunoassay using a heterologous system, with 6-keto-PGF1 alpha as radioligand and an antiserum with high cross-reactivity for 2,3-dinor-6-keto-PGF1 alpha. Sensitivity, precision and accuracy of the assay procedure are reported together with the validation of its specificity. The proposed method has been applied to the determination of this prostacyclin metabolite in human urine.

6-Ketoprostaglandin F1 alpha↗
PubMed1986

Increased synthesis of systemic prostacyclin in cirrhotic patients.

Urinary excretion of two prostacyclin metabolites was investigated in 48 subjects: 8 controls and 40 cirrhotics (9 without ascites, 22 with ascites and preserved renal function, and 9 with functional renal failure). Urinary 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha), believed to reflect renal prostacyclin production, was significantly increased in patients without ascites and in ascitic patients with preserved renal function, but cirrhotics with renal failure showed rates similar to controls. Excretion of 2,3-dinor-6-keto-PGF1 alpha (PGI-M), the major urinary metabolite of systemic prostacyclin, was increased in all groups of patients, including those with renal failure. A single dose of sulindac, a renal-sparing prostaglandin synthesis inhibitor, reduced PGI-M but not 6-keto-PGF1 alpha in 5 cirrhotic patients. This would be consistent with the predicted renal origin of the latter and the systemic origin of the former. Ascitic patients with high urinary excretion of PGI-M (above the median value) showed significantly lower mean arterial pressure and higher plasma renin activity and aldosterone than patients with excretion below the median. Urinary 6-keto-PGF1 alpha was higher in patients with low PGI-M. Finally, creatinine clearance corrected excretion of PGI-M, as an estimation of relative plasma levels correlates both with plasma renin activity and plasma aldosterone in the 31 subjects who presented with ascites. It is suggested that enhanced synthesis of systemic prostacyclin may influence hemodynamic changes in patients with liver cirrhosis. Overproduction of systemic prostacyclin in the absence of increased renal prostacyclin synthesis appears to be characteristic of patients with functional renal failure.

6-Ketoprostaglandin F1 alpha↗
PubMed1986

Effect of spironolactone on renal prostaglandin excretion in patients with liver cirrhosis and ascites.

The effect of spironolactone on the urinary excretion of prostaglandins was studied in patients with liver cirrhosis and ascites. Patients were kept in bed and given a sodium-restricted diet for at least 4 days before spironolactone treatment was considered. Starting from the 5th day of protocol, patients were treated with this diuretic if their spontaneous weight loss had been less than 600 g during the 2 previous days. Patients were distributed in groups according to weight loss during the first 4 days on diuretic therapy: Group I (high responders), II (medium responders) and III (low responders). Group I patients showed higher basal values (4th day of protocol) of urinary sodium (P less than 0.02) and urinary 6-keto-PGF1 alpha (P less than 0.02) than the other patients, but there were no significant differences in the basal excretion rates of PGE2 nor TXB2 among the groups. The therapeutic requirement for spironolactone treatment in patients from Group I was delayed as compared with the other two groups (P less than 0.001) due to the fact that their spontaneous weight loss took place over a long period. For all patients, spironolactone administration produced a significant increase in 6-keto-PGF1 alpha excretion (P less than 0.01) without affecting significantly urinary elimination of PGE2 nor TXB2. A close relationship was found between the spironolactone-induced increments in urinary sodium and urinary 6-keto-PGF1 alpha excretion (r = 0.74, P less than 0.001). It is suggested that the ability of the kidney to synthetize prostacyclin can influence the natriuretic response to spironolactone therapy in patients with liver cirrhosis.

6-Ketoprostaglandin F1 alpha↗
PubMed1986

Effect of sulindac on prostaglandin excretion and renal function in cirrhotic patients with ascites.

The effect of sulindac, a nonsteroidal anti-inflammatory drug, on renal prostaglandin synthesis and renal function variables was investigated in six cirrhotic patients with tense ascites and marked sodium retention. We studied serum thromboxane (TXB2) production, urinary prostaglandin excretion (6-keto-prostaglandin F1 alpha and TXB2) and renal function before and after administration of a therapeutic dose of sulindac (400 mg). After treatment, no significant changes were observed in urinary prostaglandin excretion, serum creatinine concentration, urine volume, or urinary sodium and creatinine clearance, whereas the serum TXB2 concentration was reduced in 89%. In five patients systemic prostaglandins were inhibited, but renal excretion remained unchallenged. However, one patient showed marked reduction of urinary prostaglandins associated with a depression of renal function. The study suggests that sulindac could be a safe substitute for other nonsteroidal anti-inflammatory drugs in cirrhotic patients with ascites. Further pharmacological trials seem to be warranted.

Ascites↗
PubMed1984

Intracerebroventricular infusion of sodium chloride-rich artificial cerebrospinal fluid in rats induces natriuresis and releases an inhibitor of prostaglandin synthesis.

Urinary sodium excretion in anaesthetized rats subjected to high-sodium artificial cerebrospinal fluid (CSF) infusion into the lateral brain ventricle, was significantly higher than in rats infused with normal-sodium CSF. Urinary immunoreactive 6-ketoprostaglandin F1 alpha, the stable derivative of prostacyclin, was significantly reduced in the high-sodium CSF group, as compared with the normal-sodium CSF group. When dog aortic endothelium was incubated in the presence of plasma, endothelial prostacyclin production was found to be inhibited by plasma from rats infused with high-sodium CSF compared with the effect of plasma from the rats infused with normal-sodium CSF. Our results indicate that intracerebroventricular infusion of high-sodium CSF induces a natriuretic response and is associated with the appearance of a humoral factor which blocks prostacyclin biosynthesis.

6-Ketoprostaglandin F1 alpha↗
PubMed1980

[Psoriatic arthropathy. A study of its frequency and clinical features in 112 psoriatic patients].

In order to determine the incidence and clinical features of psoriatic arthropathy 112 psoriatic patients have been studied. The following conclusions have been shown: 1. the incidence ratio male: female was near 2: 1 in the skin disease; 2. a prevalence of 15% has been observed in the psoriatic arthropathy, showing similar incidence in both sexes; 3. when the onset of the skin disease were analyzed either alone or with arthropathy, different frequency profiles were demonstrated; that suggest they are different biological events; 4. neither the age of onset nor the severity of the arthropathy, show any relationship with the severity of the skin disease; 5. both, negative latex and the elevation of the sedimentation rate are of value for diagnostic purposes.

Adolescent↗