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Biomedical subjects

G Mayor

Publications and source records attributed to G Mayor.

At least 19 recordsLinked to original sources

Increased serum concentrations of procollagen peptides in essential hypertension. Relation to cardiac alterations.

BACKGROUND: The serum concentrations of two procollagen-derived peptides, procollagen type III amino terminal peptide (PIIIP) and procollagen type I carboxy terminal peptide (PIP), have been proposed as useful markers of the tissue synthesis of collagen type III and type I, respectively. Therefore, this study was designed to evaluate fibrogenic activity in patients with essential hypertension by measuring serum PIIIP and PIP. Furthermore, since hypertensive heart disease is characterized by myocardial accumulation of collagen type III and type I, a second aim of the study was to assess whether some relation exists between the serum concentrations of PIIIP and PIP and several parameters of left ventricular anatomy and function in hypertensive patients. METHODS AND RESULTS: The study was performed in 50 patients with never-treated essential hypertension and in 30 normotensive control subjects. Measurements were repeated in 43 hypertensive patients after 6 months of treatment with the angiotensin-converting enzyme inhibitor lisinopril. The serum concentrations of PIIIP and PIP were measured by specific radioimmunoassay. Two-dimensional, targeted M-mode and Doppler ultrasound recordings were obtained in every subject to determine several parameters of the left ventricle anatomy and function. Ambulatory ECG monitoring was performed in each patient, and the recorded ventricular arrhythmias were categorized according to Lown-Wolf classification. Baseline serum PIIIP and PIP were increased (P < .001) in hypertensive patients as compared with normotensive subjects. An inverse correlation was found between serum PIIIP and the ratio between maximal early transmitral flow velocity and maximal late transmitral flow velocity measured during diastole (r = .3786, P < .01) in the group of hypertensive patients. Serum PIP was correlated directly with the left ventricular mass index (r = .3277, P < .05) in the group of hypertensive patients. Serum PIP concentrations increased in parallel with the increase in the grade of ventricular arrhythmias in the group of hypertensive patients. Treated patients attained normalization in blood pressure, amelioration of diastolic filling, regression of left ventricular mass index, and a diminution in the number of daily ventricular extrasystoles. In addition, serum PIIIP and PIP concentrations decreased significantly (P < .001) to normal values in patients treated with lisinopril. CONCLUSIONS: These findings suggest that tissue synthesis of collagen type III and type I is abnormally increased in essential hypertension and can be normalized by treatment with lisinopril. On the other hand, our results suggest that serum PIIIP and PIP are related to several anatomic and functional alterations of the hypertensive left ventricle. Serum procollagen peptide measurements may therefore provide indirect diagnostic information on the myocardial fibrosis associated with arterial hypertension.

Collagen

Treatment with lisinopril normalizes serum concentrations of procollagen type III amino-terminal peptide in patients with essential hypertension.

Procollagen type III amino-terminal peptide (PIIIP) is cleaved off procollagen type III during the biosynthesis of type III collagen. Thus, to assess the synthesis of collagen type III in essential hypertension, we determined the serum concentrations of PIIIP in 24 patients with never-treated essential hypertension and in 30 normotensive controls. In addition, serum concentrations of PIIIP were measured in 15 patients after receiving lisinopril during 6 months. Serum PIIIP was higher in hypertensives than controls (11.20 +/- 0.76 v 8.47 +/- 0.77 ng/mL, mean +/- SEM, P < .01). A direct correlation was found between serum PIIIP and plasma renin activity (r = 0.54, P < .01) in the group of hypertensives. In addition, serum PIIIP was correlated inversely with maximal early transmitral flow velocity measured during diastole by Doppler echocardiography (r = -0.74, P < .001) in the group of hypertensive patients. The serum PIIIP levels decreased significantly in patients treated with lisinopril (11.76 +/- 0.84 v 8.47 +/- 0.66 ng/mL, P < .01). A significant increase of plasma renin activity and a significant decrease of plasma aldosterone was observed in these patients after treatment with lisinopril. These results suggest that increased collagen type III synthesis is present in patients with essential hypertension. Abnormal synthesis of collagen type III in essential hypertension may be related to the activity of circulating renin-angiotensin-aldosterone system. Whether an excessive synthesis of myocardial collagen type III is responsible for increased serum PIIIP present in essential hypertension deserves further investigation.

Adult

Effects of antihypertensive therapy on left ventricular hypertrophy of essential hypertension: a role for insulin-like growth factor I?

In a previous work we have found than an association exists between the presence of left ventricular hypertrophy (LVH) and increased circulating levels of insulin-like growth factor I (IGF-I) in essential hypertension. To address whether this association is of pathophysiological relevance the relationship between echocardiographically determined LVH and IGF-I levels was investigated in 49 patients with essential hypertension before and after one year of antihypertensive treatment with different regimens (nonpharmacological measures, bisoprolol, captopril). The control group consisted of 30 normotensive subjects without LVH. Before treatment IGF-I levels were higher (p < 0.05) in hypertensives with LVH, n = 17, (81.3 +/- 14.3 ng/ml) compared with hypertensives without LVH, n = 32, (57.4 +/- 3.9 ng/ml) and controls (61.3 +/- 3.9 ng/ml). A positive correlation was found between IGF-I levels and LVMI in the whole group of hypertensives (r = 0.32, p < 0.05). After one year of treatment hypertensives with initial LVH separated in two subgroups: those in which LVH regressed (n = 10) and those in which LVH persisted (n = 7). A similar diminution of BP was observed in the two subgroups of hypertensives. The IGF-I levels decreased significantly in patients in which LVH regressed (101.6 +/- 21.7 vs. 61.2 +/- 8.5 ng/ml; p < 0.05) and increased slightly in patients in which LVH persisted (51.2 +/- 8.9 vs. 68.5 +/- 7.9 ng/ml). Six patients in which LVH regressed showed a diminution of IGF-I after treatment. These six patients had received captopril as treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult

[Effects of captopril on left ventricular morphology and function in essential arterial hypertension].

BACKGROUND: The presence of diastolic dysfunction in a hypertensive patient is not necessarily associated to the existence of left ventricular hypertrophy. The aim of this study was to determine whether the reduction of the left ventricular mass in hypertensive patients treated with captopril is accompanied by an improvement of the diastolic filling indexes. METHODS: Nineteen patients with essential hypertension were studied before and after one year of treatment with captopril. Different morphological indexes and diastolic function of the left ventricle were evaluated by mode M and Doppler echography. RESULTS: The indexes of left ventricular mass diminished significantly with treatment with captopril. The thickness of the ventricular walls diminished with treatment although not significantly. No significant modification was observed in the indexes of diastolic function (quotient of speed of protodiastolic filling/speed of telediastolic filling and time of deceleration of transmitral fluid during diastole) following the treatment period. CONCLUSIONS: Diminution of the left ventricular mass induced by captopril in hypertensive patients is not accompanied by an improvement in ventricular filling. It is suggested that myocardial hypertrophy is not responsible for diastolic dysfunction of arterial hypertension.

Adult

Admission screening by thyroid function tests in an acute general care teaching hospital.

To determine the incidence of unrecognized thyroid disease among admissions to a large acute care university teaching hospital, 364 samples taken on consecutive admissions were assayed for thyroid-stimulating hormone (TSH) and free thyroxine index (FTI). Patients with abnormal test results were further evaluated by determination of antimicrosomal and antithyroglobulin antibodies, and charts were reviewed for evidence of prior diagnosis of thyroid disease, especially severe illness, drug treatment that might affect thyroid function tests, and prior diagnosis of thyroid disease. Results of subsequent thyroid function tests performed during the patient's hospitalization were correlated with the admission serum assays, and data on subsequent testing during the following 6 months were also obtained. A total of 3.9% of patients had significantly depressed TSH, and 11.1% of values were significantly elevated. A total of 11.3% of patients had significantly low FTI values, and 1% had significantly elevated values. A total of 7.4% appeared to have the euthyroid sick syndrome, 5.8% appeared to have unrecognized or undertreated primary thyroid failure, 6% had apparent subclinical hypothyroidism, 2% were thyrotoxic, and 2.8% (all women) had suppressed TSH levels for inapparent reasons. Limiting testing to patients over 49 years of age, or to women, would have missed many individuals with abnormal test results. Considering widespread availability of tests, relative costs, and value of the information obtained, it is suggested that the FTI determination would provide an appropriate screening test for patients in a population such as this entering a large, acute care general hospital.

Diagnostic Tests, Routine

[The presence of diastolic dysfunction in hypertensive patients without left ventricular hypertrophy].

BACKGROUND: Hypertension is associated with abnormalities in the diastolic left ventricular function. The present study was performed to evaluate whether diastolic function is impaired independently from myocardial hypertrophy. METHODS: 41 patients with essential hypertension who had never received antihypertensive therapy were evaluated. All patients had normal systolic function. VE wave, or early diastolic filling wave, and VA, or late diastolic filling wave, were measured by Doppler echocardiography, and the VE/VA ratio was used as index of diastolic function. RESULTS: The VE/VA ratio was abnormally reduced in 23 patients, of which only 9 had left ventricular hypertrophy on echocardiographic criteria. The patients with a reduced ratio were older (p less than 0.01) than patients with a normal ratio. VE/VA ratio was not correlated with left ventricular mass, but it was correlated with age (r = 0.4186, p less than 0.01). CONCLUSIONS: Left ventricular diastolic function is impaired in hypertension independently from hypertrophy. The myocardial abnormalities associated with aging might be the major determinants of this functional impairment.

Adult

[Association of cardiovascular risk factors in hypertensive patients with left ventricular hypertrophy].

The cardiovascular morbidity-mortality is higher between the patients with essential hypertension and LVH. It is due to effects over heart provoked by the abnormal increment of the myocardial mass. However, the role of others concurrent risk factors must be determined. To analyze this possibility, we studied the distribution of the main cardiovascular risk factors in a population of 50 essential hypertensive patients non treated before. They were shared in two groups: 32 patients with LVH diagnosed by echocardiography (left ventricular mass index greater than 120 g/m2) and 18 patients without LVH. The comparison between both groups showed that the patients with LVH had higher systolic arterial pressure (p less than 0.05), higher mean arterial pressure (p less than 0.05), higher alcohol (p less than 0.01) and tobacco (p less than 0.02) consumption, higher values of triglycerides (p less than 0.05) and uric acid (p less than 0.01), and higher plasma renin activity (p less than 0.05) than those observed in the group without LVH. Plasma cholesterol was also higher (increase of 11%) in patients with LVH; then, in these patients its mean value (245 +/- 12 mg/dl, M +/- SD) was over the top of the normal limit (240 mg/dl), which discriminate the risk of cardiovascular complications for this factor. The following factors: age, sex distribution, diastolic arterial pressure, sedentary life and carbohydrate intolerance, didn't present differences between the groups. These results show that hypertensive patients with LVH, as a group, have others factors of risk, different from ventricular hypertrophy, which favour the high cardiovascular morbidity-mortality of LVH group.

Adult

Microcytic anemia in dialysis patients: reversible marker of aluminum toxicity.

Improvement of microcytic anemia after deferoxamine treatment is described in eight long-term dialysis patients with high serum aluminum concentration and other clinical signs of aluminum toxicity. Hematocrit increase of 3 to 19 vol% was associated with correction of microcytosis, significant reduction in abnormal levels of free erythrocyte protoporphyrins, and amelioration of the bone-related symptoms and neurologic signs of aluminum intoxication. Increase in hematocrit, reversal of microcytosis, and reduction in protoporphyrin levels all correlated with the aluminum burden as indicated by the pretreatment serum aluminum levels and by the peak serum aluminum levels during mobilization with deferoxamine. Furthermore, deferoxamine resulted in marked improvement in anemia despite significant reduction in serum ferritin levels. This reversal of microcytosis with deferoxamine provides objective evidence verifying the toxicity of aluminum, and suggests that microcytosis may be an easily detected marker for both clinical diagnosis as well as response to treatment in some cases of aluminum intoxication.

Adult

Attenuation of experimental tobramycin nephrotoxicity by ticarcillin.

It is well known that in vitro the combination of carbenicillin, ticarcillin, or other antipseudomonal penicillins with gentamicin, tobramycin, or other aminoglycoside antibiotics results in the inactivation of the antibacterial activity of the aminoglycoside. To assess the influence of the in vivo interaction of tobramycin and ticarcillin on experimental nephrotoxicity, male Fischer 344 rats were given either tobramycin alone (120 mg/kg per day), tobramycin (120 mg/kg per day) and ticarcillin (250 mg/kg per day) concomitantly, or the combination of these drugs at the same doses that had been preincubated for 24 h and at the time of delivery contained but 63 and 25%, respectively, of the initial concentrations of tobramycin and ticarcillin as measured by conventional analytical procedures. Initial experiments were conducted to determine the concentrations of the antibiotics in serum achieved after administration of each test solution. After a single dose of the test solution, ticarcillin concentrations in serum were higher and more prolonged in rats given tobramycin plus ticarcillin than in rats given ticarcillin alone. After 7 days of exposure to the test solutions, inulin clearance in animals given tobramycin alone was 0.15 +/- 0.1 (mean +/- 2 standard errors) ml/min per 100 g of body weight as compared with 0.53 +/- 0.1 in rats given tobramycin and ticarcillin concomitantly, 0.59 +/- 0.1 in animals given the partially inactivated tobramycin-ticarcillin mixture, and 0.79 +/- 0.1 in control rats. Although there was some improvement in inulin clearance in the group containing tobramycin alone, the three treatment groups maintained the same rank relationship in inulin clearance through 14 days of treatment. Real histology confirmed the attenuation of tubular injury in animals given tobramycin and ticarcillin concomitantly. There was no evidence of toxicity from the presumed inactivation complexes of tobramycin-ticarcillin. These results document an in vivo protective effect of ticarcillin on experimental tobramycin nephrotoxicity.

Animals

Suppression of parathyroid hormone secretion by aluminum.

The effect of aluminum on parathyroid hormone secretion was examined using collagenase-dispersed bovine parathyroid cells. An increase in the medium aluminum concentration over the range of 0.5 to 2.0 mM, in low calcium medium, progressively inhibited the secretion of radioimmuno-assayable hormone. At 2.0 mM aluminum hormone secretion was inhibited by 68% while high medium calcium, without aluminum, maximally inhibited parathyroid hormone secretion only 39%. Individually, 2.0 mM aluminum or 2.0 mM calcium inhibited isoproterenol-stimulated hormone secretion by 43%. Either metal suppressed basal and isoproterenol-stimulated cyclic AMP levels of the parathyroid cells. That the inhibitory effect of aluminum on parathyroid hormone secretion was not due to an irreversible toxic effect was demonstrated by a restoration of normal secretion when cells were returned to 0.5 mM calcium medium without aluminum. The incorporation of [3H]leucine into total cell protein, parathyroid secretory protein, proparathyroid hormone, or parathyroid hormone was not affected by aluminum. The secretion of radiolabeled protein was, however, inhibited by aluminum. These results suggest that aluminum does not affect protein biosynthesis of the parathyroid cell or the conversion of proparathyroid hormone to parathyroid hormone. Aluminum appears to directly affect the secretion of protein from dispersed parathyroid cells.

Aluminum