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Biomedical subjects

F Escobar-Jimenez

Publications and source records attributed to F Escobar-Jimenez.

18 recordsLinked to original sources
PubMed1995

Circulating alpha-actin in non-insulin-dependent diabetics with autonomic dysfunction.

Silent myocardial ischemia in non-insulin-dependent diabetic patients occurs frequently in association with autonomic dysfunction, suggesting that diabetic neuropathy may be involved in the development of this disorder. Repeated episodes of silent myocardial ischemia can induce myocardial necrosis. Recently, actin was detected with Western blotting in the serum of patients with acute myocardial infarction and angina pectoris. We found that a large proportion of non-insulin-dependent diabetic patients with neuropathy also have detectable circulating concentrations of alpha-actin, and therefore suggest that the determination by immunoblotting of serum alpha-actin in such patients is an effective method to detect myocardial cell suffering and to identify patients that may need special consideration.

Actins↗
PubMed1995

Increased plasma pancreastatin-like immunoreactivity levels in non-obese patients with essential hypertension.

DESIGN: Pancreastatin, a novel peptide, is known to inhibit insulin secretion and to have a glycogenolytic effect, and is present in many endocrine and chromaffin cells. Both the plasma insulin levels and the adrenergic activity accompanying insulin resistance have been shown to be increased in hypertensive subjects. Our working hypothesis was that pancreastatin might play a role in these pathological phenomena. METHODS: We studied the plasma pancreastatin level in non-obese essential hypertensive patients in response to an intravenous glucose load. We further measured the responses to the glucose challenge of insulin, glucagon, catecholamines and free fatty acids, as well as other factors related to insulin resistance (i.e. lipoproteins and apolipoproteins). We separated the hypertensive patients into three groups according to their response to an oral glucose-tolerance test: normoinsulinaemic, hyperinsulinaemic and glucose-intolerant. Matched normotensive control subjects were also studied. RESULTS: Pancreastatin levels did not change in the control group after the glucose challenge. However, all hypertensive patients showed an increase in plasma pancreastatin levels after glucose loading. The normoinsulinaemic hypertensive patients also had elevated basal pancreastatin levels. The increase in pancreastatin levels was in the ranking: normoinsulinaemic > hyperinsulinaemic > glucose-intolerant. The pancreastatin: insulin ratio showed that the secretion of pancreastatin and insulin may be regulated differently. Basal free fatty acid and glucagon levels were found to be elevated both in the hyperinsulinaemic and in the glucose-intolerant group. Fasting triglycerides levels were increased in all of the hypertensive patients. Other risk factors for coronary artery disease were also found to be altered: elevated very low-density lipoprotein-cholesterol and decreased high-density lipoprotein-cholesterol, with ranking: normoinsulinaemic < hyperinsulinaemic < glucose-intolerant. CONCLUSIONS: These results show an increase in pancreastatin levels in hypertensive patients, suggesting that pancreastatin might play a role in the pathophysiology of essential hypertension.

Adult↗
PubMed1991

Hyperthyroidism due to familial pituitary resistance to thyroid hormone: successful control with 3, 5, 3' triiodothyroacetic associated to propranolol.

We herein describe a family with thyroid hormone resistance. Thyroid hormones and basal TSH were elevated. Pituitary tumor or abnormality in thyroid hormone binding proteins were ruled out by appropriate tests. Mother and sister of the propositus presented similar abnormal hormonal features but no hyperthyroidism. Initially the patient was treated with carbimazole (30 mg/day): three months later a dramatic increase in the size of the thyroid gland and in TSH levels (12.5 to 28 mU/l) were noted. Thereafter, dextrothyroxine (D-T4) and 3, 5, 3'-triiodothyroacetic acid (TRIAC) were given consecutively and treatment was accompanied by a decrease of TSH levels (2 mU/l) but thyroid hormone remained elevated. The symptoms and signs of hyperthyroidism improved with the addition of propranolol (30-60 mg/day). In conclusion, the present report describes a new family with the syndrome of THR and variable degrees of involvement among relatives. We suggest the usefulness of TRIAC therapy to decrease TSH levels and propranolol to improve thyrotoxicosis due to pituitary resistance to thyroid hormone.

Adolescent↗
PubMed1988

Measurement of parathyrin in blood from thyroid veins: two radioimmunoassays compared in patients with primary hyperparathyroidism.

We measured parathyrin (PTH) in peripheral venous blood samples and in thyroid veins (both homolateral and contralateral to the lesion) in 13 patients with surgically confirmed parathyroid adenomas. Two different RIAs were used, one specific to the mid-region of the molecule (44-68, M-PTH), the other specific to the carboxy-terminal region (65-84, C-PTH). With the M-PTH assay we established a statistically significant multiple correlation (P less than 0.05) between the PTH concentrations in blood from the peripheral and thyroid veins; no significant correlation was found when we used the C-PTH assay. Our results confirm the superiority of the M-PTH RIA over the C-PTH RIA for study of hormonal secretion in primary hyperparathyroidism.

Adult↗
PubMed1980

Behavior of secretion in the hypoxia-immobilisation stress on the rat.

Secretin was determined radioimmunologically in portal vein blood and in duodenal mucosa biopsies in stressed male Wistar rats as compared to control animals. The stressed animals showd a significantly higher scretin content of the duodenalmucosa and no different levels of the portal vein blood. A stress ulcer-reducing cimetidine application does not demonstrate any influence of secretin content on duodenal mucosa. The obvious elevation of duodenal secrtin is not the result of an increased gastric acid production, but may be a consequence of a stress-reduced susceptibility of the pancreas to endogenous secretin.

Animals↗
PubMed1978

[A field study with the combination of Pindolol and Clopamid in antihpertensive therapy (author's transl)].

In a field study comprising 678 patients with arterial hypertension efficacy and tolerance of the stable combination VKB 105 consisting of 10 mg Pindolol (Visken) and 5 mg Clopamid (Brinaldix) were investigated. Treatment with 1--2 tablets of VKB per day resulted in a successful therapy in 94% of all patients corresponding on the average to a reduction in blood pressure to 145/85 mm Hg within 14 days. In mean arterial pressures ranging between 120 and 170 mm Hg a positive linear relationship between the individual initial value and the hypotensive effect of the combination could be observed. A controlled omission trial disclosed qualitatively the respective contribution to the effect of the two components Pindolol and Clopamid. With a systematic case control of the serum potassium under the combined therapy with VKB 105 and during a monotherapy with Clopamid and antihypokalaemic effect of Pindolol could be demonstrated diminishing the tendency for potassium loss. The result revealed a far-reaching potassium neutrality of diuresis-depending stimulation of renin by the beta-receptor blocker. In 61 patients altogether subjective side-effects could be recorded, such as vertigo (5%), palpitations (2.8%), fatigue (2%), insomina (1.9%), nausea (1.7%) and vomiting (0.8%). Laboratory controls gave no indication for clinically relevant changes.

Adrenergic beta-Antagonists↗
PubMed1977

Prevention by somatostatin of rise in blood pressure and plasma renin mediated by beta-receptor stimulation.

The interrelationships of increased plasma renin and elevated blood pressure following acute beta-stimulation by orcipernaline and its prevention by somatostatin was studied in normal man. During somatostatin infusion basal values of renin and blood pressure were unchanged. Following orciprenaline both variables increased significantly. Combination of somatostatin and orciprenaline reduced the rise in plasma renin activity by 49%, mean arterial blood pressure by 21% and heart rate by 19%, compared with beta-stimulation alone. The results indicate that the inhibitory action of somatostatin on plasma renin activity may be mediated via beta-receptors. The lesser increase of blood pressure under somatostatin plus orciprenaline also indicates a possible inhibitory effect of somatostatin on beta-adrenergic receptors.

Adult↗
PubMed1977

Somatostatin modulation of pancreatic glucagon, insulin, glucose and free fatty acids following beta-adrenergic stimulation.

This study was undertaken to determine the effect of somatostatin on acute, orciprenaline mediated, beta-adrenergic stimulation of free fatty acids, blood glucose, insulin, and glucagon in healthy subjects. After orciprenaline and somatostatin insulin and glucagon decreased, whereas blood glucose and free fatty acids increased, probably in part as a result of the lesser inhibition of glucagon (50%) than of insulin (83%). From these observations it is tentatively concluded that the inhibitory effects of somatostatin on insulin and glucagon release in man are a consequence of beta-adrenergic receptor involvement. These effects are possibly mediated through increased destruction of cAMP, blocking of camp dependent secretion or impairment of calcium uptake.

Adult↗
PubMed1977

The effect of somatostatin on platelets: in vivo and in vitro studies.

The influence of somatostatin on platelets was studied in healthy volunteers. After a bolus injection of 250 microgram somatostatin followed by a three hour infusion at a rate of 250 microgram somatostatin/hr a statistically significant fall of platelet count and impairment of platelet aggregation was observed. The aggregation inhibiting effect of somatostatin at the end of the three hour infusion is clinically unimportant as compared to the effect of aspirin. In vitro concentrations up to 10.0 microgram somatostatin per ml do not show any effect on platelet aggregation and platelet stickiness. Endocrinologically active doses of somatostatin in short term infusions are very unlikely to cause bleeding disorders.

Adolescent↗
PubMed1976

Inhibition of frusemide-induced hyperreninaemia by growth-hormone release-inhibiting hormone in man.

In a study of the effect of somatostatin (growth-hormone release-inhibiting hormone) on plasma-renin in healthy volunteers, plasma-renin activity was measured by radioimmunoassay after the intravenous administration of somatostatin and also during frusemide-induced hyperreninaemia. While somatostatin was being given, basal values of renin were unchanged. Injection of frusemide alone produced hyperreninaemia; but, under somatostatin, renin release was inhibited by 45%. The results indicate that somatostatin is a potent inhibitor of renin and exerts its effect independent of sodium excretion, which was unchanged under somatostatin. Conceivably, somatostatin plays an important role in the regulation of endogenous renin release.

Adult↗
PubMedDate not supplied

Detection of circulating alpha-actinin in non-insulin-dependent diabetics with autonomic dysfunction.

The presence of cardiac proteins in serum has been related to ischemic heart diseases such as acute myocardial infarction and angina pectoris, which are more frequent in non-insulin-dependent diabetic patients. Silent myocardial ischemia, which is also more frequent in these patients, occurs in association with autonomic dysfunction. We used Western blot analysis to search the myocardial protein alpha-actinin in sera from non-insulin-dependent diabetic patients with or without autonomic dysfunction. Of the 24 diabetic patients with neuropathy, 18 were positive for circulating alpha-actinin; this protein was found in only 1 of the 22 diabetic patients without neuropathy. Our results showed a significant correlation between non-insulin-dependent diabetic patients with neuropathy and detectable circulating alpha-actinin in serum, and suggest that the determination by immunoblotting of serum alpha-actinin in these patients may be an effective method to detect myocardial cell impairment, and to identify diabetic patients that may need special consideration.

Actins↗