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Biomedical subjects

J J Serrano

Publications and source records attributed to J J Serrano.

52 records · Page 3Linked to original sources
PubMed1981

The effect of trypsin of rate, force and cyclic AMP in guinea pig atria.

Trypsin (10(-6)M produced a positive inotropic and chronotropic effect in left and right atria respectively and an increase in cyclic AMP. The effects were blocked by aprotinine while propranolol, phentolamine, promethazine and cimetidine and reserpine pretreatment did not alter trypsin activity. Trypsin effects were potentiated by RO 20,1724, a phosphodiesterase inhibitor. The cardiac effects of trypsin may be due to increase in cyclic AMP and are in agreement with previous work indicating that trypsin can activate cardiac adenylate cyclase.

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PubMed1975

[Experimental study of uterine hypoplasia. II. Effect of treatment with beta mimetics].

After we had made rats' uteri hypoplastic by surgical interference with their blood supply we carried out a second part of our study by treating the animals that had been operated on with a beta-mimetic substance in order to lessen or counter completely the effects of surgical devascularisation. From our results we can conclude in a statistically significant proportion of cases that the effects of devascularisation are cancelled out by the treatment. These facts are explained by taking into account the specific pharmacological effects on the uterus of beta-mimetic substances.

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PubMedDate not supplied

Long-term antidiabetic activity of vanadyl after treatment withdrawal: restoration of insulin secretion?

In its vanadate (V5+) or vanadyl (V4+) forms, vanadium has been demonstrated to possess antidiabetic activity. Oral treatment of streptozotocin (STZ)-diabetic animals with either form is associated with correction of hyperglycemia, and prevention of diabetes-induced complications, although weight gain is unaffected. Vanadium treatment of non-diabetic animals lowers plasma insulin levels by reducing insulin demand, as these animals remain normoglycemic. These results suggest that vanadium has in vivo insulin-mimetic or insulin-enhancing effects, in agreement with several in vitro observations. Chronic treatment with vanadium has also been shown to result in sustained antidiabetic effects in STZ-diabetic animals long after treatment has ceased. Thus, at 13 weeks after withdrawal from treatment, corrected animals had normalized glucose and weight gain, and improved basal insulin levels. In addition, near-normal glucose tolerance was found despite an insignificant insulin response. Since vanadium accumulates in several tissue sites (e.g. bone, kidney) when pharmacological doses are administered, it is possible that stored vanadium may be important in maintaining near-normal glucose tolerance at least in the short-term following withdrawal from treatment. Recently, following withdrawal of vanadyl treatment up to 30 weeks, diabetic animals which had remained normoglycemic and had normalized glucose tolerance showed improvements in plasma insulin levels both in the basal state and in response to oral glucose, as compared to those which had reverted to hyperglycemia. The observed significant improvements in insulin capacity over the long-term ( > 3 months) suggests that a restored and/or preserved insulin secretion may be essential for maintained reversal of the diabetic state over a prolonged period after treatment is withdrawn.

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PubMedDate not supplied

Long-term correction of STZ-diabetic rats after short-term i.p. VOSO4 treatment: persistence of insulin secreting capacities assessed by isolated pancreas studies.

We have previously shown that 3 week oral VOSO4 treatment of streptozotocin (STZ, 60 mg/kg)-induced diabetic rats was able to correct diabetes for 13 weeks after treatment withdrawal. In the present study, we investigated whether a short-term (8 days) i.p. VOSO4 treatment was similarly able to reverse the diabetic state. Insulin secretory capacities were assessed at distance of treatment using the isolated pancreas preparation. Seven treatment-groups were performed: high dose VOSO4-treated diabetics (HVD, 1.3 mM/kg/8 days), food-restricted diabetics (FRD, food adjusted to HVD levels), low dose VOSO4-treated diabetes (LVD, 0.06 mM/kg/day), insulin-treated diabetics (ID, dose adjusted to normalize glycaemia) and VOSO4 (0.06 mM/kg/day) + insulin (dose adjusted to normalize glycaemia in the presence of vanadium)-treated diabetics (IVD), in addition to the corresponding untreated non-diabetic controls (C) and diabetics (D). Our results indicate that long-term correction of diabetes (a) can be obtained after an 8 day treatment using i.p. VOSO4 in diabetic animals retaining some degree of pancreatic function, (b) is not obtained with insulin treatment or food restriction although the association of VOSO4 and insulin was found beneficial, (c) can be prolonged in some individuals for at least 4 months, i.e. in conditions such that tissue vanadium concentrations had returned to values close to pre-treatment levels, (d) is associated with improved and in some cases normalized insulin secretion from isolated pancreas. The protective or corrective role of VOSO4 on diabetes-related pancreatic alterations, as well as the potential of the VOSO4-insulin association should be further studied in view of the possible use of vanadium derivatives in the treatment of diabetes.

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PubMedDate not supplied

Interactive computerized microscopy as a tool for quantifying vascular remodelling effects of diabetes and V1a receptor antagonist SR 49059 on rat mesenteric arterial bed.

A methodology using interactive computerized microscopy (ICM) was developed to quantify in the mesenteric arterial bed the morphometric changes associated with diabetes and the influence of treatment with SR 49059, an antagonist of vasopressin V1a receptors. Four groups of rats were studied: untreated normal (N) or streptozotocin- (60 mg/kg i.v.) induced diabetic (D), and treated (0.4 mg/g SR 49059 included in food) normal (NT) or diabetic (DT) animals. Treatment was initiated 4 days after diabetes induction and continued for 3 weeks. Nested (hierarchical) analysis of variance of ICM data was performed on raw diameter or after logarithmic normalization of area and nuclei values. Diabetes was associated with an increase in arterial diameters, and in total vessel, wall, media, adventitia, and lumen areas. The same parameters, with the exception of the lumen, were also increased in DT as compared to D. The number of nuclei in the media or adventitia was increased in D as compared to N, and in DT as compared to D. In summary, ICM is allowed to further characterize the vascular mesenteric changes and describe for the first time the enlargement of adventitia associated with diabetes. Our study also suggested that the blockade of Via receptors is unable to prevent diabetes-related vascular changes, although the slight increase in food intake associated with SR 49059 treatment may have had an indirect influence on angiopathy development.

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PubMedDate not supplied

[Experimental study of uterine hypoplasia. I. Influence of the vascular factor].

The purpose of the experiment was to prove the importance of the vascular factor in uterine hypoplasia. The animal that was chosen was the rat. The method that was used consisted of devascularisation of one of the two uterine cornua. This was done without altering the blood supply to the ovaries when the animals were 7 weeks of age, which is the immediate prepuberty stage. The results that were obtained were significant whether they were looked at macroscopically, microscopically or by weight. In experimental conditons the hypoplasia was obtained solely due to interference with the blood supply which was carried out surgically.

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PubMedDate not supplied

Cardiac beta-adrenergic receptors in diabetic rats: alteration of guanyl nucleotide regulation.

Cardiac beta-adrenergic receptors (beta AR) were studied in rats after 4 months of diabetes induced by streptozotocin (50 mg/kg, i.v.). Saturation binding studies performed using [125I]-iodocyanopindolol (ICYP) as an antagonist ligand showed that the number and affinity of beta AR were not significantly altered. Analysis of competition curves of ICYP binding by the agonist (-)-isoproterenol showed that diabetes induces an increase in the (-)-isoproterenol IC50 and a steepening of the curve ("pseudo-Hill" coefficient not significantly different from 1) in the absence of Gpp(NH)p, while these parameters were not significantly modified in the presence of Gpp(NH)p (10(-4) M). These results indicates that beta AR were not significantly reduced in number but altered in their capacity to efficiently couple with the GTP-binding protein of adenylate cyclase (AC). These data can be correlated to the alteration of beta-adrenergic stimulation of cardiac AC previously observed after 4 months of diabetes. The characteristics of beta AR alteration at this stage of the disease are similar to those of a first step of a beta AR desensitization process due to overstimulation.

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