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Biomedical subjects

J Marco

Publications and source records attributed to J Marco.

At least 145 records · Page 8Linked to original sources
PubMed1990

Inhibition of insulin and somatostatin secretion and stimulation of glucagon release by homologous galanin in perfused rat pancreas.

Results of studies on the effects of exogenous galanin on islet cell secretion are controversial. Until recently, only pig galanin has been available, and structural dissimilarities among the galanin molecules of different species might have contributed to discrepancies among the study results. Thus, we investigated the influence of synthetic rat galanin (50 nM) on unstimulated insulin, glucagon, and somatostatin release and on the responses of these hormones to arginine (10 mM), glucose (16.6 mM), and vasoactive intestinal polypeptide (VIP; 1 nM) in a homologous animal model, the perfused rat pancreas. In addition, the effect of an equimolar concentration of pig galanin on arginine-induced islet cell secretion was examined. Infusion of rat galanin reduced unstimulated insulin release (approximately 60%, P less than 0.01) and the insulin responses to arginine (approximately 30%, P less than 0.025), glucose (100%, P less than 0.01), and VIP (approximately 80%, P less than 0.025). Galanin also inhibited unstimulated somatostatin secretion (approximately 15%, P less than 0.05) and virtually abolished the somatostatin output evoked by arginine, glucose, and VIP. Conversely, rat galanin increased unstimulated glucagon output (approximately 20%, P less than 0.05), potentiated the glucagon response to arginine (approximately 50%, P less than 0.05) and VIP (approximately 90%, P less than 0.05), and counteracted the suppressor effect of glucose on alpha-cell secretion. Pig galanin inhibited the insulin output elicited by arginine (approximately 45%, P less than 0.05) but did not affect the somatostatin and glucagon responses to the aminogenic stimulus. In conclusion, the opposite effects of galanin on insulin and glucagon secretion favor the concept of galanin as a diabetogenic agent. Galanin also behaves as a potent inhibitor of somatostatin release. Finally, the importance of using homologous galanin to study the biological activity of this peptide must be emphasized.

Animals↗
PubMed1990

[Hormones and the nasal mucosa. A bibliographic review].

The development and activity of the nasal mucosa are influenced by many hormonal substances. In this work we realize a bibliographical review about the effect of adrenaline, thyroid hormones, corticosteroids and sex hormones on the nasal respiratory mucous membrane. We emphasize the clinic consequences.

Animals↗
PubMed1990

Nasal mucociliary function during the menstrual cycle in healthy women.

Nasal mucociliary transport time was studied in nine healthy women over the menstrual cycle using the vegetable charcoal powder technique. Three measurements were made at different points of the cycle: during the early follicular phase, periovulatory phase and luteal phase. The mean transport times were 10.1 +/- 3.50, 5.1 +/- 2.08 and 7.5 +/- 3.28 minutes, respectively. Transit was significantly accelerated during the periovulatory phase (p less than 0.01), when the seric estrogens are at their highest level.

Adult↗
PubMed1990

Curve of perceptive intellectual deterioration in hemodialysis patients.

In order to optimize the results of kidney transplant, i.e. patient's acceptance and speedy recovery, the available organ resources must be combined with appropriate "preparation" of the patient's mental state. In order to plot the "mental deterioration curve" of patients on a hemodialysis program, the present study was made on 62 patients in a general hospital in Spain. The possible repercussions of treatment of kidney disease on intellectual (Weschler's Adult Intelligence Scale-WAIS test) and perceptive (Benton test) capacity were investigated. Samples were grouped according to whether they had been on dialysis for up to four years (less than 4) or more than four years (greater than 4). The WAIS test for the greater than 4 group indicated a lower I.Q. These results indicated that it was after four years on dialysis that greater negative effects began to be seen in perceptive-intellectual capacity. The Benton test indicated that time on hemodialysis adversely affected the patient's capacities. A sharp decline was seen particularly between two and four years in the less than 4 group, suggesting that patients' mental conditions vary with time on dialysis but that their resources and capacities are still fairly untroubled by the treatment in the first two years. In the light of these findings, the deterioration curve should be taken into account when planning kidney transplant, in order to take advantage of the initial period if possible.

Adult↗
PubMed1989

Pancreastatin inhibits insulin secretion as induced by glucagon, vasoactive intestinal peptide, gastric inhibitory peptide, and 8-cholecystokinin in the perfused rat pancreas.

Pancreastatin is a 49-amino acid straight chain molecule isolated from porcine pancreatic extracts. In the perfused rat pancreas, this peptide has been shown to inhibit unstimulated insulin release and the insulin responses to glucose, arginine, and tolbutamide. To further explore the influence of pancreastatin on islet cell secretion, the effect of synthetic porcine pancreastatin (a 2-micrograms priming dose, followed by constant infusion at a concentration of 15.7 nmol/L) was studied on the insulin, glucagon, and somatostatin responses to 1 nmol/L vasoactive intestinal peptide (VIP), 1 nmol/L gastric inhibitory peptide (GIP), and 1 nmol/L 26 to 33 octapeptide form of cholecystokinin (8-CCK). The effect of pancreastatin on the insulin and somatostatin secretion elicited by glucagon (20 nmol/L) was also examined. Pancreastatin infusion consistently reduced the insulin responses to VIP, GIP, and 8-CCK without modifying glucagon or somatostatin release. It also inhibited the insulin release but not the somatostatin output induced by glucagon. These observations broaden the spectrum of pancreastatin as an inhibitor of insulin release. The finding that pancreastatin does not alter glucagon or somatostatin secretion supports the concept that it influences the B cell directly, and not through an A cell or D cell paracrine effect.

Animals↗
PubMed1989

[Primary failure of pericardial valvular heterografts].

From July 1981 to October 1984, 79 Hancock pericardial valves were implanted in 74 patients surviving the hospital period and with a mean age of 64.2 years. Fifty-two patients underwent aortic valve replacement, 16 had mitral valve replacement, 5 bad a double replacement and 19 associated procedures were performed. The mean survival is 48 months. Until 1st June 1987, 11 primary failures have required reoperation (14.9%), 4 in the mitral position (4.6% patient-years), 7 in the aortic position (3.01% patient-years). The time to reoperation was 48.4 months for the aortic orifice and 36.5 months for the mitral orifice. The lesions most frequently encountered were tears (7 cases), calcifications (5 cases) and stretching of valvular tissue (2 cases); two patients died during the postoperative phase of this operation. Despite the small number of patients followed, this series demonstrates of high incidence of dysfunction due to primary tissue degeneration as, after the 5th year, the actuarial rate of absence of primary lesion is 85.3 +/- 8% with no significant difference between the aortic and the mitral orifices, although dysfunction appears to occur more rapidly in mitral prostheses. These results are much less favourable than those obtained with Ionescu bioprostheses in the aortic position of those obtained with porcine bioprostheses in either position. This justifies very regular clinical and echocardiographic follow-up of patients with Hancock pericardial valvular heterografts.

Actuarial Analysis↗
PubMed1988

In vitro effects of BAY K 8644, a dihydropyridine derivative with hypoglycaemic properties, on hepatic glucose production and pancreatic hormone secretion.

In rats, oral administration of BAY K 8644 (methyl 1,4-dihydro-2,6-dimethyl-3-nitro-4-(2-trifluoromethylphenyl)-pyridine-5- carboxylate), a dihydropyridine derivative, Ca2+-channel activator, lowers fasting glycaemia and improves glucose tolerance to carbohydrate loading without elevating peripheral plasma insulin. To study the hypoglycaemic mechanism of this compound, we have examined its effects on glucose production by isolated rat hepatocytes and on hormone secretion by the perfused rat pancreas. Incorporation of BAY K 8644 (0.2-10 microM) into the hepatocyte incubation medium failed to significantly modify glycogenolysis, gluconeogenesis or L-lactate production. Hepatocyte glycogen phosphorylase a (EC 2.4.1.1) activity and fructose 2,6-bisphosphate levels were also unaffected by BAY K 8644. In the perfused rat pancreas, BAY K 8644 markedly stimulated insulin release without modifying glucagon or somatostatin output. Thus, the possibility that this compound exerts its hypoglycaemic effect by provoking insulin secretion should be further investigated.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1988

Effects of pancreastatin on insulin, glucagon and somatostatin secretion by the perfused rat pancreas.

Pancreastatin is a novel peptide, isolated from porcine pancreatic extracts, which has been shown to inhibit glucose-induced insulin release "in vitro". To achieve further insight into the influence of pancreastatin on pancreatic hormone secretion, we have studied the effects of this peptide on unstimulated insulin, glucagon and somatostatin output, as well as on the responses of these hormones to glucose and to tolbutamide in the perfused rat pancreas. Pancreastatin strongly inhibited unstimulated insulin release as well as the insulin responses to glucose and to tolbutamide. It did not significantly affect glucagon or somatostatin output under any of the above-mentioned conditions. These findings suggest that pancreastatin inhibits B-cell secretory activity directly, and not through an A-cell or D-cell paracrine effect.

Animals↗
PubMed1988

Effects of galanin on islet cell secretory responses to VIP, GIP, 8-CCK, and glucagon by the perfused rat pancreas.

Exogenous galanin has been shown to suppress insulin secretion as elicited by a number of secretagogues such as glucose, arginine, tolbutamide, carbachol, and oral nutrients. To achieve further insight into the influence of galanin on the endocrine pancreas, we have investigated the effect of synthetic porcine galanin (a 200 ng bolus followed by constant infusion at a concentration of 16.8 ng/mL for 16 to 24 minutes) on unstimulated insulin, glucagon, and somatostatin release, as well as on the responses of these hormones to 1 nmol/L vasoactive intestinal peptide (VIP), 1 nmol/L gastric inhibitory peptide (GIP), 1 nmol/L 26 to 33 octapeptide form of cholecystokinin (8-CCK) or 10 nmol/L glucagon in the perfused rat pancreas. Galanin infusion reduced unstimulated insulin secretion by 60% without modifying glucagon and somatostatin output. Galanin also blocked insulin release elicited by VIP, GIP, and 8-CCK, it did not affect the glucagon responses to VIP and GIP, or the somatostatin responses to VIP, GIP, and 8-CCK. Finally, galanin inhibited the insulin output, but not the somatostatin release induced by glucagon. In conclusion, in the perfused rat pancreas, galanin appears to behave as a general inhibitor of insulin secretion. Since this neuropeptide does not modify glucagon or somatostatin release, a direct effect of galanin on the B-cell seems plausible.

Animals↗
PubMed1988

The combined use of diastolic counterpulsation and coronary dilation in unstable angina due to multivessel disease under unstable hemodynamic conditions.

Sixteen patients with multivessel ischemic heart disease and severely jeopardized myocardium required intra-aortic balloon counterpulsation subsequent to a deterioration in hemodynamics during or following a coronary angioplasty procedure. They had all suffered unstable angina which was refractory to intensive medical therapy, consisting of a combination of nitroglycerin, beta-adrenergic antagonists, and calcium blockers. Thirty angioplasties had been attempted (1.9 artery stem/patient) with a primary success rate of 90%. The symptoms of prolonged myocardial ischemia had disappeared, and the patient's blood pressure had normalized. No complications were associated with the use of the mechanical circulatory assistance. There were no deaths related to the procedure itself, and no myocardial infarctions. Emergency surgery was not required. One patient did die in hospital, however, due to cerebrovascular accident which occurred 4 days after removal of the mechanical circulatory support. Two also died suddenly later. One patient also required later elective coronary arterial bypass surgery and another needed repeated coronary dilation. The 12 remaining patients are asymptomatic at a follow-up with mean value of 22 months. Temporary intra-aortic diastolic counterpulsation is a useful adjunct to coronary angioplasty in patients with multivessel unstable angina and compromised hemodynamics.

Adult↗
PubMed1988

Absence of steroid-dependent, endogenous opioid peptide suppression of pulsatile luteinizing hormone release between diestrus 1 and diestrus 2 in the rat estrous cycle.

The objective of this study was to determine whether the negative feedback action of ovarian steroids on pulsatile luteinizing hormone (LH) release in the diestrous 1 (D1)-diestrous 2 (D2) interval of the rat estrous cycle is mediated by endogenous opioid peptides (EOPs), by examining the pulsatile LH release response to naloxone infusions in the presence or absence of D1-D2 levels of estradiol (E2) and progesterone (P). As plasma E2 and P levels increased between D1 and D2, mean blood LH levels decreased due solely to a decrease in LH pulse amplitude as frequency remained stable. However, ovariectomy increased both parameters of pulsatile LH release, indicating the effect of loss of ovarian steroid-negative feedback in this interval. Replacement of D1-D2 plasma levels of E2 and P restored D2 values for both parameters of pulsatile LH release, and E2 + P did not alter in vivo pituitary responsiveness to LH-releasing hormone (LHRH). In ovariectomized rats lacking the negative feedback provided by E2 + P in this cycle interval, continuous infusion of naloxone caused a further dose-dependent augmentation in both LH pulse amplitude and frequency. This stimulatory action of naloxone was prevented by simultaneous infusion with morphine, and was not associated with any change in in vivo pituitary responsiveness to LHRH, indicating that this was an action exerted through centrally located EOP receptors. Naloxone also increased both parameters of pulsatile LH release in E2 + P-treated rats. However, the magnitudes of the naloxone-induced increments in LH pulse amplitude and frequency in ovariectomized, steroid-treated rats were not greater than those seen in ovariectomized, nonsteroid-treated rats given naloxone versus saline. In addition, mean values for both parameters of pulsatile LH secretion during EOP receptor blockade in steroid-treated rats were reduced when compared to values in ovariectomized, nonsteroid-treated rats infused with naloxone. Thus the stimulatory effect of naloxone on pulsatile LH release was similar in the presence or absence of the negative feedback action of D1-D2 plasma levels of E2 + P. This indicates that the negative feedback effect of E2 + P on pulsatile LH release in this interval is not mediated by EOPs whose actions are blocked by naloxone.

Animals↗
PubMed1988

Actuality in the treatment of unstable angina pectoris.

In an attempt to relieve ischaemic symptoms and to prevent progression to myocardial infarction, coronary angioplasty was attempted in 236 multivessel coronary heart disease patients with unstable angina, refractory to medical treatment including oral Ca2+ antagonists, beta blockers and nitroglycerin drugs. Unstable angina was defined as ischaemic chest pain at rest lasting for at least 20 min, accompanied by reversible ST-T changes. The initial angioplasty success rate was 87% (205/236 cases). Vessel occlusion necessitating urgent bypass surgery occurred in five patients (2.1%). There was evidence of myocardial infarction in eight patients (3.4%). There were seven deaths (2.9%) related to the procedure. 191 of the 205 successfully dilated patients were followed up for 14 months on the average. Late mortality occurred in 4.2% (8/191), late nonfatal infarction in 2.6%, 127 patients remained asymptomatic and 11 were considered to be disabling angina (New York Heart Association classification III or IV). Recurrent angina rate with progression in ischaemic disease (restenosis and native vessel stenosis) occurred in 30%. For this reason, repeated angioplasty and elective bypass surgery were performed in 48 and 14 cases, respectively. These results support the growing evidence that angioplasty as an emergency procedure in multivessel disease patients with unstable angina pectoris refractory to intensive medical treatment can restore coronary blood flow with an acceptable risk and a good initial and short-term success rate.

Adult↗
PubMed1988

[Transluminal angioplasty of the coronary vessels in patients with pluritruncular unstable angina].

Between October, 1979 and August, 1987, 489 patients with multivessel coronary disease and unstable angina underwent transluminal angioplasty of coronary arteries with the following results: primary success in 90 p. 100 of the patients, emergency bypass surgery of occlusive dissection in 1.8 p. 100, myocardial infarction in 2.9 p. 100, death in 1.4 p. 100. These results were similar to those obtained in 369 patients with stable angina whose coronary vessels were dilated by the same group during the same period. The death rate was significantly higher in elderly people and in women. 398/489 patients were followed up for 2 to 45 months: 1.8 p. 100 died, 2 p. 100 developed myocardial infarction and 2.3 p. 100 underwent coronary bypass. 46 patients had repeat angioplasty for restenosis. After single or repeat angioplasty, 68 p. 100 of the primary success patients followed up were asymptomatic, and 73 p. 100 had lasting clinical improvement. Among 221 patients studied with different numbers of vessels treated, the degree of revascularization did not make any significant difference in the percentage of symptom-free patients. Data from the literature concerning the medical treatment of unstable angina indicate a high incidence of complications and a mediocre long-term functional benefit, while data concerning surgical treatment show a better long-term functional result. Compared with these two types of treatment, transluminal coronary angioplasty appears as a satisfactory method to treat unstable angina in patients with multivessel coronary disease.

Adult↗
PubMed1988

[A new procedure for the study and treatment of myocardial infarction in the acute phase: percutaneous coronary angioscopy].

The recent development of small diameter optical fibers, which are also very flexible allows us to realise percutaneous coronary angioscopy. First of all we visualized normal dog's arteries, bifurcations, origin of small branches; then we created and visualized intimal tears, dissections and experimental thrombi. The second part of this work consisted in applying this new technic in three patients who had an evolving myocardial infarction and an occluded right coronary artery. In all three cases a clot has been visualized, occluding the lumen of the artery. This small experiment shows that percutaneous angioscopy is a feasible, quick and save procedure. Its developments will be very important according to the development of percutaneous interventional therapies.

Animals↗
PubMed1987

Steroid-independent endogenous opioid peptide suppression of pulsatile luteinizing hormone release between estrus and diestrus in the rat estrous cycle.

We have previously demonstrated an absence of ovarian steroid negative feedback on pulsatile luteinizing hormone (LH) release between estrus and early diestrus 1 (D1) in the rat estrous cycle. The object of the present study was to determine if there was a steroid-independent endogenous opioid peptide (EOP) suppression of pulsatile LH release in this same 24-h interval, and if so, which parameter(s) of pulsatile LH release were affected. Rats were bled on estrus, or 24 h following sham ovariectomy (OVX), or OVX at 08.30-10.00 h on estrus. At the time of bleeding all rats were infused i.v. for 4 h either with 0.9% saline (0.5 ml/h) or naloxone (0.005, 0.05, 0.5, or 2 mg/kg/h). At 1 h after the infusion began, rats were bled for 3 h (40 or 50 microliters whole blood/5 min) between 09.30 and 12.30 h. Mean blood LH levels increased between estrus and early D1 due to increases in LH pulse amplitude and frequency. OVX on estrus decreased plasma levels of estradiol and progesterone 24 h later, but did not augment the increase in pulsatile LH release. However, naloxone infusion augmented the increase in pulsatile LH secretion in sham ovariectomized rats in a dose-dependent fashion. While infusion of 0.005 or 0.05 mg/kg/h had no effect, 0.5 or 2 mg/kg/h increased blood LH levels by increasing both LH pulse amplitude and frequency. The stimulatory effect of naloxone on pulsatile LH release was blocked by simultaneous infusion of morphine, demonstrating that the effect was mediated by EOP receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗