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Biomedical subjects

G Anfossi

Publications and source records attributed to G Anfossi.

At least 73 records · Page 4Linked to original sources
PubMed1988

Insulin-induced hypoglycaemia increases plasma concentrations of angiotensin II and does not modify atrial natriuretic polypeptide secretion in man.

Insulin-induced hypoglycaemia causes profound haemodynamic changes, commonly ascribed to catecholamine increase. The aim of the present study was to investigate the influence of insulin-induced hypoglycaemia on non-adrenergic factors potentially involved in haemodynamic regulation: angiotensin II and alpha-human atrial natriuretic polypeptide. Fourteen healthy male subjects, aged 25.5 +/- 0.74 years, body mass index 23.81 +/- 0.68 kg/m2, received (after an overnight fast and at least 60 min rest in a supine position) an i.v. bolus injection of human regular insulin (Actrapid HM, Novo, Bagsvaerd, Denmark: 3.84 U/m2). Serial venous blood samples were drawn in the following 150 min, to measure plasma glucose, angiotensin II, alpha-human natriuretic polypeptide, and factors potentially involved in the regulation of the renin-angiotensin-aldosterone system. During the study, we observed a plasma glucose fall, reaching a nadir of 1.95 +/- 0.11 mmol/l between 25 and 30 min, and an increase of angiotensin II (from 7.6 +/- 0.8 to 13.5 +/- 1.1 pg/ml, p = 0.01, quadratic model evaluated by an analysis of the variance for repeated measures), whereas atrial natriuretic polypeptide remained unchanged. As far as the regulation of the renin-angiotensin-aldosterone system is concerned, the increase of angiotensin II is attributable to the increased plasma renin activity, whereas angiotensin converting enzyme was not modified. The increase of plasma renin activity, in turn, is attributable both to the increased catecholamine concentrations and to the decreased potassium levels. Both adrenocorticotropic hormone and angiotensin II are potentially involved in the hypoglycaemia-induced increase of aldosterone concentrations.

Adrenocorticotropic Hormone↗
PubMed1988

Influence of urapidil on in vitro platelet response to adrenaline and other aggregating agents.

The effects of hypotensive drug urapidil on human platelet functions were investigated. Urapidil failed to evidence direct aggregating properties or potentiating effects. Furthermore, drug high concentrations inhibited the platelet response to ADP, PAF, collagen, adrenaline and bovine thrombin, and influenced the platelet release reaction induced by ADP and PAF. Data indicate that urapidil possesses negligible agonistic effects on human platelet alpha 2-adrenoceptors and interferes at high concentrations with the platelet activation, as evidenced for other anti-aggregating compounds.

Adenosine Diphosphate↗
PubMed1988

Effect of labetalol on human platelet function.

1. The effects of the alpha-beta-adrenergic antagonist labetalol on the activation of human platelets by adrenaline and other aggregating stimuli have been investigated. 2. Labetalol inhibited platelet aggregation and secretion induced by collagen and the second phase of aggregation caused by ADP, platelet activating factor, adrenaline and ionophore A23187. Adrenaline-induced platelet activation was inhibited by the lowest labetalol concentration. The response to Na arachidonate was minimally affected and the arachidonate-induced thromboxane B2 generation was only partially prevented. 3. The pre-incubation with low concentration of ionophore A23187 overcame labetalol's inhibition of collagen-induced platelet aggregation. 4. Labetalol did not influence intraplatelet cyclic AMP levels. 5. The present investigation provided evidences that the modulation of human platelet function by labetalol could be related also to a decreased Ca2+ availability.

Adult↗
PubMed1988

Insulin directly reduces platelet sensitivity to aggregating agents. Studies in vitro and in vivo.

The aim of this study was to investigate the influence of insulin on platelet function, both in vitro and in vivo. For the in vitro investigation, we evaluated whether insulin affects platelet function at a physiological hormone concentration by incubating the platelet-rich plasma (PRP) of fasting subjects with human regular insulin at the final concentration of 40 microU/ml for 30 min; we observed a significant reduction of platelet sensitivity to all the aggregating agents employed, i.e., ADP, platelet-activating factor (PAF), epinephrine, collagen, and Na+ arachidonate. To investigate whether the insulin effect on platelets is dose dependent, we incubated the PRP of fasting subjects with different concentrations of human regular insulin (40, 80, 120, and 160 microU/ml) for 5 min, and we observed that the insulin-induced reduction of platelet sensitivity to aggregating agents is a dose-dependent phenomenon. Furthermore, the comparison between the platelet responses after 5 and 30 min of incubation with insulin showed that the insulin effect on platelet aggregation is time dependent. The lack of specificity of its inhibiting activity suggests that insulin does not interfere with the initial binding of each aggregating agent at specific sites but does influence a common step of platelet aggregation. Our study rules out the possibility that insulin reduces platelet-function-modifying intraplatelet cAMP levels or thromboxane A2 production, because this hormone decreases the platelet concentrations of cAMP--a phenomenon that, per se, promotes platelet aggregation--and does not modify collagen or Na+ arachidonate--induced platelet production of thromboxane A2, measured by radioimmunoassay of its stable-metabolite thromboxane B2.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Diphosphate↗
PubMed1988

Postprandial exercise in type I diabetic patients on multiple daily insulin injection regimen.

This study shows the influence on plasma glucose concentrations of 45 min of mild exercise (48 +/- 4% of maximum aerobic capacity) performed 180 min after breakfast and 195 min after a subcutaneous injection of regular insulin by six type I (insulin-dependent) diabetic patients on a three-daily insulin injection regimen (regular insulin before breakfast and lunch, regular + intermediate insulin before supper). It has been observed that such exercise does not induce a large plasma glucose decrease. Actually, plasma glucose concentrations were 99 +/- 18 mg/dl before exercise, reached a nadir of 78 +/- 17 mg/dl at 35 min, and were 81 +/- 15 mg/dl at the end of exercise. During the control study at rest, in the same 45-min time interval, plasma glucose decreased from 146 +/- 31 to 128 +/- 31 mg/dl. In the exercise study, one patient began exercising while hypoglycemic, and another patient developed asymptomatic hypoglycemia during exercise. In the control study at rest, one patient showed hypoglycemic glucose concentrations. Throughout the exercise study, plasma free-insulin concentrations decreased (from 32 +/- 5 to 20 +/- 4 microU/ml) as a result of the pharmacokinetics of subcutaneously injected insulin.

Adult↗
PubMed1988

Urinary enzyme release following aminoglycoside administration in single low dose.

Urinary enzyme excretion was investigated in healthy volunteers before and after infusion of single low doses of aminoglycoside (gentamicin, tobramycin and amikacin) in the same subjects. Significant increases were detected in urinary leucine aminopeptidase, lactate dehydrogenase and alkaline phosphatase following gentamicin infusion; after amikacin administration only urinary release of leucine aminopeptidase was found to be increased. No difference was detected compared to basal values in enzyme excretion after tobramycin infusion. Urinary enzyme release in our conditions suggests low tubular damage after single doses of gentamicin and amikacin.

Adult↗
PubMed1986

Influence of age on polymorphonuclear leukocytes in vitro: phagocytic activity in healthy human subjects.

Polymorphonuclear leukocytes (PMNs) represent an important defensive mechanism against infectious agents. Some of their functions are impaired in old people, with a decreased effectiveness of nonspecific immunity. In vitro PMN phagocytic activity was studied with different techniques on 74 healthy subjects (20-82.5 years; 40 males, 34 females). Serum-mediated ingestion resulted to be impaired with age with a lower ratio of active PMNs and a lower activity of phagocytosing cells. The behavior of these parameters was age-related, without significant difference between males and females; the decline was found to be a continuous phenomenon with no threshold age. Serum-independent ingestion had very low values and was not impaired with aging. The present data can represent a further explanation for the finding of a higher incidence and mortality of bacterial diseases in elderly population.

Adult↗
PubMed1986

Studies on mechanisms involved in hypoglycemia-induced platelet activation.

The aim of our study was to investigate the mechanisms involved in hypoglycemia-induced platelet activation. Sixteen healthy male subjects received a 60-min intravenous infusion of human regular insulin at the rate of 64 mU . m-2 . min-1: throughout 150 min, we serially measured plasma concentrations of glucose, insulin, and counterregulatory hormones; platelet sensitivity to ADP, thrombin and platelet-activating factor; plasma concentrations of platelet markers for specific proteins of in vivo release reaction (beta-thromboglobulin and platelet factor 4). Our study showed that insulin-induced hypoglycemia causes a significant increase in platelet sensitivity to aggregating agents in vitro and a platelet release reaction in vivo. Hypoglycemia-induced platelet activation was not correlated with plasma glucose concentrations at nadir and occurred before the increase of plasma growth hormone and cortisol. To further elucidate the mechanisms of hypoglycemia-induced platelet activation, we incubated in vitro platelet-rich plasma (PRP) of seven fasting healthy subjects with the same concentrations of insulin, epinephrine, glucagon, growth hormone, and cortisol measured in vivo during insulin-induced hypoglycemia. Only epinephrine was able to increase platelet sensitivity to aggregating agents. To investigate the role of alpha-adrenergic receptors in this phenomenon, we also studied four healthy subjects on another occasion, repeating the above-described insulin infusion together with intravenous infusion of phentolamine (-15 to +150 min), 5 mg over 2 min followed by 500 micrograms/min. alpha-Blockade was able to suppress hypoglycemia-induced increase of platelet sensitivity to aggregating agents.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Urinary enzyme excretion in acute and subacute experimental lithium administration.

Blood lithium (Li) levels, renal functional parameters and urine excretion of enzymatic activities having different intracellular sites were investigated on rats submitted to acute and subacute Li chloride administration. In acute experiments increased levels of all detected enzymes were assayed following Li single doses of 5 and 10 mEq/kg b.w. In subacute poisoning, urine output of lactate dehydrogenase, aspartate transaminase and alanine transaminase was significantly over the basal ranges following 15 days in concomitance with marked elevation of plasma Li levels and exhibited progressive increase until 30 days; on the 10th day following Li withdrawal, elevated excretion of enzymatic activities was still assayed. The results are in agreement with data about the localization of the histologic lesions involving different sites of the nephron in acute Li poisoning and the distal tubular tract in subacute toxicity. In subacute administration the output of cytoplasmic and mitochondrial activities can be assumed as an index of damage of the nephron cells which can persist following Li withdrawal. Our findings indicate that the urine enzyme assay is a valuable tool to detect renal damage in experimental Li nephropathy.

Alanine Transaminase↗
PubMed1982

Urinary enzyme excretion and renal lactate dehydrogenase isoenzyme pattern in acute HgCl2 nephropathy of rat.

The activity of several enzymes with different intracellular sites was determined in urine at various times following nonfatal acute tubular necrosis induced by mercuric chloride administration. The excretion rate of all tested enzymes rose on the 1st and 2nd day; in the next observations (days 7-15) enzymatic values approached the basal values. The lactate dehydrogenase isoenzyme pattern of the renal cortical zone showed an early shift towards cathodic fractions and later (7 days) an increase of middle ones; the normal anodic zymogram recovered after a suitable time interval (30 days). The isoenzymatic changes are related both to the renal hypoxia and to the appearance of less differentiated cells. The behaviour of functional parameters (urine flow, osmolality, urea clearance, creatinine clearance) were well in agreement with the observed enzyme and renal isoenzyme changes.

Acid Phosphatase↗
PubMed1979

Renal lactate dehydrogenase (LDH) isoenzyme pattern in short-term experimental obstructive nephropathy.

The lactate dehydrogenase isoenzyme pattern of different zones of rat kidney has been investigated at different stages after unilateral ureteral obstruction. In the obstructed kidney, the cortical tissue showed an early (3 days) progressive shift toward a cathodic zymogram; at 7 days LDH-5 isoenzyme was the predominant fraction (44.7 +/- 2.5). In the outer medullary tissue a similar change was observed even though middle fractions were always quite evident. No significant changes were found in the inner medullary tissue. The observed enzymatic abnormalities are related to renal hypoxia and to the occurrence of a less differentiated nephronic cell population. They represent a metabolic marker of the morphologic and functional alterations which occur in obstructive nephropathy.

Animals↗
PubMed1979

[Acute calculous cholecystitis (author's transl)].

The authors studied 333 acute cholecystitis out of 2,200 operated on for lithiasis of the gall-bladder, 186 bacteriological tests were carried out on the vesicular liquid and wall. They insist on the main anatomo-pathological characteristic: early, partial or total destruction of the mucous together with acute inflammatory lesions of the wall and even sometimes necrosis. This irreversible lesion is due to the acute obstruction of the gall-bladder by blockage of a calculus. Acute cholecystitis are practically always aseptic at the beginning. Sepsis is a secondary complication. These anatomo-pathological and bacteriological elements have two therapeutic corollaries: 1. The patient has to be operated very early at the aseptic stage. 2. Preliminary antibiotherapy becomes useless. Under these conditions there is practically no death before the age of 65. Mortality concern old people, operated late and suffering from other disease.

Acute Disease↗