Biomedical subjects

G Girardi

Publications and source records attributed to G Girardi.

At least 19 recordsLinked to original sources

PubMed1997

Effects of clenbuterol as a repartitioning agent on beta-adrenoceptor concentrations in heart, bronchi and brain of veal calves.

The effects induced by dietary clenbuterol (20 micrograms kg-1 body weight day-1 for 40 days) on beta-adrenergic receptor (beta-AR) subtypes in the heart, bronchial smooth muscles and the CNS of veal calves were investigated using a binding method. Clenbuterol exposure caused a significant (P < 0.05, P < 0.01, P < 0.001) decrease in beta 1-AR and beta 2-AR in both cardiac atria and ventricles of treated animals (excluding the beta 2-AR of the right atrium). Similarly, a significant (P < 0.01, P < 0.001) down-regulation of beta-AR subtypes in bronchial smooth muscles of treated calves was observed. In the CNS (cerebral cortex, hippocampus, hypothalamus and cerebellum) the down-regulation was limited to beta 2-AR, with the exception of the hippocampus in which both beta 1-AR and beta 2-AR concentrations were significantly (P < 0.05; P < 0.01) reduced. Scatchard analysis of the binding of the beta-AR antagonist, (-) [3H]CGP 12177, revealed that the down-regulation of beta-AR was not associated with any modification in binding affinity, as Kd values were unaffected by clenbuterol treatment. Data obtained indicated that prolonged clenbuterol exposure induced a remarkable beta-AR down-regulation in the heart, bronchi and brain of veal calves.

Adrenergic beta-Agonists↗

PubMed1996

Glomerular compromise in mercuric chloride-induced nephrotoxicity.

We have examined the effects of mercuric chloride on renal glomerular structure. Isolated glomeruli from mercury-treated rats (HgCl2, 5 mg/kg body wt, s.c.) 1 hour post injection presented a diminished cross-sectional area as compared with control glomeruli [control (micron2) = 26,310 +/- 2,545, HgCl2 (micron2) = 18,474 +/- 1,828] and higher glomerular calcium content (control = 23 +/- 6 nmoles/mg prot, HgCl2 = 43 +/- 7 nmoles/mg prot). Renal sections prepared for immunohistochemical and histochemical analysis showed larger deposits of fibronectin and lipids and enhanced cellularity in glomerular structures from HgCl2-treated rats. Moreover, mieloperoxidase activity measured in isolated glomeruli were also increased as compared with control preparations [MPO (U/mg prot): control = 59 +/- 7, HgCl2 = 134 +/- 10]. When the animals were studied 24 hours post HgCl2 injection, glomerular cross-sectional area values were not different from control values (25,276 +/- 1,983 micron2), while calcium contents were higher than values observed 1 hour after treatment (92 +/- 9 nmoles/mg prot). A similar pattern was observed in fibronectin deposits. Hypercellularity in glomerular structures and the higher mieloperoxidase levels were maintained at this time (MPO HgCl2-rats 24 h = 148 +/- 31 U/mg prot). The effects observed in this study are consistent with an inflammatory response in the glomerular structure of HgCl2-treated rats that could explain the altered renal function described in previous reports in our laboratory.

Animals↗

PubMed1995

Evidence for renal ischaemia as a cause of mercuric chloride nephrotoxicity.

The present study was undertaken to investigate if the source of oxidative stress and the renal injury produced by mercuric chloride could be renal ischaemia. Verapamil Vp was used because it was described that calcium channel blockers protect cells from nephrotoxicants and from ischaemia. Vp (75 micrograms/kg, i.v.; 30 min before HgCl2 injection) prevented mercuric chloride renal injury observed 1 h post-HgCl2 injection as measured by clearance techniques. Vp also prevented the diminution of non-protein-sulfhydryls (NPSH) and the increased lipid peroxidation (LPO) induced by HgCl2 in renal tissue. Hg2+ toxicokinetic alterations were not observed in Vp plus HgCl2 treated rats, nor was Vp ability found as a free radical scavenger in renal tissue homogenates. The results described in this study give some evidence for the role of renal ischaemia in the production of oxidative stress, generating LPO and functional and morphological renal injury described in mercuric chloride treated rats.

Animals↗

PubMed1995

Mercuric chloride effects on rat renal redox enzymes activities: SOD protection.

This study was done to determine the effect of mercuric chloride treatment on the redox cycle enzymes in rat kidney ex-vivo. Glutathione peroxidase (GSH-Px) and catalase (Cat) activities were measured in kidney homogenates from rats with different nonprotein sulfhydrils levels and different mercury content. The results indicated that GSH-Px activity was enhanced in mercury-treated rats in direct relationship with kidney mercury content, whereas Cat activity was increased in the presence of the highest mercury kidney content obtained. Superoxide dismutase (SOD) was administered to rats prior to mercury chloride injection and renal function, development of lipid peroxidation and renal glutathione level were measured 1 h later. Renal function, renal glutathione, and renal lipid peroxidation production were maintained similar to control values. Moreover, SOD pretreatment also protected kidney from mercuric chloride histological alterations observed 24 h post mercury treatment. Thus, an inhibition of renal redox cycle enzymes "in vivo," did not appear to be an important determinant of the increased lipid peroxidation observed during mercuric chloride nephrotoxicity.

Animals↗

PubMed1995

[Evaluation of the synergism between ketorolac and morphine in the treatment of postoperative pain].

BACKGROUND: The aim of the study is to determine what concentration of ketorolac and morphine administered together i.v. achieve best synergic effect between NSAID antiinflammatory and opioids analgesic properties. DESIGN: Randomized comparative study was carried out on 180 patients, ASA II-IV, undergoing major general surgery, in an University Clinic. METHODS: Postoperative pain therapy by i.v. PCA: group 1 morphine 0.75 mg.ml + ketorolac 0.75 mg.ml; group 2 morphine 0.50 mg.ml + ketorolac 1.50 mg.ml; group 3 morphine 0.25 mg.ml + ketorolac 1.50 mg.ml; in saline solution. Initial bolus: 2 ml. Continuous infusion 1.5 ml.h. Demand bolus: 0.2 ml. Lockout time: 30 minutes. Evaluations included: pain intensity (T0, T3, T18); total amount of infused drugs (T18); number of valid demands and attempts (T18); amount of autoadministered analgesic drugs in percent of highest available amount (T18); side effects (T18); patient's judgment. DATA ANALYSIS: ANOVA and Student's "t"-test. RESULTS: A statistically significant reduction of pain intensity was found after 3 and 18 hours in the three groups, no differences were found among the groups. Group 2 required an amount of autoadministered drugs significantly lower than other groups. Rare side effects. Patient's judgment was generally positive. CONCLUSIONS: Results suggest a greater synergetic effect between morphine and ketorolac in concentrations used in group 2.

Analgesics, Non-Narcotic↗

PubMed1994

[Effect of dopexamine in splanchnic perfusion during surgery of the abdominal aorta].

Abdominal aortic surgery has significant effects on cardiac and splanchnic perfusion. The purpose of this study was to examine the effects of dopexamine, an inodilator drug, on hemodynamic and splanchnic perfusion with measurement of gastric intramucosal pH, by the method of gastric tonometry, during abdominal aneurysm resection. Twenty-five patients undergoing excision of an aortic abdominal aneurysm were randomly divided into two groups. During aortic cross-clamping Group II patients received dopexamine infusion, at a dose of 1 microgram/kg/m, and at a dose of 0.5 micrograms/kg/m from declamping to the end of the surgery. Whereas Group I patients did not receive a dopexamine infusion. During aortic cross-clamping the intramucosal pH value decreased in Group I patients, but did not change in Group II patients. Heart rate, cardiac index, and mixed venous oxygen saturation increased significantly during dopexamine infusion, whereas systemic vascular resistance was reduced. During aortic cross-clamping dopexamine was a useful agent in improving splanchnic blood flow, cardiac index venous saturation. Also, since the drug produces dose related hemodynamic changes of rapid onset and reversibility, it is possible to interrupt the infusion before aortic declamping to avoid the decrease in the intramucosal pH value.

Aged↗

PubMed1994

[Anesthesia with isoflurane in air and with isoflurane and nitrous oxide].

BACKGROUND: The aim of this study is to control the depth, the quality of recovery of total inhalation isoflurane anesthesia with or without nitrous oxide. DESIGN: Controlled comparative study was carried out on 51 patients, aged 40-54 yr, ASA 1, undergoing saphenectomy, in an University Clinic. METHODS: Induction: thiopental (3.5 mg kg), atracurium (0.6 mg kg) i.v. Patients were randomly assigned to: group 1 (26 patients), 5% isoflurane in air, by mask; group 2 (25 patients), 3% isoflurane and 60% N2O, by mask. Maintenance: group 1, 2% isoflurane in air; group 2, 1.2% isoflurane and 60% N2O. During anesthesia, consciousness and analgesia level were monitored by EEG Compressed Spectral Array, and clinical signs of pain by Evans' test; arousal time evaluation by "Time to correct response test". The subjective impressions, eventual dreams and recalls were collected using a standard set of questions one hour after the end of anesthesia and 24 hours later. One hour before anesthesia and two hours after the end of surgical procedures, a psychomotor performance recovery evaluation was performed using Zazzo's "deux barrages" test. DATA ANALYSIS: Student's "t" test. RESULTS: Adequate anesthetic depth was documented in all patients. Recovery time was statistically longer in isoflurane group (group 1 16.7 sd 2.2 minutes vs 10.3 sd 1.9 minutes group 2, p < 0.01). No patient reported recalls relative to anesthetic period. Two hours after recovery no significant differences in psychomotor performance tests were recorded. CONCLUSIONS: Isoflurane anesthesia in air, in adequate concentrations, provides a sufficient level of analgesia, hypnosis, amnesia, without clinical side effects.

Adult↗

PubMed1993

Effect of different renal glutathione levels on renal mercury disposition and excretion in the rat.

Mercury renal disposition has been studied following HgCl2 injection (5.0 mg/kg body wt., s.c.) in controls, diethylmaleate and N-acetylcysteine-treated rats. The different treatments were used to generate statistically different degrees of non-protein sulfhydryls concentration in kidneys. Diethylmaleate (4 mmol/kg body wt., i.p.) diminished kidney glutathione levels to 25% and N-acetylcysteine (2 mmol/kg body wt., i.p.) increased kidney non-protein sulfhydryls levels up to 75% compared with new controls. The amount of mercury in the kidneys, the mercury excretion rate in urine and the mercury plasma disappearance curves were calculated during 3 h post HgCl2 injection. BUN was measured in plasma at the same time period to determine the onset of kidney damage. The results indicate a higher HgCl2 renal clearance in N-acetylcysteine-treated rats compared to controls and less renal mercury accumulation. The data agree with diminished renal toxicity. On the other hand, renal mercury accumulation was higher and mercury renal clearance lower in diethylmaleate-treated animals, associated with higher renal toxicity. The results suggest that non-protein sulfhydryl levels (principally glutathione) might determine renal accumulation of mercury as well as its elimination rate and hence might enhance or mitigate the nephrotoxicity induced by the metal.

Acetylcysteine↗

PubMed1992

Acetaminophen nephrotoxicity in male Wistar rats.

Acute acetaminophen (APAP) nephrotoxicity was studied in male Wistar rats 1 h after different APAP single doses (200, 500 and 1000 mg/kg body wt, i.p.). Significant impairments in glomerular filtration rate (GFR) and clearance of p-aminohippuric acid (ClPAH) were observed in a dose-dependent way, although tubular parameters measured, water and electrolyte fractional excretion, remained at control values, while the urine to plasma osmolality ratios (Uosm/Posm) were diminished in APAP-1000 rats (control = 2.93 +/- 0.20, APAP-1000 = 1.40 +/- 0.04). The time course of renal function was also studied in APAP-1000 mg/kg-treated animals; parallel impairments were observed in GFR, ClPAH and tubular functions. Maximal alteration was observed at 16 h and restorement began at 24 h post-injection. Glucose renal handling, either at low or at high tubular glucose loads, remained at control values. Thus, our data suggest that the early stage of acetaminophen nephrotoxicity might be due to renal hemodynamic changes which might induce an alteration in tubular function principally in distal structures of medullary tissue, as shown by the Uosm/Posm results. These effects occurred coupled with a diminution in hepatic glutathione (GSH) levels at every APAP dose and in renal GSH levels in APAP-1000 mg/kg-treated rats. Moreover, renal damage was observed both in the presence or absence of hepatic damage.

Acetaminophen↗

PubMed1991

Effectiveness of N-acetylcysteine in protecting against mercuric chloride-induced nephrotoxicity.

Mercuric chloride (HgCl2)-induced nephrotoxicity, as measured by functional and biochemical parameters was evaluated in rats at different kidney non-protein sulfhydryls (NPS) levels. Diethylmaleate (DEM) induced a 75% of NPS diminution 1 h after the administration. Renal function (clearance) and biochemical measurements (gamma-glutamyltranspeptidase activity in urine, and lipoperoxides in kidney tissue) were impaired when the animals were HgCl2-treated. Values were highly impaired when the kidneys were NPS-depleted and were improved when NPS pools were previously increased although they were not similar to control values. DEM treatment promoted a higher accumulation of HgCl2 in both kidney and liver while NAC-treatment reduced significantly the metal content in these organs. These data are in favour of a positive relationship among mercury content and organ injury. On the other hand, mercury content increased while NPS levels diminished. NPS might play a role in the HgCl2 detoxification and thus avoids mercury accumulation and mercury effects.

Acetylcysteine↗

PubMed1989

[Therapy with ketotifen in breast-fed infants with asthma].

Fifty asthmatic infants under 10 months of age included in a double blind placebo controlled trial lasting nine months. The whole group received continuous bronchodilator therapy with fenoterol + ipratropium in the first month. This was gradually discontinued in the second month, and half of the children began to receive ketotifen 0.35 mg each 12 hours, and the other placebo. The treatment was maintained for months. During this period, both groups received bronchodilators only in the presence of wheezing attacks. Bronchodilator consumption, symptoms registered in a diary card, results of a medical examination practiced each 10 days, and symptoms/bronchodilator requirements relationship were considered in the evaluation. Both groups showed a significant reduction in their symptom after the continuous bronchodilator use period. Control group did not experience further improvement within the next months, despite raising bronchodilators use. Ketotifen group improved all parameters evaluated and diminished their bronchodilator consumption. These changes reached statistical significance after three months ketotifen treatment. In the follow-up posttreatment, ketotifen group remained with significative less symptoms (p less than 0.001).

Asthma↗

PubMed1986