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Biomedical subjects

F Cosentino

Publications and source records attributed to F Cosentino.

At least 19 recordsLinked to original sources
PubMed1995

Tetrahydrobiopterin and dysfunction of endothelial nitric oxide synthase in coronary arteries.

BACKGROUND: The L-arginine/nitric oxide pathway plays a key role in the regulation of arterial tone. Biosynthesis of nitric oxide requires activation of nitric oxide synthase in the presence of tetrahydrobiopterin as a cofactor. Biochemical studies demonstrated that activation of purified nitric oxide synthase at suboptimal concentrations of tetrahydrobiopterin leads to production of hydrogen peroxide. The present experiments were designed to determine whether in coronary arteries inhibition of tetrahydrobiopterin synthesis may favor nitric oxide synthase-catalyzed production of hydrogen peroxide. METHODS AND RESULTS: Primary branches of canine left anterior descending artery were incubated for 6 hours in minimum essential medium in the presence or in the absence of the tetrahydrobiopterin synthesis inhibitor 2,4-diamino-6-hydroxypyrimidine (DAHP; 10(-2) mol/L). Arterial rings were suspended for isometric tension recording. Production of cGMP was measured by radioimmunoassay. Experiments were performed in the presence of indomethacin (10(-5) mol/L). During contractions to the thromboxane A2/prostaglandin H2 receptor agonist U46619 (10(-7) mol/L), calcium ionophore A23187 (10(-9) to 10(-6) mol/L) caused endothelium-dependent relaxations. A nitric oxide synthase inhibitor, NG-nitro-L-arginine methyl ester (3 x 10(-4) mol/L), significantly inhibited these relaxations. In DAHP-treated arteries, relaxations to A23187 and its stimulating effect on cGMP production were significantly reduced in the presence of catalase (1200 U/mL). By contrast, catalase did not exert any effect in rings incubated in the absence of DAHP. Furthermore, the inhibitory effect of catalase on A23187-induced relaxations was abolished when coronary arteries were incubated in the presence of DAHP plus a liposoluble analogue of tetrahydrobiopterin, 6-methyltetrahydropterin (10(-4) mol/L). CONCLUSIONS: The present study suggests that hydrogen peroxide may be a mediator of endothelium-dependent relaxations in coronary arteries depleted of tetrahydrobiopterin. This initially compensatory response, triggered by a dysfunctional nitric oxide synthase, may represent an important mechanism underlying oxidative vascular injury.

Amino Acid Oxidoreductases↗
PubMed1995

Glossopharyngeal neuralgia with cardiac syncope.

Glossopharyngeal Neuralgia is an uncommon craniofacial pain syndrome that is occasionally associated with cardiac syncope. Involvement of the glossopharyngeal nerve may be painless or may be marked by true episodic neuralgia, and this justifies the term neuralgia reported here. We present 5 cases of this uncommon syndrome, of a total of 15 observed cases of glossopharyngeal neuralgia, successfully treated by section of the rootlets of Cranial Nerves IX and X or by microvascular decompression in the posterior cranial fossa. We also analyze the relevant literature and discuss the pathogenesis and treatment of the syndrome.

Cranial Fossa, Posterior↗
PubMed1994

Risk factors influencing survival in ICU acute renal failure.

Factors influencing survival in ICU patients with acute renal failure (ARF) requiring dialysis were analysed from data collected prospectively in an ARF registry. A total of 363 patients were analysed. Overall mortality was 79.1% and did not differ between medical and surgical patients. Factors associated with an increased risk of dying included the development of any concomitant organ system failure, the number of failed organs, APACHE II score at the time of renal consultation for medical patients, pre-existing chronic liver disease, and the number of days from ICU admission to institution of dialysis. Male gender reached borderline significance. Survivors recovered renal function and discontinued dialysis in 65.7% of cases. We conclude that mortality rates for ARF in ICU patients continues to be high. Multi-system organ failure (MSOF) occurs frequently and is the major cause of death.

Acute Kidney Injury↗
PubMed1994

[Intracranial actinomycosis].

Actinomycosis is a bacterial infection mainly affecting the cervico-oro-facial area, abdomen and lungs, sometimes spreading to the central nervous system. Extremely rare is the primary cerebral location of the disease.

Actinomyces↗
PubMed1993

Effect of endothelinA-receptor antagonist BQ-123 and phosphoramidon on cerebral vasospasm.

The present study was designed to determine whether an endothelinA (ETA)-receptor antagonist BQ-123 (cyclo[Dtrp, Dasp, pro-D-Val-Leu]) or an ET-converting enzyme inhibitor phosphoramidon may prevent development of cerebral vasospasm after subarachnoid hemorrhage (SAH). A "double hemorrhage" canine model of the disease was used (n = 17 dogs), and the degree of vasospasm of the basilar artery was assessed by angiography. Mongrel dogs of either sex were divided into three experimental groups: animals treated with daily intracisternal injections of BQ-123 (10(-4) M; n = 6) or phosphoramidon (2 x 10(-4) M; n = 6) and control animals treated with saline solution (n = 5). Diameter of basilar arteries in animals treated with saline solution was reduced by SAH to 56 +/- 7% of control diameter. BQ-123 and phosphoramidon did not significantly affect SAH-induced vasospasm (diameters were 62 +/- 0% and 56 +/- 10% of control diameters for BQ-123 and phosphoramidon, respectively). In contrast, in isolated canine basilar arteries BQ-123 (10(-5) M) selectively inhibited concentration-dependent contractions to ET-1 (10(-11)-3 x 10(-8) M; n = 5). Levels of immunoreactive ET in plasma and cerebrospinal fluid were not affected by development of vasospasm. These results suggest that intracisternal injections of ETA-receptor antagonist or phosphoramidon cannot prevent SAH-induced cerebral vasospasm and that ET-1 may not be the major mediator responsible for the decrease in cerebral arterial diameter associated with SAH.

Amino Acid Sequence↗
PubMed1992

Sympathetic overactivity in patients with chronic renal failure.

BACKGROUND: Hypertension is a frequent complication of chronic renal failure, but its causes are not fully understood. There is indirect evidence that increased activity of the sympathetic nervous system might contribute to hypertension in patients with end-stage renal disease, but sympathetic-nerve discharge has not been measured directly in patients or animals with chronic renal failure. METHODS: We recorded the rate of postganglionic sympathetic-nerve discharge to the blood vessels in skeletal muscle by means of microelectrodes inserted into the peroneal nerve in 18 patients with native kidneys who were undergoing long-term treatment with hemodialysis (of whom 14 had hypertension), 5 patients receiving hemodialysis who had undergone bilateral nephrectomy (of whom 1 had hypertension), and 11 normal subjects. RESULTS. The mean (+/- SE) rate of sympathetic-nerve discharge was 2.5 times higher in the patients receiving hemodialysis who had not undergone nephrectomy than in the normal subjects (58 +/- 3 vs. 23 +/- 3 bursts per minute, P < 0.01). In contrast, the rate of sympathetic-nerve discharge was similar in the patients receiving hemodialysis who had undergone bilateral nephrectomy (21 +/- 6 bursts per minute) and the normal subjects. The rate of sympathetic-nerve discharge in the patients receiving hemodialysis who had not undergone nephrectomy was also significantly higher (P < 0.01) than that in the patients with bilateral nephrectomy, and it was accompanied in the former group by higher values for vascular resistance in the calf (45 +/- 4 vs. 22 +/- 4 units, P < 0.05) and mean arterial pressure (106 +/- 4 vs. 76 +/- 14 mm Hg, P < 0.05). The rate of sympathetic-nerve discharge was not correlated with either plasma norepinephrine concentrations or plasma renin activity. CONCLUSIONS: Chronic renal failure may be accompanied by reversible sympathetic activation, which appears to be mediated by an afferent signal arising in the failing kidneys.

Angiotensin II↗
PubMed1992

Phase I study of FUDR continuous infusion with circadian variability in advanced cancer patients.

A phase I study of floxuridine circadian infusion was performed in 14 patients with advanced solid tumors (9 colonic, 1 gastric, 4 renal). The starting dose was 0.15 mg/kg/day for 14 days followed by a 14-day therapy-free interval. Sixty-eight percent of the daily dose was infused between 3pm and 9pm. The dose was increased by 0.025 mg/kg/day for each successive course. Eighty-one cycles of therapy were given for a total of 1134 days of treatment. The mean dose intensity was 0.868 mg/kg/day for the entire group. The highest dose achieved (maximum tolerated dose) was 0.325 mg/kg/day. The most frequent toxicity was diarrhea (4.9% of all courses) and nausea-vomiting (3.7% of all courses). These side effects were of a low grade and all were resolved without hospitalization. Our results suggest the circadian modulation of floxuridine infusion.

Adult↗
PubMed1992

[Endoscopic laser therapy in the palliative treatment of cancer of the esophagus].

Frequently when dysphagia first becomes manifest, esophageal carcinoma is already unresectable. Endoscopic laser therapy is a recently introduced method which can be used for the palliative treatment of esophageal cancer. By using the method the tumour is destroyed and the esophagus is recanalized, there is low incidence of complications, and the patient can be fed naturally thus improving quality of life. The method has been perfected over the past years and now offers excellent results.

Esophageal Neoplasms↗
PubMed1992

HN-10200 causes endothelium-independent relaxations in isolated canine arteries.

HN-10200, a nonselective inhibitor of phosphodiesterase, has positive inotropic and vasodilator activity. The present study was designed to determine the role of endothelium in causing relaxation to HN-10200 in isolated canine femoral and basilar arteries. Rings with and without endothelium were suspended for isometric tension recording in Krebs-Ringer bicarbonate solution bubbled with 94% O2, 6% CO2 (t = 37 degrees C; pH = 7.4). HN-10200 and another nonselective phosphodiesterase inhibitor, 3-isobutyl-1-methyl-xanthine (IBMX), caused similar concentration-dependent relaxations in femoral arteries with and without endothelium. In femoral arteries without endothelium, HN-10200 and IBMX significantly augmented relaxations to prostacyclin, but did not affect relaxations to a nitric oxide donor 3-morpholinosydnonimine (SIN-1) or endothelium-derived relaxing factor (EDRF) released by bradykinin. In basilar arteries, relaxations to HN-10200 were augmented by the removal of endothelium, whereas relaxations to IBMX were not affected. Relaxations to prostacyclin, SIN-1, and EDRF were not affected by the presence of phosphodiesterase inhibitors. The results of the present study suggest that HN-10200 causes endothelium-independent relaxations. In addition, it may augment relaxations to prostacyclin but does not affect relaxations to EDRF.

1-Methyl-3-isobutylxanthine↗
PubMed1992

Electrocardiographic changes in subarachnoid hemorrhage secondary to cerebral aneurysm. Report of 70 cases.

Electrocardiographic (ECG) alterations in the course of sub-arachnoid hemorrhage (SAH) have frequently been reported. The most frequent anomalies reported were lengthening of the QT interval, very negative or positive deep T waves, elevation or depression of the ST segment and the presence of U waves. We report 70 cases of SAH secondary to rupture of intracranial aneurysm (part of a larger group of 150) with ECG changes. We review the literature with particular regard to discussion of the possible pathogenesis of ECG changes and to the way they may affect the general clinical course.

Adult↗
PubMed1991

Prophylactic sclerotherapy in high-risk cirrhotics selected by endoscopic criteria. A multicenter randomized controlled trial.

Controlled trials of sclerotherapy for the prevention of the first variceal hemorrhage in cirrhotics have given conflicting results. In the present study, 106 cirrhotics were randomized to sclerotherapy (55 patients) or control group (51 patients). Admission criteria were no history of previous variceal bleeding and the presence of high-risk varices, i.e., a variceal score less than or equal to 0 according to Beppu et al. Sclerotherapy sessions were performed at time zero, 7 days, 30 days, and then monthly until eradication. Follow-up endoscopies were performed at 6-month intervals thereafter. Control patients underwent repeat endoscopy at 6-month intervals. Bleeding episodes were treated by sclerotherapy in both groups, whenever possible. Mean follow-up was 24 months. Analysis of the results was performed by the intention-to-treat method. Variceal bleeding occurred in 19 sclerotherapy patients (34.5%) and in 17 controls (35.4%, P = NS). Overall mortality was 34.5% in sclerotherapy patients and 50% in controls (P = NS). Seven of the 19 sclerotherapy patients (36.8%) and 11 of the 17 controls (64.7%) who bled died of hemorrhage (P less than 0.05, log-linear model). It is concluded that prophylactic sclerotherapy does not reduce the incidence of first variceal bleeding in cirrhotics. However, there seems to be a trend toward a lower bleeding-related mortality in sclerotherapy patients than in controls.

Esophageal and Gastric Varices↗
PubMed1990

Distal splenorenal shunt versus endoscopic sclerotherapy in the prevention of variceal rebleeding. First stage of a randomized, controlled trial.

In 1984 we started a prospective controlled trial comparing endoscopic sclerotherapy (ES) with the distal splenorenal shunt (DSRS) in the elective treatment of variceal hemorrhage in cirrhotic patients. The study population included 40 patients with cirrhosis and portal hypertension referred to our department from October 1984 to March 1988. These patients were drawn from a pool of 173 patients who underwent either elective surgery or endoscopic sclerotherapy during this time. Patients were assigned to one of the two groups according to a random-number table: 20 to DSRS and 20 to ES. During the postoperative period, no DSRS patient died, while one ES patient died of uncontrolled hemorrhage. One DSRS patient had mild recurrent variceal hemorrhage despite an angiographically patent DSRS. Four ES patients suffered at least one episode of gastrointestinal bleeding: two from varices and two from esophageal ulcerations. Five ES patients developed transitory dysphagia. Long-term follow-up was complete in all patients. Two-year survival rates for shunt (95%) and ES (90%) groups were similar. One DSRS patient rebled from duodenal ulcer, while three ES patients had recurrent bleeding from esophagogastric sources (two from varices and one from hypertensive gastropathy). One DSRS and two ES patients have evolved a mild chronic encephalopathy; four DSRS and two ES patients suffered at least one episode of acute encephalopathy. Two ES patients had esophageal stenoses, which were successfully dilated. Preliminary data from this trial seem to indicate that DSRS, in a subgroup of patients with good liver function and a correct portal-azygos disconnection, more effectively prevents variceal rebleeding than ES. However no significant difference in the survival of the two treatment groups was noted.

Adult↗
PubMed1989

The safety of cumulative doses of labetalol in perioperative hypertension.

Intravenous labetalol is commonly used in the management of hypertensive emergencies or urgencies as well as postoperative hypertension. The maximum recommended dose in any clinical setting is 300 mg in 24 hours. The safety of administering high doses of intravenous labetalol (greater than 300 mg in 24 hours) was evaluated in neurosurgical patients (n = 9). During 15 distinct periods of 24 hours or less, the mean dose of labetalol given was 623 +/- 86 mg. Adverse hemodynamic and biochemical effects were minor and easily reversible. Intravenous labetalol can safely be used in doses exceeding 300 mg per 24 hours in neurosurgical patients.

Adult↗