Angel Belmonte

Effects of amphetamine on T-cell immune response in mice

Mice chronically injected with amphetamine (0.4 mg/kg/day) showed a reduction in thymus and spleen cellularity, and in peripheral T lymphocyte population. The blastogenic response of spleen lymphoid cells was assessed and amphetamine was found to inhibit T-cell proliferation. Amphetamine also reduced the capacity of mice to the development and passive transfer of immunity to Listeria monocytogenes.

Effects of alprazolam on T-cell immunosuppressive response to surgical stress in mice

Mice submitted to surgical stress induced by laparotomy and treated with chronic alprazolam (1 mg/kg) showed a reduction in stress-induced suppression of thymus and spleen cellularity, as well as in peripheral T lymphocyte population. The blastic response of spleen lymphoid cells was also assessed and found to partially supress the inhibitory effect of surgery.

Effects of alprazolam on the development of MTV-induced mammary tumors in female mice under stress

Female C3H/He mice carrying the mammary tumor virus (MTV) were monitored for mammary tumor incidence and latent periods while subjected to a daily intraperitoneal (i.p.) injection of placebo or alprazolam (1 mg/kg per day). Although all of the mice were potential candidates for MTV-induced breast cancer, those injected with alprazolam were partially protected against adverse effects of stress induced by the daily administration of placebo.

Effects of alprazolam on influenza virus infection in stressed mice.

The review of the literature shows that stress can adversely affect influenza A virus infection. In this report, we study the effects of chronic alprazolam (1 mg/kg/day), a central benzodiazepine agonist anxiolytic, on the influenza A (PR-8/34) virus specific immune injury in mice exposed to a chronic auditory stressor. Treatment with alprazolam resulted in a significant reduction of stress-induced increase of virus titters and pulmonary vascular permeability. A correlation with the lethality of mice was also observed.

Effects of midazolam on T-cell immunosuppressive response to surgical stress in mice

Mice submitted to surgical stress induced by laparotomy and treated with chronic midazolam (1 mg/kg) showed a reduction in stress-induced suppression of thymus and spleen cellularity and in peripheral lymphocyte population. The blastogenic response of spleen lymphoid cells was also assessed and midazolam was found to partially attenuate the suppressive effect of surgery.

Effect of Desmethyl Tirilazad, Dizocilpine Maleate and Nimodipine on Brain Nitric Oxide Synthase Activity and Cyclic Guanosine Monophosphate during Cerebral Ischemia in Rats

The present study was designed to evaluate the effects of pretreatment with a combination of desmethyl tirilazad (21-aminosteroid) plus dizocilpine maleate (N-methyl-D-aspartate receptor antagonist) and nimodipine (calcium channel antagonist) on constitutive nitric oxide synthase (cNOS) activity and cyclic guanosine monophosphate (cGMP) levels in brain homogenates of rats subjected to global cerebral transient ischemia induced by bilateral clamping of the carotids for 30 min and reduction of arterial pressure (to 50–60 mm Hg) by intravenous infusion of trimethaphan (30 mg/kg). Our results show that cerebral ischemia produced an increase in cNOS activity and cGMP levels in brain homogenates. Pretreatment with desmethyl tirilazad or dizocilpine maleate or nimodipine individually significantly suppressed (p < 0.01) the increase in cNOS activity and cGMP levels induced by cerebral ischemia, which may be related to their neuroprotective effect. Similar results were obtained with pretreatment by a combination of desmethyl tirilazad plus dizocilpine maleate plus nimodipine.

Effect of Tirilazad on Brain Nitric Oxide Synthase Activity during Cerebral Ischemia in Rats

The effect of the 21-aminosteroid tirilazad mesylate (10 mg/kg, i.p.) on nitric oxide synthase (NOS) activity in the brain cortex was studied in male Wistar rats subjected to cerebral global transient ischemia induced by bilateral clamping of the carotids for 10 min and reduction of arterial pressure (to 50 mm Hg) by intravenous infusion of 1.5 ml of a solution of trimethaphan (5 mg/ml). NOS activity was determined by measuring the rate of conversion of [3H]arginine to [3H]citrulline in brain cortex. Our results show for the first time that tirilazad suppresses the increase of NOS activity in brain cortex induced by cerebral ischemia (136 +/- 16 vs. 60 +/- 9 pmol [3H]citrulline/min per mg protein) and also suppresses the increase in K(m) of NOS (5.7 +/- 0.1 vs. 1.2 +/- 0.2 mumol/l). These effects are attributed to the fact that tirilazad acts as a scavenger of oxygen free radicals formed during cerebral ischemia. These results document the neuroprotective efficacy of tirilazad mesylate in cerebral ischemia.

Effects of amphetamine on the activity of phagocytosis in mice

Experiments were conducted to evaluate the influences of chronic treatment with amphetamine (0.4 mg/kg/day) on the activity of phagocytosis in mice. Results show a decrease of the in vitro and in vivo phagocytosis measured by using the zymosan-particle uptake method and the carbon clearance test, respectively.

Autoradiographic evidence of 125I-β-endorphin binding sites in the articular cartilage of the rat

After 125I-beta-endorphin was intravenously injected to rats, an autoradiographic study of distal femur articular cartilage was performed. Results show a specific binding of 125I-beta-endorphin to chondrocytes, suggesting the possible existence of an opiate modulation of articular cartilage.

Effects of midazolam on the activity of phagocytosis in mice submitted to surgical stress

Abstract Mice submitted to surgical stress and treated with chronic midazolam (1 mg/kg) showed a reduction in stress-induced suppression of the in vitro and in vivo activity of phagocytosis, both measured using the zymosan-particle uptake method and the carbon clearance test, respectively.