Browse

You are looking at 91 - 100 of 128 items for

  • Refine by Access: all x
  • By Author: Heros, Roberto C. x
Clear All
Restricted access

Roberto C. Heros

Restricted access

Roberto C. Heros

Restricted access

Roberto C. Heros

Restricted access

Gabriel Gonzales-Portillo and Roberto C. Heros

Full access

Gabriel Gonzales-Portillo and Roberto C. Heros

Restricted access
Restricted access

Kiyoyuki Yanaka, Paul J. Camarata, Stephen R. Spellman, James B. McCarthy, Leo T. Furcht, Walter C. Low, and Roberto C. Heros

✓ Leukocytes play an important role in the development of ischemia—reperfusion injury. This study was conducted to ascertain whether synthetic peptides corresponding to the cell- and heparin-binding sequences of fibronectin that disturb leukocyte adhesion molecules were effective in neuronal protection after transient focal cerebral ischemia in rats. The authors evaluated the efficacy of peptides on infarction size, leukocyte infiltration in the ischemic tissue, and neurological outcome in rats subjected to 1 hour of cerebral ischemia and 48 hours of reperfusion. Twenty-one animals were divided into three groups: transient ischemia without treatment (Group I), transient ischemia with administration of vehicle (Group II), and transient ischemia with administration of fibronectin peptides (Group III). The mean myeloperoxidase activity (U/g wet wt) in the ischemic area was as follows: Group I, 0.19% ± 0.05; Group II, 0.21% ± 0.03; and Group III, 0.08% ± 0.02. The mean size of the infarction as a percentage of the total hemispheric volume was as follows: Group I, 38.35% ± 1.34%; Group II, 39.21% ± 2.42%; and Group III, 25.81% ± 4.87%. Group III showed a significant decrease in myeloperoxidase activity in the lesion and the infarction size was smaller when compared to Groups I and II (p < 0.05). The neurological grade in Group III was significantly better than in Groups I and II at 48 hours after reperfusion (p < 0.01). This study is the first to explore the therapeutic potential of synthetic fibronectin peptides in brain protection after transient focal ischemia, and the results also serve as a basis for studies of important cellular and molecular events that contribute to tissue damage.

Restricted access
Restricted access

Sun Ho Lee, Roberto C. Heros, John C. Mullan, and Kazuyoshi Korosue

✓ The ability of hemodilution to lower blood viscosity and increase cerebral blood flow has been proven experimentally; however, the optimum hematocrit for maximum oxygen delivery to ischemic brain tissue is not known, and a study was designed to determine this. Fifty dogs were selected for inclusion in the study using criteria based on changes in somatosensory evoked potentials at the time of arterial occlusion, which were found in a previous study to predict the development of a moderate infarction of relatively constant size. Infarctions were induced by permanent occlusion of the left middle cerebral artery and the azygous anterior cerebral artery. The animals selected for inclusion were divided into five groups of 10 dogs each: 1) a control group; 2) a group with 25% hematocrit; 3) a group with 30% hematocrit; 4) a group with 35% hematocrit; and 5) a group with 40% hematocrit. Isovolemic hemodilution was accomplished 1 hour after occlusion of vessels using dextran infusion and blood withdrawal. The animals were sacrificed after 6 days and infarction volume was determined from fluorescein-stained sections. Statistical analysis was performed using Student's t-test and one-way analysis of variance.

Mean infarction volume for each group, expressed as a percentage of total hemispheric volume ± 1 standard error of the mean, was 28.3% ± 2.8% for the control group, 33.6% ± 3.4% for the 25% hematocrit group, 17.1% ± 2.2% for the 30% hematocrit group, 29.2% ± 4.3% for the 35% hematocrit group, and 29.9% ± 2.1% for the 40% hematocrit group. The 30% hematocrit group showed the smallest average infarction size and this size differed significantly (p = 0.02) from the average infarction size in the control animals. These results show that, in this model of focal ischemia, a hematocrit of approximately 30% is optimum for protecting the brain.