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Abstract Objectives: This study assessed the cardio- and renoprotective effect of remote ischemic Preconditioning (PreC) in patients undergoing percutaneous coronary intervention (PCI). Background: Myocyte necrosis and contrast induced nephropathy (CIN) occur frequently in PCI and are associated with subsequent cardiovascular events. Methods: Two hundred consecutive patients undergoing elective PCI with normal baseline troponin-I (cTnI) values were recruited. Subjects were systematically allocated into 2 groups: 100 patients received PreC (created by three 5 min inflations of a blood pressure cuff to 200 mmHg around the upper arm, separated by 5 min intervals of reperfusion) 2 h before the PCI procedure, and control group (n= 100). Results: The incidence of PCI-related myocardial infarction (MI 4a) at 24 h after PCI was lower in the PreC group compared with control group (41% vs 64%, P =0.02). Subjects who received PreC had significant trend toward lower incidence of CIN at 72 h after contrast exposure (4 vs. 11, P = 0.05) and less chest pain during stent implantation compared to control group. At 3 months, the major adverse event rate was lower in the PreC group (6 vs. 14 events; P =0.04). Conclusions: The use of PreC 2 h before PCI, reduces the incidence of PCI-related MI 4a, tends to decrease the incidence of CIN and improves ischemic symptoms in patients undergoing elective PCI. The observed cardio- and renoprotection appears to confer sustained benefit on reduced major adverse events at 3 month follow-up beyond what is seen with judicious pre- and post-hydration (ClinicalTrials.gov identifier: NCT02313441).

Abstract Objectives: This study assessed the cardio- and renoprotective effect of remote ischemic Preconditioning (PreC) in patients undergoing percutaneous coronary intervention (PCI). Background: Myocyte necrosis and contrast induced nephropathy (CIN) occur frequently in PCI and are associated with subsequent cardiovascular events. Methods: Two hundred consecutive patients undergoing elective PCI with normal baseline troponin-I (cTnI) values were recruited. Subjects were systematically allocated into 2 groups: 100 patients received PreC (created by three 5 min inflations of a blood pressure cuff to 200 mmHg around the upper arm, separated by 5 min intervals of reperfusion) 2 h before the PCI procedure, and control group (n= 100). Results: The incidence of PCI-related myocardial infarction (MI 4a) at 24 h after PCI was lower in the PreC group compared with control group (41% vs 64%, P =0.02). Subjects who received PreC had significant trend toward lower incidence of CIN at 72 h after contrast exposure (4 vs. 11, P = 0.05) and less chest pain during stent implantation compared to control group. At 3 months, the major adverse event rate was lower in the PreC group (6 vs. 14 events; P =0.04). Conclusions: The use of PreC 2 h before PCI, reduces the incidence of PCI-related MI 4a, tends to decrease the incidence of CIN and improves ischemic symptoms in patients undergoing elective PCI. The observed cardio- and renoprotection appears to confer sustained benefit on reduced major adverse events at 3 month follow-up beyond what is seen with judicious pre- and post-hydration (ClinicalTrials.gov identifier: NCT02313441).

Abstract Objectives: This study assessed the cardio- and renoprotective effect of remote ischemic Preconditioning (PreC) in patients undergoing percutaneous coronary intervention (PCI). Background: Myocyte necrosis and contrast induced nephropathy (CIN) occur frequently in PCI and are associated with subsequent cardiovascular events. Methods: Two hundred consecutive patients undergoing elective PCI with normal baseline troponin-I (cTnI) values were recruited. Subjects were systematically allocated into 2 groups: 100 patients received PreC (created by three 5 min inflations of a blood pressure cuff to 200 mmHg around the upper arm, separated by 5 min intervals of reperfusion) 2 h before the PCI procedure, and control group (n= 100). Results: The incidence of PCI-related myocardial infarction (MI 4a) at 24 h after PCI was lower in the PreC group compared with control group (41% vs 64%, P =0.02). Subjects who received PreC had significant trend toward lower incidence of CIN at 72 h after contrast exposure (4 vs. 11, P = 0.05) and less chest pain during stent implantation compared to control group. At 3 months, the major adverse event rate was lower in the PreC group (6 vs. 14 events; P =0.04). Conclusions: The use of PreC 2 h before PCI, reduces the incidence of PCI-related MI 4a, tends to decrease the incidence of CIN and improves ischemic symptoms in patients undergoing elective PCI. The observed cardio- and renoprotection appears to confer sustained benefit on reduced major adverse events at 3 month follow-up beyond what is seen with judicious pre- and post-hydration (ClinicalTrials.gov identifier: NCT02313441).

Abstract Objectives: This study assessed the cardio- and renoprotective effect of remote ischemic Preconditioning (PreC) in patients undergoing percutaneous coronary intervention (PCI). Background: Myocyte necrosis and contrast induced nephropathy (CIN) occur frequently in PCI and are associated with subsequent cardiovascular events. Methods: Two hundred consecutive patients undergoing elective PCI with normal baseline troponin-I (cTnI) values were recruited. Subjects were systematically allocated into 2 groups: 100 patients received PreC (created by three 5 min inflations of a blood pressure cuff to 200 mmHg around the upper arm, separated by 5 min intervals of reperfusion) 2 h before the PCI procedure, and control group (n= 100). Results: The incidence of PCI-related myocardial infarction (MI 4a) at 24 h after PCI was lower in the PreC group compared with control group (41% vs 64%, P =0.02). Subjects who received PreC had significant trend toward lower incidence of CIN at 72 h after contrast exposure (4 vs. 11, P = 0.05) and less chest pain during stent implantation compared to control group. At 3 months, the major adverse event rate was lower in the PreC group (6 vs. 14 events; P =0.04). Conclusions: The use of PreC 2 h before PCI, reduces the incidence of PCI-related MI 4a, tends to decrease the incidence of CIN and improves ischemic symptoms in patients undergoing elective PCI. The observed cardio- and renoprotection appears to confer sustained benefit on reduced major adverse events at 3 month follow-up beyond what is seen with judicious pre- and post-hydration (ClinicalTrials.gov identifier: NCT02313441).

Background: Lead exposure can cause adverse effects on the reproductive system. This study aimed to evaluate the protective and therapeutic effects of vitamin E on lead-induced pituitary and gonadal dysfunctions and the possible mechanisms underlying these effects. Material and methods: 104 Albino Wistar adult rats were divided into four groups: group I: 12 rats received vehicle of lead and 12 rats received vehicle of vitamin E; Group II: 40 rats subdivided into 2 subgroups: Group IIa: 20 rats injected with lead acetate (10 mg/kg/day 5 times/week, i.p. for 6 weeks) and Group IIb: 20 rats injected with lead as previous then stopped for 6 weeks; Group III: 20 rats injected with lead acetate as previous followed by oral administration of vitamin E (50 mg/kg/day 5 times/week); Group IV: 20 rats received vitamin E simultaneously with lead acetate as previous. At the end of the experiment the animals were scarified and blood samples were collected for measurement of gonadotrophic, gonadal hormones, malondialdehyde (MDA), total antioxidant capacity (TAC) and caspase 3 by ELISA kits. The pituitary gland, testes, and ovaries were processed for histopathological examination. Results: Lead administration significantly decreased the plasma levels of gonadotrophic, and gonadal hormones, and TAC but significantly increased the plasma levels of MAD and caspase 3. Meanwhile, vitamin E administration with or after lead exposure significantly increased gonadotrophic, gonadal hormones and TAC and markedly decreased MAD and caspase 3. Conclusion: Vitamin E has protective and therapeutic effects on lead-induced gonadal dysfunction. This effect mediated by inhibition of oxidative stress and apoptosis.

Background: Lead exposure can cause adverse effects on the reproductive system. This study aimed to evaluate the protective and therapeutic effects of vitamin E on lead-induced pituitary and gonadal dysfunctions and the possible mechanisms underlying these effects. Material and methods: 104 Albino Wistar adult rats were divided into four groups: group I: 12 rats received vehicle of lead and 12 rats received vehicle of vitamin E; Group II: 40 rats subdivided into 2 subgroups: Group IIa: 20 rats injected with lead acetate (10 mg/kg/day 5 times/week, i.p. for 6 weeks) and Group IIb: 20 rats injected with lead as previous then stopped for 6 weeks; Group III: 20 rats injected with lead acetate as previous followed by oral administration of vitamin E (50 mg/kg/day 5 times/week); Group IV: 20 rats received vitamin E simultaneously with lead acetate as previous. At the end of the experiment the animals were scarified and blood samples were collected for measurement of gonadotrophic, gonadal hormones, malondialdehyde (MDA), total antioxidant capacity (TAC) and caspase 3 by ELISA kits. The pituitary gland, testes, and ovaries were processed for histopathological examination. Results: Lead administration significantly decreased the plasma levels of gonadotrophic, and gonadal hormones, and TAC but significantly increased the plasma levels of MAD and caspase 3. Meanwhile, vitamin E administration with or after lead exposure significantly increased gonadotrophic, gonadal hormones and TAC and markedly decreased MAD and caspase 3. Conclusion: Vitamin E has protective and therapeutic effects on lead-induced gonadal dysfunction. This effect mediated by inhibition of oxidative stress and apoptosis.