The potential protective role of the standardized leaf extract of ginkgo biloba (EGb761) on hypertension with hypercholesterolemia-induced renal injury was investigated in rats. Hypertension was induced by L-N(G)-nitroarginine methyl ester (L-NAME) and hypercholesterolemia was induced by feeding rats with a diet containing 1% cholesterol. In these animals repeated treatment with EGb761 produced a progressive reduction in the systolic, diastolic and mean arterial blood pressure (BP). EGb761 increased the progressive reduction in the systolic, diastolic and mean arterial BP induced by repeated administration of losartan with simvastatin. EGb761 corrected the compromised serum lipid profile and enhanced the effect of losartan with simvastatin on lipid profile. EGb761 protected against hypertension with hypercholesterolemia-induced renal injury as assessed by measurement of serum renal function markers and by histopathological examination. EGb761 enhanced the renoprotective effect of losartan with simvastatin in these rats. Concomitantly, hypertension with hypercholesterolemia-induced elevation of renal tissue malondialdehyde (MDA) and nitrite levels and reduction of intracellular reduced glutathione (GSH) level were inhibited by repeated treatment with EGb761. In addition, hypertension with hypercholesterolemia-induced increases in tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6) and interleukin-1β (IL-1β) levels in renal tissues were inhibited by treatment with EGb761. Also, EGb761 inhibited hypertension with hypercholesterolemia-induced decrease in endothelial nitric oxide synthase (eNOS) protein expression and increase in the protein expressions of inducible NO synthase (iNOS), TNF-α, IL-6 and IL-1β in the kidney tissues. Losartan with simvastatin produced similar effects on renal tissues oxidative stress, nitrite and inflammatory markers levels and on protein expressions of eNOS, iNOS, TNF-α, IL-6 and IL-1β. EGb761 enhanced losartan with simvastatin effects. These results indicate that EGb761 has the ability to protect against hypertension with hypercholesterolemia-induced renal injury. The ability of EGb761 to provide this renoprotective effect may positively correlate, besides its antihypertensive and antihypercholesterolemic effects, to its ability to suppress renal oxidative stress, nitrosative stress and inflammation.

The potential protective role of the standardized leaf extract of ginkgo biloba (EGb761) on hypertension with hypercholesterolemia-induced renal injury was investigated in rats. Hypertension was induced by L-N(G)-nitroarginine methyl ester (L-NAME) and hypercholesterolemia was induced by feeding rats with a diet containing 1% cholesterol. In these animals repeated treatment with EGb761 produced a progressive reduction in the systolic, diastolic and mean arterial blood pressure (BP). EGb761 increased the progressive reduction in the systolic, diastolic and mean arterial BP induced by repeated administration of losartan with simvastatin. EGb761 corrected the compromised serum lipid profile and enhanced the effect of losartan with simvastatin on lipid profile. EGb761 protected against hypertension with hypercholesterolemia-induced renal injury as assessed by measurement of serum renal function markers and by histopathological examination. EGb761 enhanced the renoprotective effect of losartan with simvastatin in these rats. Concomitantly, hypertension with hypercholesterolemia-induced elevation of renal tissue malondialdehyde (MDA) and nitrite levels and reduction of intracellular reduced glutathione (GSH) level were inhibited by repeated treatment with EGb761. In addition, hypertension with hypercholesterolemia-induced increases in tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6) and interleukin-1β (IL-1β) levels in renal tissues were inhibited by treatment with EGb761. Also, EGb761 inhibited hypertension with hypercholesterolemia-induced decrease in endothelial nitric oxide synthase (eNOS) protein expression and increase in the protein expressions of inducible NO synthase (iNOS), TNF-α, IL-6 and IL-1β in the kidney tissues. Losartan with simvastatin produced similar effects on renal tissues oxidative stress, nitrite and inflammatory markers levels and on protein expressions of eNOS, iNOS, TNF-α, IL-6 and IL-1β. EGb761 enhanced losartan with simvastatin effects. These results indicate that EGb761 has the ability to protect against hypertension with hypercholesterolemia-induced renal injury. The ability of EGb761 to provide this renoprotective effect may positively correlate, besides its antihypertensive and antihypercholesterolemic effects, to its ability to suppress renal oxidative stress, nitrosative stress and inflammation.

The potential protective role of the standardized leaf extract of ginkgo biloba (EGb761) on hypertension with hypercholesterolemia-induced renal injury was investigated in rats. Hypertension was induced by L-N(G)-nitroarginine methyl ester (L-NAME) and hypercholesterolemia was induced by feeding rats with a diet containing 1% cholesterol. In these animals repeated treatment with EGb761 produced a progressive reduction in the systolic, diastolic and mean arterial blood pressure (BP). EGb761 increased the progressive reduction in the systolic, diastolic and mean arterial BP induced by repeated administration of losartan with simvastatin. EGb761 corrected the compromised serum lipid profile and enhanced the effect of losartan with simvastatin on lipid profile. EGb761 protected against hypertension with hypercholesterolemia-induced renal injury as assessed by measurement of serum renal function markers and by histopathological examination. EGb761 enhanced the renoprotective effect of losartan with simvastatin in these rats. Concomitantly, hypertension with hypercholesterolemia-induced elevation of renal tissue malondialdehyde (MDA) and nitrite levels and reduction of intracellular reduced glutathione (GSH) level were inhibited by repeated treatment with EGb761. In addition, hypertension with hypercholesterolemia-induced increases in tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6) and interleukin-1β (IL-1β) levels in renal tissues were inhibited by treatment with EGb761. Also, EGb761 inhibited hypertension with hypercholesterolemia-induced decrease in endothelial nitric oxide synthase (eNOS) protein expression and increase in the protein expressions of inducible NO synthase (iNOS), TNF-α, IL-6 and IL-1β in the kidney tissues. Losartan with simvastatin produced similar effects on renal tissues oxidative stress, nitrite and inflammatory markers levels and on protein expressions of eNOS, iNOS, TNF-α, IL-6 and IL-1β. EGb761 enhanced losartan with simvastatin effects. These results indicate that EGb761 has the ability to protect against hypertension with hypercholesterolemia-induced renal injury. The ability of EGb761 to provide this renoprotective effect may positively correlate, besides its antihypertensive and antihypercholesterolemic effects, to its ability to suppress renal oxidative stress, nitrosative stress and inflammation.

The potential protective role of the standardized leaf extract of ginkgo biloba (EGb761) on hypertension with hypercholesterolemia-induced renal injury was investigated in rats. Hypertension was induced by L-N(G)-nitroarginine methyl ester (L-NAME) and hypercholesterolemia was induced by feeding rats with a diet containing 1% cholesterol. In these animals repeated treatment with EGb761 produced a progressive reduction in the systolic, diastolic and mean arterial blood pressure (BP). EGb761 increased the progressive reduction in the systolic, diastolic and mean arterial BP induced by repeated administration of losartan with simvastatin. EGb761 corrected the compromised serum lipid profile and enhanced the effect of losartan with simvastatin on lipid profile. EGb761 protected against hypertension with hypercholesterolemia-induced renal injury as assessed by measurement of serum renal function markers and by histopathological examination. EGb761 enhanced the renoprotective effect of losartan with simvastatin in these rats. Concomitantly, hypertension with hypercholesterolemia-induced elevation of renal tissue malondialdehyde (MDA) and nitrite levels and reduction of intracellular reduced glutathione (GSH) level were inhibited by repeated treatment with EGb761. In addition, hypertension with hypercholesterolemia-induced increases in tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6) and interleukin-1β (IL-1β) levels in renal tissues were inhibited by treatment with EGb761. Also, EGb761 inhibited hypertension with hypercholesterolemia-induced decrease in endothelial nitric oxide synthase (eNOS) protein expression and increase in the protein expressions of inducible NO synthase (iNOS), TNF-α, IL-6 and IL-1β in the kidney tissues. Losartan with simvastatin produced similar effects on renal tissues oxidative stress, nitrite and inflammatory markers levels and on protein expressions of eNOS, iNOS, TNF-α, IL-6 and IL-1β. EGb761 enhanced losartan with simvastatin effects. These results indicate that EGb761 has the ability to protect against hypertension with hypercholesterolemia-induced renal injury. The ability of EGb761 to provide this renoprotective effect may positively correlate, besides its antihypertensive and antihypercholesterolemic effects, to its ability to suppress renal oxidative stress, nitrosative stress and inflammation.

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BACKGROUND: Addiction to tramadol, a widely used analgesic, is becoming increasingly common. Tramadol can also induce seizures even after a single clinical dose. We tested whether the epileptogenicity of tramadol was associated with any changes in cortical excitability and inhibitory transmission using transcranial magnetic stimulation (TMS). METHODS: The study included 16 tramadol dependent patients and 15 age and sex matched healthy volunteers. Clinical evaluation was conducted using an addiction severity index. TMS assessment of excitability was conducted on the motor cortex since the response to each TMS pulse at that site is easily measured in terms of the amplitude of the twitches it evokes in contralateral muscles. Measures included resting and active motor threshold (RMT and AMT respectively), motor evoked potential (MEP) amplitude, cortical silent period (CSP) duration, transcallosal inhibition (TCI), and short interval intracortical inhibition and facilitation (SICI and ICF respectively). Urinary level of tramadol was measured immediately before assessing cortical excitability in each patient. RESULTS: RMT and AMT were significantly lower, the duration of the CSP was shorter and SICI was reduced in patients compared with the control group. These findings are suggestive of increased neural excitability and reduced GABAergic inhibition following exposure to tramadol. Also there were negative correlations between the severity of tramadol dependence and a number of cortical excitability parameters (AMT, RMT, and CSP with P=0.002, 0.005, and 0.04 respectively). CONCLUSIONS: The results provide evidence for hyperexcitability of the motor cortex coupled with inhibitory deficits in tramadol dependent patients.

BACKGROUND: Addiction to tramadol, a widely used analgesic, is becoming increasingly common. Tramadol can also induce seizures even after a single clinical dose. We tested whether the epileptogenicity of tramadol was associated with any changes in cortical excitability and inhibitory transmission using transcranial magnetic stimulation (TMS). METHODS: The study included 16 tramadol dependent patients and 15 age and sex matched healthy volunteers. Clinical evaluation was conducted using an addiction severity index. TMS assessment of excitability was conducted on the motor cortex since the response to each TMS pulse at that site is easily measured in terms of the amplitude of the twitches it evokes in contralateral muscles. Measures included resting and active motor threshold (RMT and AMT respectively), motor evoked potential (MEP) amplitude, cortical silent period (CSP) duration, transcallosal inhibition (TCI), and short interval intracortical inhibition and facilitation (SICI and ICF respectively). Urinary level of tramadol was measured immediately before assessing cortical excitability in each patient. RESULTS: RMT and AMT were significantly lower, the duration of the CSP was shorter and SICI was reduced in patients compared with the control group. These findings are suggestive of increased neural excitability and reduced GABAergic inhibition following exposure to tramadol. Also there were negative correlations between the severity of tramadol dependence and a number of cortical excitability parameters (AMT, RMT, and CSP with P=0.002, 0.005, and 0.04 respectively). CONCLUSIONS: The results provide evidence for hyperexcitability of the motor cortex coupled with inhibitory deficits in tramadol dependent patients.

BACKGROUND: Addiction to tramadol, a widely used analgesic, is becoming increasingly common. Tramadol can also induce seizures even after a single clinical dose. We tested whether the epileptogenicity of tramadol was associated with any changes in cortical excitability and inhibitory transmission using transcranial magnetic stimulation (TMS). METHODS: The study included 16 tramadol dependent patients and 15 age and sex matched healthy volunteers. Clinical evaluation was conducted using an addiction severity index. TMS assessment of excitability was conducted on the motor cortex since the response to each TMS pulse at that site is easily measured in terms of the amplitude of the twitches it evokes in contralateral muscles. Measures included resting and active motor threshold (RMT and AMT respectively), motor evoked potential (MEP) amplitude, cortical silent period (CSP) duration, transcallosal inhibition (TCI), and short interval intracortical inhibition and facilitation (SICI and ICF respectively). Urinary level of tramadol was measured immediately before assessing cortical excitability in each patient. RESULTS: RMT and AMT were significantly lower, the duration of the CSP was shorter and SICI was reduced in patients compared with the control group. These findings are suggestive of increased neural excitability and reduced GABAergic inhibition following exposure to tramadol. Also there were negative correlations between the severity of tramadol dependence and a number of cortical excitability parameters (AMT, RMT, and CSP with P=0.002, 0.005, and 0.04 respectively). CONCLUSIONS: The results provide evidence for hyperexcitability of the motor cortex coupled with inhibitory deficits in tramadol dependent patients.