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John H. Mcneill - One of the best experts on this subject based on the ideXlab platform.

  • N-acetylcysteine prevents nitrosative stress-associated depression of Blood Pressure and heart rate in streptozotocin diabetic rats.
    Journal of cardiovascular pharmacology, 2006
    Co-Authors: Prabhakara R. Nagareddy, Zhengyuan Xia, Kathleen M. Macleod, John H. Mcneill
    Abstract:

    Previous studies have indicated that cardiovascular abnormalities such as Depressed Blood Pressure and heart rate occur in streptozotocin (STZ) diabetic rats. Chronic diabetes, which is associated with increased expression of inducible nitric oxide synthase (iNOS) and oxidative stress, may produce peroxynitrite/nitrotyrosine and cause nitrosative stress. We hypothesized that nitrosative stress causes cardiovascular depression in STZ diabetic rats and therefore can be corrected by reducing its formation. Control and STZ diabetic rats were treated orally for 9 weeks with N-acetylcysteine (NAC), an antioxidant and inhibitor of iNOS. At termination, the mean arterial Blood Pressure (MABP) and heart rate (HR) were measured in conscious rats. Nitrotyrosine and endothelial nitric oxide synthase (eNOS) and iNOS expression were assessed in the heart and mesenteric arteries by immunohistochemistry and Western blot experiments. Untreated diabetic rats showed Depressed MABP and HR that was prevented by treatment with NAC. In untreated diabetic rats, levels of 15-F(2t)-isoprostane, an indicator of lipid peroxidation increased, whereas plasma nitric oxide and antioxidant concentrations decreased. Furthermore, decreased eNOS and increased iNOS expression were associated with elevated nitrosative stress in Blood vessel and heart tissue of untreated diabetic rats. N-acetylcysteine treatment of diabetic rats not only restored the antioxidant capacity but also reduced the expression of iNOS and nitrotyrosine and normalized the expression of eNOS to that of control rats in heart and superior mesenteric arteries. The results suggest that nitrosative stress depress MABP and HR following diabetes. Further studies are required to elucidate the mechanisms involved in nitrosative stress mediated depression of Blood Pressure and heart rate.

Edward J. Johns - One of the best experts on this subject based on the ideXlab platform.

  • Rilmenidine and reflex renal sympathetic nerve activation in wistar and hypertensive rats
    British journal of pharmacology, 1996
    Co-Authors: Tao Zhang, Edward J. Johns
    Abstract:

    1. This study sets out to examine the effect of rilmenidine administered systemically on basal and reflexly activated renal nerve activity in Wistar and stroke prone spontaneously hypertensive rats (SHRSP). 2. Animals were anaesthetized with chloralose/urethane, stimulating electrodes were placed on the brachial plexi and the renal nerves were isolated and put on recording electrodes. Both brachial nerves were stimulated electrically at 0.8, 1.6 and 3.2 Hz (15 V, 0.2 ms) in the absence and in the presence of rilmenidine given at 100 and 200 micrograms kg-1 i.v. in a cumulative manner. 3. Stimulation of the brachial nerves caused graded increases in Blood Pressure, heart rate and integrated renal nerve activity (P < 0.05) in both Wistar and SHRSP. Fast Fourier transformation of the renal nerve activity signal to generate a power spectrum demonstrated that both total power and percentage power at heart rate was higher in the SHRSP than Wistar (P < 0.05). Total power was raised during brachial nerve stimulation in both Wistar and SHRSP by some 200-300% (P < 0.05) but the percentage power at heart rate was decreased by some 60% (P < 0.01) in the Wistar but was raised by some 40-50% (P < 0.05) in the SHRSP. 4. Administration of rilmenidine caused dose-related decreases in Blood Pressure and heart rate and integrated renal nerve activity in both Wistar and SHRSP (all P < 0.05). Both doses of rilmenidine decreased (P < 0.05) the total power in the signal in both strains of rat by about one-half but the power occurring at heart rate only fell at the higher dose of compound in the Wistar, whereas in the SHRSP it was decreased by both doses by approximately 60-70%. In the presence of rilmenidine, coherence of the renal nerve signal was reduced in the Wistar and SHRSP and although the drug had no effect on phase difference in the Wistar, this parameter was decreased in the SHRSP by the low and high doses of rilmenidine (P < 0.05). 5. In the presence of 100 micrograms kg-1 rilmenidine, stimulation of the brachial nerves caused increases in total power in the Wistar and SHRSP (two to three fold, P < 0.05), together with a decrease (P < 0.05) in the percentage power occurring at heart rate in the Wistar, of some 60%, and an increase (P < 0.01) in the SHRSP, of some two to three times, which were very similar in magnitude and pattern to those obtained in the absence of the drug. Following the 200 micrograms kg-1 dose of rilmenidine, brachial nerve stimulation increased total power in the Wistar and SHRSP groups (P < 0.05) and whereas in the Wistar the percentage power at heart rate did not change in the SHRSP it was again increased in response to the electrical stimulation of the brachial plexus (P < 0.001) by between two to three fold. 6. These results showed that in both the Wistar and SHRSP rilmenidine Depressed Blood Pressure, heart rate and integrated renal nerve activity. Moreover, rilmenidine did not affect the reflex activation of renal nerve activity via the somatosensory system although the characteristics within the power spectra underwent certain changes which might have a functional impact at the level to the kidney.

Prabhakara R. Nagareddy - One of the best experts on this subject based on the ideXlab platform.

  • N-acetylcysteine prevents nitrosative stress-associated depression of Blood Pressure and heart rate in streptozotocin diabetic rats.
    Journal of cardiovascular pharmacology, 2006
    Co-Authors: Prabhakara R. Nagareddy, Zhengyuan Xia, Kathleen M. Macleod, John H. Mcneill
    Abstract:

    Previous studies have indicated that cardiovascular abnormalities such as Depressed Blood Pressure and heart rate occur in streptozotocin (STZ) diabetic rats. Chronic diabetes, which is associated with increased expression of inducible nitric oxide synthase (iNOS) and oxidative stress, may produce peroxynitrite/nitrotyrosine and cause nitrosative stress. We hypothesized that nitrosative stress causes cardiovascular depression in STZ diabetic rats and therefore can be corrected by reducing its formation. Control and STZ diabetic rats were treated orally for 9 weeks with N-acetylcysteine (NAC), an antioxidant and inhibitor of iNOS. At termination, the mean arterial Blood Pressure (MABP) and heart rate (HR) were measured in conscious rats. Nitrotyrosine and endothelial nitric oxide synthase (eNOS) and iNOS expression were assessed in the heart and mesenteric arteries by immunohistochemistry and Western blot experiments. Untreated diabetic rats showed Depressed MABP and HR that was prevented by treatment with NAC. In untreated diabetic rats, levels of 15-F(2t)-isoprostane, an indicator of lipid peroxidation increased, whereas plasma nitric oxide and antioxidant concentrations decreased. Furthermore, decreased eNOS and increased iNOS expression were associated with elevated nitrosative stress in Blood vessel and heart tissue of untreated diabetic rats. N-acetylcysteine treatment of diabetic rats not only restored the antioxidant capacity but also reduced the expression of iNOS and nitrotyrosine and normalized the expression of eNOS to that of control rats in heart and superior mesenteric arteries. The results suggest that nitrosative stress depress MABP and HR following diabetes. Further studies are required to elucidate the mechanisms involved in nitrosative stress mediated depression of Blood Pressure and heart rate.

Tao Zhang - One of the best experts on this subject based on the ideXlab platform.

  • Rilmenidine and reflex renal sympathetic nerve activation in wistar and hypertensive rats
    British journal of pharmacology, 1996
    Co-Authors: Tao Zhang, Edward J. Johns
    Abstract:

    1. This study sets out to examine the effect of rilmenidine administered systemically on basal and reflexly activated renal nerve activity in Wistar and stroke prone spontaneously hypertensive rats (SHRSP). 2. Animals were anaesthetized with chloralose/urethane, stimulating electrodes were placed on the brachial plexi and the renal nerves were isolated and put on recording electrodes. Both brachial nerves were stimulated electrically at 0.8, 1.6 and 3.2 Hz (15 V, 0.2 ms) in the absence and in the presence of rilmenidine given at 100 and 200 micrograms kg-1 i.v. in a cumulative manner. 3. Stimulation of the brachial nerves caused graded increases in Blood Pressure, heart rate and integrated renal nerve activity (P < 0.05) in both Wistar and SHRSP. Fast Fourier transformation of the renal nerve activity signal to generate a power spectrum demonstrated that both total power and percentage power at heart rate was higher in the SHRSP than Wistar (P < 0.05). Total power was raised during brachial nerve stimulation in both Wistar and SHRSP by some 200-300% (P < 0.05) but the percentage power at heart rate was decreased by some 60% (P < 0.01) in the Wistar but was raised by some 40-50% (P < 0.05) in the SHRSP. 4. Administration of rilmenidine caused dose-related decreases in Blood Pressure and heart rate and integrated renal nerve activity in both Wistar and SHRSP (all P < 0.05). Both doses of rilmenidine decreased (P < 0.05) the total power in the signal in both strains of rat by about one-half but the power occurring at heart rate only fell at the higher dose of compound in the Wistar, whereas in the SHRSP it was decreased by both doses by approximately 60-70%. In the presence of rilmenidine, coherence of the renal nerve signal was reduced in the Wistar and SHRSP and although the drug had no effect on phase difference in the Wistar, this parameter was decreased in the SHRSP by the low and high doses of rilmenidine (P < 0.05). 5. In the presence of 100 micrograms kg-1 rilmenidine, stimulation of the brachial nerves caused increases in total power in the Wistar and SHRSP (two to three fold, P < 0.05), together with a decrease (P < 0.05) in the percentage power occurring at heart rate in the Wistar, of some 60%, and an increase (P < 0.01) in the SHRSP, of some two to three times, which were very similar in magnitude and pattern to those obtained in the absence of the drug. Following the 200 micrograms kg-1 dose of rilmenidine, brachial nerve stimulation increased total power in the Wistar and SHRSP groups (P < 0.05) and whereas in the Wistar the percentage power at heart rate did not change in the SHRSP it was again increased in response to the electrical stimulation of the brachial plexus (P < 0.001) by between two to three fold. 6. These results showed that in both the Wistar and SHRSP rilmenidine Depressed Blood Pressure, heart rate and integrated renal nerve activity. Moreover, rilmenidine did not affect the reflex activation of renal nerve activity via the somatosensory system although the characteristics within the power spectra underwent certain changes which might have a functional impact at the level to the kidney.

Takeshi Shichijo - One of the best experts on this subject based on the ideXlab platform.

  • Temporary stenting in a case of Stanford type A aortic dissection complicated with left main coronary ischemia
    General Thoracic and Cardiovascular Surgery, 2020
    Co-Authors: Shu Yamamoto, Tatsuya Ogawa, Tomohiro Hayashida, Gentaro Kato, Takeshi Shichijo
    Abstract:

    A 54-year old man suffering from back pain was diagnosed with Stanford type A aortic dissection in our emergency unit. During the preparation of the operating room, he developed coronary ischemia with chest pain and Depressed Blood Pressure accompanied with abnormal electro- and echocardiography findings. He was transported to the catheter laboratory where stent placement into the left main coronary artery was successfully performed. Thereafter, he underwent total arch replacement, during which the stent was removed intentionally without performing coronary artery bypass graft. His postoperative course was uneventful and he is doing well without any ischemic event for 2 years after the surgery.