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  • 1
    Electronic Resource
    Electronic Resource
    Benidipine:A New Ca2+ Channel Blocker with a Cardioprotective Effect (1999)
    Oxford, UK : Blackwell Publishing Ltd
    Cardiovascular drug reviews 17 (1999), S. 0 
    Details
    ISSN: 1527-3466
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1527-3466.1999.tb00001.x
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  • 2
    Electronic Resource
    Electronic Resource
    Brief myocardial ischemia affects free radical generating and scavenging systems in dogs (1993)
    Springer
    Heart and vessels 8 (1993), S. 115-120 
    Details
    ISSN: 1615-2573
    Keywords: Sublethal ischemia ; Neutrophil function ; Superoxide dismutase ; Glutathione redox state
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary This study examined whether brief repeated myocardial ischemia altered free radical generating and scavenging activity in a dog model. In dogs preconditioned with four 5-min left anterior descending coronary artery (LAD) occlusions and reperfusions, we examined transcardiac changes in both the function of neutrophils, cells which are major free radical generators, and in myocardial antioxidant enzyme activity, as an indication of free radical scavenging. Neutrophil function was assessed by determining luminol-enhanced whole blood chemiluminescence (CL) induced by zymosan. Blood was taken simultaneously from the carotid artery and the cardiac vein running along the occluded LAD. Preconditioning with sublethal ischemia significantly reduced whole blood CL in the cardiac vein compared with the carotid artery after the first and fourth 5-min reperfusions, while there was no difference in neutrophil count between these sampling sites. Immediately after brief repeated ischemia and reperfusion, manganese-superoxide dismutase (SOD) activity was significantly enhanced, and glutathione reductase activity was markedly reduced in the ischemic, compared with the non-ischemic, myocardium. There were no differences in the myocardial activities of copper, zinc-SOD, glutathione peroxidase, and glutathione S-transferase between the ischemic and non-ischemic regions. Also, no difference was observed between the reduced myocardial glutathione levels in these regions, although the oxidized glutathione level was significantly higher in the ischemic regions of the subepicardial and subendocardial areas. We demonstrated that brief repeated ischemia affects free radical generating and scavenging systems in the ischemic myocardium.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01744795
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  • 3
    Electronic Resource
    Electronic Resource
    levation of Plasma Adenosine Levels May Attenuate the Severity of Chronic Heart Failure (1998)
    Springer
    Cardiovascular drugs and therapy 12 (1998), S. 307-309 
    Details
    ISSN: 1573-7241
    Keywords: NYHA ; ejection fraction ; cytokines ; dipyridamole ; dilazep
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Adenosine is known to be an endogenous cardioprotective substance. Since we have reported that adenosine levels increase in patients with chronic heart failure, we tested whether further elevation of the adenosine levels due to dipyridamole or dilazep for 6 months modulates the pathophysiology of chronic heart failure. In patients with chronic heart failure, either dipyridamole (300 mg/d n = 17) or dilazep (300 mg/d n = 5) were administered for 6 months. Twenty-two patients (mean ± SE age 58 ± 4 years old) attending a specialized chronic heart failure (CHF) clinic over 6 months and judged as in New York Heart Association (NYHA) function class II or III were examined. The other drugs used for the treatment of CHF were not altered during the study. There were 5 patients with CHF caused by ischemic heart diseases, and 17 patients with either valvular heart diseases or dilated cardiomyopathy. We found that increases in the plasma adenosine levels (202 ± 34 and 372 ± 74) nmol/L before and after dipyridamole administration, P 〈 0.005 ameliorate the severity of CHF (NYHA: 2.1 ± 0.5 to 1.7 ± 0.2). Both ejection fraction and maximal oxygen consumption increased. These improvements in the severity of chronic heart failure returned to baseline levels 6 months after discontinuation of dipyridamole. Comparable results were obtained in the dilazep protocol. We suggest that the elevation of plasma adenosine levels improves the pathophysiology of CHF.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1007726018470
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  • 4
    Electronic Resource
    Electronic Resource
    Intracoronary Administration of Adenosine Triphosphate Increases Coronary Blood Flow and Attenuates the Severity of Myocardial Ischemic Injury in Dogs (1999)
    Springer
    Cardiovascular drugs and therapy 13 (1999), S. 407-414 
    Details
    ISSN: 1573-7241
    Keywords: NO ; NO synthase ; adenosine ; fractional shortening ; lactate extraction ratio
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract ATP generates nitric oxide (NO) via activation of P2y receptors, and is degraded to adenosine. This study was undertaken to examine whether ATP causes coronary hyperemic flow via purinoceptors-, NO- and adenosine-dependent mechanisms, and attenuates the severity of contractile and metabolic dysfunction in the ischemic myocardium. In the non-ischemic canine hearts, the infusions of ATP into the coronary artery dose-dependently increased coronary blood flow. The levels of adenosine and end-product of NO in coronary venous blood over the arterial blood also increased. This hyperemic flow was partially attenuated by either 8-sulfophenyltheophylline (8SPT) or Lο-nitro arginine methyl ester (L-NAME), and completely blocked by the treatment with 8SPT, L-NAME and suramin (SRM). During myocardial ischemia, exogenous ATP increased coronary blood flow, and attenuated myocardial metabolic and contractile dysfunction, which was completely blunted by the treatment with 8SPT, L-NAME and SRM. We conclude that exogenous ATP increases coronary blood flow in the non-ischemic and ischemic myocardium mainly via either NO- or adenosine-dependent mechanisms.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1007899822136
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  • 5
    Electronic Resource
    Electronic Resource
    Chronic Treatment with FK506 Increases p70 S6 Kinase Activity Associated with Reduced Nitric Oxide Synthase Activity in Rabbit Hearts (2000)
    Springer
    Cardiovascular drugs and therapy 14 (2000), S. 329-336 
    Details
    ISSN: 1573-7241
    Keywords: FK506 ; nitric oxide synthase ; p70 S6 kinase ; hypertrophy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract FK506, an immunosuppressant, modulates phosphorylation of nitric oxide (NO) synthase, and induces cardiac hypertrophy in clinical settings. Having recently reported that chronic treatment with an inhibitor of NO synthase induces cardiac hypertrophy associated with the activation of 70-kD S6 kinase (p70S6K), which plays an important role in cardiac hypertrophy by regulating protein synthesis, we investigated the effects of chronic administration of FK506 on NO synthase and p70S6K activities in hearts. Twenty rabbits were divided into four groups: untreated rabbits, those treated with low-dose FK506 (0.10 mg/kg), those treated with medium-dose FK506 (0.20 mg/kg), and those treated with high-dose FK506 (0.40 mg/kg). FK506 was administered intravenously twice a day. After 4 weeks of treatment with FK506, calcium-dependent NO synthase activity in myocardium in the high-dose FK506 group was lower (P 〈 0.05) than in the untreated group. p70S6K activity in myocardium in the high-dose group was higher (P 〈 0.05) than in the untreated group. There was a significant (P 〈 0.05) inverse correlation between NO synthase and p70S6K activities in myocardium. However, the endothelial-dependent vasodilation of aortic rings or plasma levels of NO metabolites during experimental protocols did not differ among the groups studied. These findings suggest that chronic treatment of FK506 activates p70S6K and reduces NO synthase activity in rabbit hearts. Reduced NO synthase and/or activated p70S6K activities in hearts might contribute to the cardiac hypertrophy observed in some patients receiving FK506.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1007890827297
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  • 6
    Electronic Resource
    Electronic Resource
    Nisoldipine Selectively Induces Coronary Vasodilation and Improves Mild Myocardial Ischemia in Dogs: A Potential Role of Cellular Acidosis (1998)
    Springer
    Cardiovascular drugs and therapy 12 (1998), S. 533-541 
    Details
    ISSN: 1573-7241
    Keywords: nisoldipine ; calcium channel blocker ; coronary vessels ; myocardium ; Na+-H+ exchange ; amiloride ; cellular acidosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We examined whether nisoldipine, a calcium (Ca) channel blocker, increases coronary blood flow (CBF) without decreasing aortic blood pressure (AoP) with ischemic and nonischemic hearts, and whether the presence of cellular acidosis in ischemic myocardium contributes to the augmentation of coronary vasodilation due to nisoldipine. In 42 dogs, coronary perfusion pressure (CPP) was reduced so that CBF decreased to 60% of the baseline, and CPP was maintained constant thereafter. First, we administered nisoldipine into a systemic vein in the ischemic and nonischemic hearts. Second, nisoldipine was administered into the canine coronary artery of the ischemic myocardium with and without administration of either sodium bicarbonate (NaHCO3), sodium hydroxide (NaOH), or amiloride. Nisoldipine (0.25–4.0 mg/kg, IV) increased CBF by 59% in the ischemic myocardium more than the nonischemic myocardium (by 34%) without reducing AoP. The infusion of nisoldipine (40 ng/kg/min, IC) increased CBF markedly by about 55% in the ischemic myocardium with increases in fractional shortening (FS; 11 ± 2% to 21 ± 2%) and lactate extraction ratio (LER; −19 ± 4% to 15 ± 2%). Increases in CBF, FS, and LER were markedly attenuated during administration of nisoldipine with concomitant administration of either NaHCO3 or NaOH. Furthermore, the extent of increases in CBF (54 ± 2 mL/100 g/min), FS (13 ± 2%), and LER (−17 ± 4%) were also markedly attenuated due to the concomitant treatment with amiloride. We conclude that myocardial cellular acidosis plays an important role in mediating coronary vasodilation affected by nisoldipine in the ischemic myocardium. H+ may modulate the property of voltage-dependent Ca channels via Na+–H+ exchange.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1007714718298
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  • 7
    Electronic Resource
    Electronic Resource
    Inhibition of Nitric Oxide Synthesis Induces Coronary Vascular Remodeling and Cardiac Hypertrophy Associated with the Activation of p70 S6 Kinase in Rats (2000)
    Springer
    Cardiovascular drugs and therapy 14 (2000), S. 533-542 
    Details
    ISSN: 1573-7241
    Keywords: rapamycin ; ACE inhibitor ; hydralazine ; L-NAME ; protein synthesis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Chronic inhibition of nitric oxide (NO) synthesis is reported to induce the thickening of coronary artery walls and cardiac hypertrophy in vivo via angiotensin II receptors. Increased protein synthesis is the main feature of these structural changes. Activation of 70 kD S6 kinase (p70S6K) phosphorylates the 40S ribosomal protein S6 that regulates protein synthesis. We examined the role of p70S6K in the vascular and myocardial structural changes induced by the chronic inhibition of NO synthesis. The following 5 groups were studied: untreated Wister-Kyoto rats, those treated with an inhibitor of NO synthase, N ω-nitro-L-arginine methyl ester (L-NAME), those treated with L-NAME and an angiotensin I converting enzyme inhibitor (imidapril), those treated with L-NAME and hydralazine, and those treated with L-NAME and an inhibitor of p70S6K (rapamycin). After 8 weeks, wall-to-lumen ratio in myocardium and cardiomyocyte cross-sectional areas were quantified. L-NAME increased systolic blood pressure, wall-to-lumen ratio, and cardiomyocyte cross-sectional area compared with control animals. Imidapril or rapamycin, but not hydralazine, markedly reduced these structural changes. L-NAME increased p70S6K activity in myocardium compared with control rats. Imidapril or rapamycin prevented the activation of p70S6K activity in myocardium induced by L-NAME. These results suggest that activation of p70S6K plays an important role in coronary vascular remodeling and cardiac hypertrophy induced by the chronic inhibition of nitric oxide synthesis in vivo.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1007897308187
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  • 8
    Electronic Resource
    Electronic Resource
    The effect of CV-4151, a selective inhibitor of thromboxane synthetase, on prostanoid formation and platelet aggregation in humans (1988)
    Springer
    Cardiovascular drugs and therapy 2 (1988), S. 693-700 
    Details
    ISSN: 1573-7241
    Keywords: CV-4151 ; thromboxane synthetase inhibitor ; prostanoids ; platelet aggregation ; prostaglandins
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The pharmacokinetics and pharmacologic effects of a potent, selective inhibitor of thromboxane synthetase, CV-4151 [(E)-7-phenyl-7-(3-pyridyl)-6-heptenoic acid] on prostanoid formation and platelet aggregation were studied in 42 healthy male volunteers. The drug was well tolerated. After oral administration of 10 to 100 mg of CV-4151, peak plasma levels of 1–6 μg/mL were reached in a dose-dependent mannor within 1 hour. Elimination followed first-order fashion with elimination half-life of about 1 hour. Serum levels of thromboxane B2 reduced to 4% to 15% of control at 2 hours after drug ingestion dose-dependently. Serum levels of 6-Keto-prostaglandin F1α increased to about four to six times basal levels. Platelet aggregation induced by collagen and arachidonate was inhibited in most eases. Such pharmacologic effects outlasted serum drug levels. In repeated administration, stable inhibition of serum thromboxane B2 production and platelet aggregation in proportion to the enhancement of serum 6-keto-prostaglandin F1α production was observed although no drug accumulation was found. These results indicate that CV-4151 may be suitable for clinical trials in cardiovascular diseases in which imbalance between thromboxane and prostacyclin may be involved in the pathogenesis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00054211
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