SUT-8701, a Cholecystokinin Analog, Prevents the Cholinergic Degeneration in the Rat Cerebral Cortex Following Basal Forebrain Lesioning

Takahashi, Masahide; Sugaya, Kiminobu; Kojima, Kumi; Katoh, Tsuyoshi; Ueki, Masaaki; Kubota, Keiichi

doi:10.1254/jjp.62.1

Cited by 4 publications

(3 citation statements)

References 43 publications

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“…However, the mechanisms that support this possible protection have not been completely identified [2,5,8,9,15,26,27,29]. Although these studies suggest a beneficial effect of these drugs, experimental studies have not yet produced definitive results concerning this cardioprotective role.…”

Section: Discussionmentioning

confidence: 99%

“…Different mechanisms have been suggested as the cause of this hypoxia-reoxygenation syndrome, and numerous therapeutic strategies have been put into practice to prevent this situation. Calcium channel blockers (mainly nifedipine) seem to exert a cardioprotective effect during hypoxia-reoxygenation through mechanisms that have not yet been well-defined [5,27].…”

Section: Introductionmentioning

confidence: 99%

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Coronary vasomotor disorders during hypoxia-reoxygenation: do calcium channel blockers play a protective role?

et al. 1999

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During heart surgery, myocardial dysfunction may occasionally appear when extracorporeal circulation is discontinued, causing serious haemodynamic disorders. Many mechanisms are involved in this hypoxia-reoxygenation syndrome. The aim of this experimental study was to characterize the vasomotor disorders that take place in the isolated porcine coronary artery during in vitro hypoxia-reoxygenation and to analyse the effect of nifedipine on them. Rings of porcine coronary artery were placed in an organ chamber connected to a system that recorded isometric forces. The vascular rings were divided into two groups: control group (no nifedipine) and study group (nifedipine, 10(-6) mol/l). The vascular rings were precontracted with 30 mmol/l KCl and then hypoxia-reoxygenation was induced. Control arterial rings showed important changes in coronary vasomotor tone: severe hypoxic contraction (from 14.48+/-1.16 g of stable contraction to 17.6+/-0.44 g after the imposition of hypoxia), and transient vasodilation during reoxygenation (69.9+/-10.1% of the maximum contraction achieved). The nifedipine group experienced a slow, progressive, vasodilation throughout the whole experiment (73+/-3.5% of the maximum contraction). Neither hypoxic vasospasm nor fluctuations of the coronary vascular tone occurred. Thus, at the end of the hypoxia, the control vessels presented a degree of contraction similar to the initial level. However, in the rings treated with nifedipine, the percentage of dilation was 73+/-3.5% (P<0.05). In the isolated porcine coronary artery with intact endothelium undergoing a situation of hypoxia-reoxygenation, we have detected transient vasoconstriction during the first period of hypoxia, followed by vasodilation during reoxygenation. The intracoronary administration of nifedipine prior to the imposition of hypoxia prevents hypoxic contraction, achieving a greater and more stable degree of coronary vasorelaxation during the complete process of hypoxia-reoxygenation.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Coronary vasomotor disorders during hypoxia-reoxygenation: do calcium channel blockers play a protective role?

et al. 1999

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“…Therefore, an increased coronary flow during reperfusion as well as an inhibition of ischemic contracture seems to play a crucial role in improving the myocardial dysfunction of ischemic-reperfused hearts (Umeda & Saida, 1993). However, whether the benefits of IPC extend beyond the myocyte and protect the vasculature from sustained ischemia is a topic of some controversy (Przyklenk & Kloner, 1998).…”

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confidence: 99%

Acute Ischemic Preconditioning and High Subchronic Co Exposure Independently Increase Myocardial Tolerance to Ischemia

Rochetaing¹

2001

Inhalation Toxicology

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This study was designed to investigate whether exposure to carbon monoxide (CO) could alter or raise the ischemic tolerance induced by preconditioning. To this end, isolated rat hearts were aerobically perfused for 20 min. Hearts were then randomized to two groups: (1) a further 20-min aerobic perfusion, and (2) ischemic preconditioning (2 cycles of 5 min of ischemia followed by 5 min of reperfusion). Hearts were then subjected to 25 min of low-flow (0.3 ml/min.) global ischemia (37 degrees C) and 30 min of reperfusion. In parallel studies, the same protocols were performed in hearts from rats previously exposed to subchronic CO (600 ppm for 2 wk). Ischemic preconditioning accelerated the development of ischemic contracture (onset = 6.0 +/- 0.3 vs. 8.6 +/- 0.9 min), increased the preischemic coronary flow (19.0 +/- 1.0 vs. 11.6 +/- 0.6 ml/min/g), improved contractile recovery (73.7 +/- 8.9 vs. 30.8 +/- 7.5%), but was without effect on reactive hyperemia (151.2 +/- 4.7 vs. 149.2 +/- 5.1%) and incidence of ventricular arrhythmia during reperfusion (55.6 vs. 60.0%) compared to a control group. CO exposure alone increased the baseline coronary flow (20.1 +/- 1.5 vs. 12.8 +/- 0.6 ml/min/g) and the contracture magnitude (54.8 +/- 6.8 vs. 37.1 +/- 4.8%), improved both contractile recovery (66.1 +/- 6.3 vs. 30.8 +/- 7.5%) and ventricular arrhythmia incidence (22.2 vs. 60.0%), and increased the hyperemic coronary flow (26.7 +/- 1.5 vs. 19.1 +/- 0.7%). Preconditioning after CO exposure exacerbated ischemic contracture (shorter onset and higher magnitude), and increased the reactive hyperemia (29.8 +/- 1.4%), but raised the beneficial effects on contractile recovery (85.4 +/- 8.4%) without alteration of ventricular tachycardia prevention (22.2%). Thus, CO-exposed hearts could be preconditioned in the same way as normal myocardium.

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Improvement of ischemic myocardial dysfunction by nisoldipine

Saida

Umeda

Itakura

1994

Cardiovasc Drug Ther

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We examined the cardioprotective effect of nisoldipine against myocardial dysfunction during ischemia and reperfusion in Langendorff perfused rabbit hearts. Nisoldipine was administered to the hearts before 60 minutes of global ischemia. This agent inhibited the increase of end-diastolic pressure during ischemia and also improved the recovery of left ventricular developed pressure and coronary flow during reperfusion in a concentration-dependent manner. The maximal cardioprotective effect was observed in 10(-8) M nisoldipine. The beneficial effect was associated with an increase of coronary flow during reperfusion. Therefore, both the nisoldipine-increased coronary flow during reperfusion and the inhibition of ischemic contracture by nisoldipine seem to play a crucial role in improving myocardial dysfunction of ischemic-reperfused hearts.

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SUT-8701, a Cholecystokinin Analog, Prevents the Cholinergic Degeneration in the Rat Cerebral Cortex Following Basal Forebrain Lesioning

Cited by 4 publications

References 43 publications

Coronary vasomotor disorders during hypoxia-reoxygenation: do calcium channel blockers play a protective role?

Coronary vasomotor disorders during hypoxia-reoxygenation: do calcium channel blockers play a protective role?

Acute Ischemic Preconditioning and High Subchronic Co Exposure Independently Increase Myocardial Tolerance to Ischemia

Improvement of ischemic myocardial dysfunction by nisoldipine

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