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yohimbine/infarkt

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ArtiklidKliinilistes uuringutesPatendid
Leht 1 alates 24 tulemused

Protective effect of FR35447 on experimental cerebral infarction.

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Logi sisse
The protective effect of 2-(5-chloro-2-phenoxyanilino)-2-imidazoline [FR35447] on cerebral infarction was examined in animal models. FR35447 in p.o. doses of 1 mg/kg or more caused a marked reduction of arachidonate-induced cerebral infarction in rats. Since FR35447 (10(-6) M) inhibited platelet
Acute coronary syndrome (ACS) covers a spectrum of clinical conditions ranging from unstable angina, Non-ST segment elevation myocardial infarction (NSTEMI), or ST segment elevation myocardial infarction (STEMI). This study encompasses patients with acute coronary syndrome, who were receiving the
To evaluate whether cervical spinal neurons can influence cardiac indices and myocyte viability in the acutely ischemic heart, the hearts of anesthetized rabbits subjected to 30 min of LAD coronary arterial occlusion (CAO) were studied 3h after reperfusion. Control animals were compared to those
Changes in platelet alpha 2 adrenoreceptors and their relation to plasma catecholamine concentrations were studied in 11 patients with acute transmural myocardial infarction. A radiolabelled alpha 2 adrenoreceptor antagonist, [3H]-yohimbine, was used to assay alpha 2 adrenoreceptors on platelet
Onset of sudden death, myocardial infarction, and stroke occurs more likely in the morning hours. Similarly, a morning increase in epinephrine-induced platelet aggregation was observed accompanied by an increase in plasma catecholamines. Inhibition of the morning increase in platelet aggregation
Clonidine, a alpha(2)-adrenergic receptor agonist, has been demonstrated to be neuroprotective when administered during ischemia. It is not known whether clonidine can precondition brain against ischemia. We examined this possibility using a transient forebrain ischemia model. Rats received 40
Pharmacological preconditioning limits myocardial infarct size after ischemia/reperfusion. Dexmedetomidine is an α(2)-adrenergic receptor agonist used in anesthesia that may have cardioprotective properties against ischemia/reperfusion injury. We investigate whether dexmedetomidine administration
BACKGROUND Dexmedetomidine (DEX) is an α2-adrenergic receptor agonist commonly used during perioperative periods due to its sedation and analgesia effect. It is confirmed that DEX has cardioprotective effects against ischemia/reperfusion (I/R) injury. We investigated whether DEX administration is
A brain ischemia rat model was established by middle cerebral artery occlusion (MCAO) for 2h and reperfusion for 4h to investigate the underlying mechanism of the neuroprotection action of clonidine, a classical alpha-2 adrenergic agonist, on cerebral ischemia. Clonidine and yohimbine were
A 43-year-old man was found dead in a hotel room during a sexual relation with a colleague.He was treated both for cardiovascular disease and for erectile dysfunction with VIAGRA. A pillbox was found in the room with several tablets of verapamil (Isoptine), trimetazidine (Vastarel), yohimbine and

Platelet alpha 2 adrenoceptor characteristics during the morning increase in platelet aggregability.

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Logi sisse
The incidence of myocardial infarction and sudden cardiac death increases in the morning, as do platelet aggregability and sympathetic activity. We considered the possibility that increased platelet aggregability in the morning was due to an increase in platelet alpha 2 adrenergic receptor number or

Ambulatory infusion of noradrenaline for long-term treatment of Shy-Drager syndrome.

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Logi sisse
A 70-year-old female patient with advanced Shy-Drager syndrome exhibited severe orthostatic hypotension, low serum catecholamine levels, and autonomic dysfunction. She was bedridden despite oral medication with fludrocortisone, etilefrin, dihydroergotamine, L-dopa, yohimbine, and amezinium methyl
OBJECTIVE To investigate whether dexmedetomidine (DEX) preconditioning could alleviate the inflammation caused by myocardial ischemia/reperfusion (I/R) injury by reducing HMGB1-TLR4-MyD88-NF-кB signaling. METHODS Seventy rats were randomly assigned into five groups: sham group, myocardial I/R group
To investigate the mechanism of dexmedetomidine (Dex) in improving brain damage induced by cerebral ischemia-reperfusion injury in rats.Rats were randomly divided into a sham operation group, ischemia-reperfusion group, Dex group, piracetam group, and

Peri-interventional coronary vasomotion.

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A percutaneous coronary intervention (PCI) is a unique condition to study the effects of ischemia and reperfusion in patients with severe coronary atherosclerosis when coronary vasomotor function is compromised by loss of endothelial and autoregulatory vasodilation. We studied the effects of
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