ABSTRACT
Xylometazoline, a sympathomimetic available as over the counter drug, acts as a nasal decongestant and has been reported as an independent risk factor for hemorrhagic and ischemic stroke. The chronic use of xylometazoline leads to either increased release of more potent vasoconstrictor norepinephrine in the presynaptic region, or acts directly on central adrenoreceptors which leads to dysfunction resulting in chronic progressive vasculopathy that manifests as an ischemic stroke. Sympathomimetics also activate 12-lipoxygenase pathways which induce proliferation and migration of vascular smooth muscle cells. 12-lipoxgenase also plays a significant role in regulating the degree and stability of platelet activation, as its activation significantly strengthens platelet activation and uncontrolled platelet activation, which may lead to myocardial infraction and stroke. The present case reports a rare case of young adult suffering from isolated left medial cerebellar peduncle infarct related to the chronic use of xylometazoline. Acute cerebellar stroke is rare, especially in young adults and represent only 3% of total ischemic and hemorrhagic strokes. Clinical symptoms, patient age at the onset of stroke, and lesion size had no significant effect on the clinical outcome. Symptoms are frequently underestimated and misdiagnosed which further lead to serious complications and poor functional outcomes.
ABSTRACT
BACKGROUND: Ischemic preconditioning(IP) is known to be effective in the protection of myocardial necrosis, arrhythmia, and the restoration of the myocardial function in the ischemia-reperfusion state of the heart. However the exact mechanism is not clearly understood. The purpose of this study was to elucidate the trigger mechanism of IP on the restoration of the myocardial function after ischemia-reperfusion. MATERIAL AND METHOD: By connecting a Langendorff perfusion apparatus with an isolated heart of a rat, the normal temperature of the heart was maintained. The experiment was conducted in seven groups, which were divided according to the preconditioning stimuli and blockage methods: Group I(n=10) was a group without IP, Group II(n=10) a group of three-minute IP, Group III(n=10) a group of PEIP, Group IV(n=10) a group of clonidine IP, Group V(n=10) a group of IP after reserpine, Group VI(n=10) a group of PE & prazosin IP, and Group VII(n=10) a group of clonidine & yohimbine IP. Hemodynamic parameters of DP, LVEDP, +/-dP/dT and the changes of perfusion in the coronary artery were evaluated. RESULT: Developed pressure and +dP/dT changed per unit time. After 20 minutes of reperfusion, those of Group II and III were 63.1+/-3.7%, 64.8+/-4.6% and 64.5+/-4.6%, 63.8+/-4.4%, which improved more significantly than those of Group I(P<0.05). However, there were no significant differences between the Groups V and VI, and Group I. CONCLUSION: The Brief ischemic preconditioning and pharmacological preconditioning using alpha-receptor sympathomimetics have protecting effects on the restoration of myocardial function after reperfusion. And the protecting effect of preconditioning seems to be related to sympathetic neurotransmitters and to the selective action of the alpha1-adrenergic receptor.