LEYKOTSITLAR, QON–MIYA TO‘SIG‘I BUZILISHI VA NO-REFLOW FENOMENINING SEREBROVASKULYAR PATOLOGIYALARDAGI ANATOMIK O‘RNI

Authors

  • Xalilov Sanjar Abdivohid o'g'li Author
  • Xalilov Hikmatulla Dilshod o`g`li Author
  • Erolov Lochunbek Hamdam o'g'li Author

Keywords:

leykoitsit, neytrofil, makrofag, qon-miya to‘sig‘i, no-reflow fenomeni, mikrovaskulyar disfunksiya, serebrovaskulyar kasallik, ishemik insult, reperfuzion shikastlanish, mikroinfarkt.

Abstract

Serebrovaskulyar kasalliklar, jumladan ishemik insult va o‘tkir miya qon aylanishi yetishmovchiligi, global miyali o‘lim va nogironlikning yetakchi sabablaridan biridir. So‘nggi o‘n yillikda klinik va eksperimental tadqiqotlar qon-miya to‘sig‘i (QMT) buzilishi va uni tiklashdan keyingi davrda sodir bo‘ladigan "no-reflow" fenomenining patogenetik muhimligini chuqur o‘rganishga qaratildi. Ushbu sharhli maqolaning maqsadi leykotsitlar, ayniqsa neytrofillar va monotsitlar/makrofaglar, QMT buzilishi, mikroinfarktlar rivojlanishi va no-reflow fenomenidagi anatomik va molekulyar mexanizmlarni, 2015-2025 yillar oralig‘ida chop etilgan eng so‘nggi ilmiy ma’lumotlar asosida tahlil qilishdan iborat. Maqolada leykotsitlarning faollashuvi, endotelga yopishishi va adgeziyasi, shuningdek ular tomonidan ishlab chiqariladigan sitokinlar, kimyoatraktantlar va reaktiv kislorod turlarining endotel disfunksiyasi, bazal membrana shikastlanishi, perisit apoptosiga olib kelishi va kapillyar darajasidagi obstruktsiyaga hissasi muhokama qilinadi. No-reflow hodisasi, ya’ni qon tomir to‘sig‘i olib tashlangandan keyin ham to‘liq reperfuzion oqim tiklanmasligi, nafaqat makrovaskulyar, balki mikrovaskulyar darajada ham, leykotsitlarning jismoniy blokirovkasi, mikrotromboz va vazogenik shish tufayli yuzaga kelishi tahlil qilinadi. Ushbu jarayonlarning anatomik asoslari: miyaning oq moddasidagi kapillyarlarning tuzilishi, astratsit oyoqchalarining dinamikasi va glymfatik tizim bilan o‘zaro ta’siri ko‘rib chiqiladi. Yaqindagi klinik va preklinik tadqiqotlar leykotsitlar bilan bog‘liq yo‘llarni nishonlash (masalan, P-selektin, ICAM-1, CD11b/CD18 integrinlari) no-reflow ni kamaytirish va neyroproteksiyani oshirish uchun yangi terapevtik strategiyalarni taklif qilishini ko‘rsatadi. Bu sharh ushbu murakkab jarayonlarni birlamchi anatomik o‘zgarishlar nuqtayi nazaridan tizimlashtirib, kelajakdagi tadqiqotlar uchun yo‘nalishlar va potensial klinik qo‘llash imkoniyatlarini taklif etadi. [1,2,3]

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Published

2026-01-13