Effects of different nitric oxide synthases on pulmonary and systemic hemodynamics in hypoxic stress rat model

-д хадгалсан:
Номзүйн дэлгэрэнгүй
-д хэвлэсэн:Animal Models and Experimental Medicine vol. 8, no. 2 (Feb 1, 2025), p. 344
Үндсэн зохиолч: Zhang, Huan
Бусад зохиолчид: Zhang, Yu, Wang, Xiaojun, Liu, Jie, Zhang, Wei
Хэвлэсэн:
John Wiley & Sons, Inc.
Нөхцлүүд:
Онлайн хандалт:Citation/Abstract
Full Text
Full Text - PDF
Шошгууд: Шошго нэмэх
Шошго байхгүй, Энэхүү баримтыг шошголох эхний хүн болох!

MARC

LEADER 00000nab a2200000uu 4500
001 3172388553
003 UK-CbPIL
022 |a 2576-2095 
024 7 |a 10.1002/ame2.12453  |2 doi 
035 |a 3172388553 
045 0 |b d20250201 
100 1 |a Zhang, Huan  |u Research Center for High Altitude Medicine, Qinghai University, Xining, Qinghai, China 
245 1 |a Effects of different nitric oxide synthases on pulmonary and systemic hemodynamics in hypoxic stress rat model 
260 |b John Wiley & Sons, Inc.  |c Feb 1, 2025 
513 |a Journal Article 
520 3 |a Background Under hypoxia, exaggerated compensatory responses may lead to acute mountain sickness. The excessive vasodilatory effect of nitric oxide (NO) can lower the hypoxic pulmonary vasoconstriction (HPV) and peripheral blood pressure. While NO is catalyzed by various nitric oxide synthase (NOS) isoforms, the regulatory roles of these types in the hemodynamics of pulmonary and systemic circulation in living hypoxic animals remain unclear. Therefore, this study aims to investigate the regulatory effects of different NOS isoforms on pulmonary and systemic circulation in hypoxic rats by employing selective NOS inhibitors and continuously monitoring hemodynamic parameters of both pulmonary and systemic circulation. Methods Forty healthy male Sprague–Dawley (SD) rats were randomly divided into four groups: Control group (NG‐nitro‐D‐arginine methyl ester, D‐NAME), L‐NAME group (non‐selective NOS inhibitor, NG‐nitro‐L‐arginine methyl ester), AG group (inducible NOS inhibitor group, aminoguanidine), and 7‐NI group (neurological NOS inhibitor, 7‐nitroindazole). Hemodynamic parameters of rats were monitored for 10 min after inhibitor administration and 5 min after induction of hypoxia [15% O2, 2200 m a. sl., 582 mmHg (76.5 kPa), Xining, China] using the real‐time dynamic monitoring model for pulmonary and systemic circulation hemodynamics in vivo. Serum NO concentrations and blood gas analysis were measured. Results Under normoxia, mean arterial pressure and total peripheral vascular resistance were increased, and ascending aortic blood flow and serum NO concentration were decreased in the L‐NAME and AG groups. During hypoxia, pulmonary arterial pressure and pulmonary vascular resistance were significantly increased in the L‐NAME and AG groups. Conclusions This compensatory mechanism activated by inducible NOS and endothelial NOS effectively counteracts the pulmonary hemodynamic changes induced by hypoxic stress. It plays a crucial role in alleviating hypoxia‐induced pulmonary arterial hypertension. 
651 4 |a United States--US 
651 4 |a China 
653 |a Carotid arteries 
653 |a Physiology 
653 |a Nitrates 
653 |a Software 
653 |a Blood flow 
653 |a Chemical elements 
653 |a Animals 
653 |a Catheters 
653 |a Hypoxia 
653 |a Altitude 
653 |a Isoforms 
653 |a Drugs 
653 |a Vasoconstriction 
653 |a Nitric-oxide synthase 
653 |a Polyethylene 
653 |a Hemodynamics 
653 |a Surgery 
653 |a Blood gas analysis 
653 |a Blood pressure 
653 |a Ostomy 
653 |a Edema 
653 |a Veins & arteries 
653 |a Data collection 
653 |a Nervous system 
653 |a Nitric oxide 
653 |a Peripheral blood 
653 |a Pulmonary arteries 
653 |a Ultrasonic imaging 
653 |a Variance analysis 
653 |a Rodents 
700 1 |a Zhang, Yu  |u Department of Basic Medicine, Qinghai University, Xining, Qinghai, China 
700 1 |a Wang, Xiaojun  |u Department of Basic Medicine, Qinghai University, Xining, Qinghai, China 
700 1 |a Liu, Jie  |u Department of Pathology, Xi'an Chest Hospital, Xi'an, Shaanxi, China 
700 1 |a Zhang, Wei  |u Research Center for High Altitude Medicine, Qinghai University, Xining, Qinghai, China 
773 0 |t Animal Models and Experimental Medicine  |g vol. 8, no. 2 (Feb 1, 2025), p. 344 
786 0 |d ProQuest  |t Biological Science Database 
856 4 1 |3 Citation/Abstract  |u https://www.proquest.com/docview/3172388553/abstract/embedded/7BTGNMKEMPT1V9Z2?source=fedsrch 
856 4 0 |3 Full Text  |u https://www.proquest.com/docview/3172388553/fulltext/embedded/7BTGNMKEMPT1V9Z2?source=fedsrch 
856 4 0 |3 Full Text - PDF  |u https://www.proquest.com/docview/3172388553/fulltextPDF/embedded/7BTGNMKEMPT1V9Z2?source=fedsrch