Cerebral vasospasm is the most serious and common complication of subarachnoid hemorrhage, and it is an important factor affecting the survival rate and quality of life of patients. In the 20th century, a lot of research has been conducted on the mechanism of cerebral vasospasm caused by SAH, but it has not been fully elucidated so far. With the development of molecular biology technology, some progress has been made in the study of the mechanism of its occurrence, especially the study of vasoactive substances, microcirculation and related genes have made some new discoveries, mainly in the following aspects: (i) vasoactive substances 1. Hemolysis products: Previous studies found that the high molecular hemolysis product oxyhemoglobin is the most initial key factor causing cerebral vasospasm, and its mechanism may be the generation of oxygen radicals through lipid peroxidation, the induction of endothelin production, the combination with nitric oxide (NO) to prevent the vasodilatory effect of NO, and the spasmogenic effect of its breakdown product bilirubin. The low-molecular hemolysis product ATP may increase intracellular calcium ions in smooth muscle cells and vasoconstriction through P2 receptor-mediated calcium channels. The current study suggests that the action of hemolysis products may occur mainly in the early stages of cerebral vasospasm and act as initiating factors, leading to the onset of delayed cerebral vasospasm. 2. endothelium-dependent vasoactive factor: NO is released from endothelial cells into adjacent smooth muscle cells, activating soluble guanylate cyclase (GC), which produces cyclic guanosine monophosphate (cGMP), activating intracellular calcium pumps, allowing free calcium to enter cells and causing smooth muscle diastole. oxyhemoglobin, a hemolysis product after SAH, binds NO, and the decrease in NO inactivates GC, which then leads to vasoconstriction. The decrease of NO inactivates GC, which leads to vasoconstriction. 3, endothelial derived contractile factor (EDCF): endothelin (ET) is the strongest vasoconstrictor found so far, its vasoconstrictive effect is 10 times that of angiotensin, ET is involved in cerebral vasospasm after SAH, the mechanism may be activation of protein kinase C (PKC); activation of GC to increase cGMP; inhibition of adenylate cyclase to reduce cAMP, ET in plasma and cerebrospinal fluid concentrations and whether ET receptor antagonists have therapeutic effects on cerebral vasospasm are inconsistently reported in the literature. 4.Calcitonin gene-related peptide (CGRP): CGRP is a bioactive peptide composed of 37 amino acid residues, which has strong vasodilatory effect, and its effect does not depend on the integrity of endothelial cells. 5.Neuropeptide Y (NPY): peptidergic neurons and their protrusions are closely connected with local cerebral arteries, which can cause strong and long-lasting vasoconstriction. 6, the common effect of vasoactive substances: cerebral vasospasm after SAH is biphasic, the initial 1~3 days is the acute phase, followed by the delayed cerebral vasospasm phase, current research suggests that the mechanism of vasospasm in the two phases is different, the acute phase may be mainly involved by Ca2+, while the delayed phase may be mainly mediated by PKC without Ca2+ involvement, many known vasoactive substances are through the activation of various Ca2+ channels, causing Ca2+ to flow inward and bind to its receptor calmodulin (CaM). (B) Microcirculatory studies of cerebral vasospasm 1. Fluid shear stress: Under normal physiological conditions, vascular shear stress regulates vessel diameter and affects the morphology of vascular endothelial cells, as well as their function. fluid shear stress complicates the process of cerebral vasospasm through its effect on vascular endothelial cells. Whether or not the subarachnoid clot is cleared, the artery has normal contractility, but compliance decreases, indicating that the vasculature undergoes adaptive changes. Smooth muscle cells are damaged during vasospasm making vasodilation dysfunctional until endothelial cell function is restored and vasospasm is relieved. 2. Microvascular perfusion during SAH: Although the importance of microcirculation on cerebral ischemia-reperfusion damage is well known, its role on cerebral vasospasm is not clear. Early inhibition of microvascular function is manifested by reduced carbon utilization in the hypothalamus and brainstem, and microvessels may be the target of SAH effects. The first finding of diminished microcirculatory function is the activation of leukocytes during SAH, which can lead to microvascular occlusion and blood-brain barrier disruption with secondary cerebral edema. Some SAH patients present with reduced cerebral blood flow and cerebral tissue blood perfusion without detecting cerebral vasospasm, which may be due to SAH using numerous purine and pyrimidine receptors in the brain and different intracellular signaling pathways to affect the microcirculation and its regulatory mechanisms, causing changes in the molecular mechanisms of the microvasculature itself. 3.Conducted vascular response: clinically, it is found that most of the vessels spasming after SAH are adjacent to the site of blood clots, but sometimes there are also distant cerebral vasospasms, and even vasospasms and cerebral ischemia in the contralateral cerebral hemisphere, and the mechanism of their occurrence is unknown. This may explain why patients with no or only mild cerebral vasospasm develop a large cerebral ischemic semidark band. (C) Genetic research on cerebral vasospasm 1. Gene introduction or knockdown: With the development of recombinant DNA technology, it was found that normal cerebral arterial vascular outer membrane endothelial cell type NOS (eNOS) gene expression can regulate vascular tension, so applying NO donors or increasing eNOS activity while selectively inhibiting nNOS and iNOS is a better therapeutic measure. The inhibitor aminoguanidine has been applied to clinical treatment of cerebral ischemia. 2, mRNA regulation: antisense oligo-DNA in vitro experiments can be effectively used for DNA functional analysis, Ohkuma through recombinant DNA technology can make the gene precisely transduced to the blood vessels, in order to maintain the integrity of oligo-DNA and stability in a considerable period of time, not to be broken down is very important. 3. Gene activation: Many stress conditions, especially cerebral ischemia, can have gene activation, as in the case of direct early gene activation, in addition to the expression of stress proteins, such as heat shock proteins, but it is still unclear which of SAH or cerebral vasospasm leads to the appearance of stress proteins, and the expression of local stress genes can be used to evaluate the efficacy of SAH therapeutic drugs.