Anatomy, physiology, and histology of the skin
Michael Parker, Charlie James in Fundamentals for Cosmetic Practice, 2022
Vasospasm is the process of constriction of blood vessels by the smooth muscle which surrounds arteries and arterioles. This reduces blood loss in the local area for minutes to hours and is likely triggered by direct damage to smooth muscle, the release of chemokines from activated platelets and reflexes initiated by nociceptors (pain receptors). Adrenaline is a potent vasospastic agent and is released in response to painful stimuli, as well as being included within certain local anaesthetic agents to encourage vasospasm and decrease bleeding. One must be careful, however, when using adrenaline-containing local anaesthetic agents in close proximity to end arteries (such as the angular artery) as its vasospastic effects can cause localised tissue necrosis due to tissue hypoxia. In these regions, it is safest to avoid local anaesthetic solutions which contain adrenaline.
Overview of the cardiovascular system
Neil Herring, David J. Paterson in Levick's Introduction to Cardiovascular Physiology, 2018
Conduit and feed arteries have a rich sympathetic innervation and can change their diameter actively. Dilatation facilitates the local increase in blood flow to skeletal muscle during exercise. Contraction reduces peripheral blood flow, spectacularly so in diving mammals. Vasospasm is an intense and sustained contraction of conduit arteries. This can be lifesaving in accidents, as demonstrated by a motorcycle crash victim brought into the Accident and Emergency department with one leg severed at the knee. Although the popliteal artery was torn in half, it was scarcely bleeding because shed blood platelets had triggered vasospasm. This prevented the patient from bleeding to death. Less beneficial is the cerebral artery vasospasm evoked by cerebral haemorrhage, which can cause a stroke, and the vasospasm of diseased coronary arteries, which can cause cardiac angina at rest (variant angina).
Histopathologic Patterns in Hypertensive Nephrosclerosis in African Americans
Meguid El Nahas in Kidney Diseases in the Developing World and Ethnic Minorities, 2005
2. Vasoreactivity: What then could account for the extensive global glomerulosclerosis in African American patients with hypertensive nephro-sclerosis? We speculate that the coexistence of solidified glomeruli with segmental glomerulosclerosis in our biopsy study could reflect an increased vasoreactivity in susceptible populations (22). African Americans tend to show a larger increase in blood pressure level than Caucasians during stress, particularly to stimuli that elicit a vasoconstrictor response (24–26). Autoregulatory response to hypertension, resulting in vasospasm, could be excessive in patients susceptible to develop hypertension, like in some African Americans (27). Thus, we speculate that global vasoconstrictive ischemia could result in complete collapse and solidification of the glomerulus. Further, we hypothesize that adaptation and segmental resistance to collapse and/or reflow, with possible attendant segmental hypertension/hyper-filtration, could give rise to segmental sclerotic lesions associated with solidification in those patients. Thus, vasospasm could reflect primary microvascular injury and endothelial dysfunction that then caused hypertension, or occurred in response to hypertension, in susceptible patients. It is thus possible that a primary renal microvascular disease results in hypertension, glomerulosclerosis, and interstitial fibrosis (28).
Comparison of radiological versus clinical cerebral vasospasm after aneurysmal subarachnoid hemorrhage: is vasospasm always present?
Published in Neurological Research, 2020
Djula Djilvesi, Igor Horvat, Bojan Jelaca, Jagos Golubovic, Filip Pajicic, Petar Vulekovic
Cerebral vasospasm (CV) is a pathologic, reversible narrowing of the cerebral arteries, which develops after subarachnoid hemorrhage (SAH). SAH, significant enough to cause vasospasm, occurs most frequently due to the rupture of cerebral aneurysm. According to the distribution, vasospasms could be classified into: 1. focal, 2. segmental and 3. Diffuse [1]. Based on the intensity, CV may be: 1. mild (0–33%), 2. moderate (34–66%), and 3. severe (67–100%) [2]. CV involves intradural part of the cerebral arteries, and the distribution and degree of vasospasm correlates with the location and size of SAH. Vasospasm primarily affects larger arteries in the subarachnoid space, which are exposed to a greater flow of circulation. Depending on the severity of SAH, vasospasm could affect distal parts of the arteries as well, even parenchymal arterioles [3]. It is considered that the cause of vasospasm is the presence of a blood clot in the subarachnoid space. There is no single accepted theory of the pathogenesis of CV, as evidenced by the presence of a number of theories that attempt to explain its etiopathogenesis [4]. The incidence of angiographic vasospasm after SAH is approximately 60%, ranging from 20% up to 97% as a result of unequal criteria for the determination of vasospasm intensity [5]. CV develops in the first week after SAH (most often on Day 3 or 4) and is most pronounced in the second week, diminishing during the third week. The presence of vasospasm in the first 48 hours after SAH correlates with the probability of occurrence of severe symptomatic vasospasm and worse outcome.
Heparin infusions in aneurysmal subarachnoid hemorrhages: clinical considerations for use beyond anticoagulation
Published in Expert Review of Clinical Pharmacology, 2022
Zsanett Kormanyos, Justin P. Reinert, Paul Brady
Limitations of this evaluation include the discrepancies regarding the definition of vasospasm, cerebral ischemia and delayed neurological deficits in the included studies, as well as the methods used to measure their incidence. There was also a large variability among the included studies of what outcomes were measured, the approach similar outcomes were reported (different disability scales), and in the primary intervention (dose, treatment duration, aPTT goal). The included studies also encompass the treatment approach of the last 20 years. Over this time, the treatment of SAH associated vasospasm has advanced. For example in recent years, ‘triple H’ therapy with induced hypertension, hypervolemia, and hemodilution for the prevention and treatment of vasospasm has fallen out of favor due to significant complications associated with its use, including pulmonary edema, hyponatremia, cerebral edema, and increased cardiac workload leading to myocardial infarction [23]. Surgical and endovascular methods, instruments and techniques are also rapidly evolving posing the question if patient outcomes can truly be directly compared. The Aneurysmal Subarachnoid Hemorrhage Trial Randomizing Heparin (ASTROH) is a phase 2 randomized multicenter trial currently enrolling subjects with low-grade aneurysmal SAH and significant hemorrhage burden undergoing endovascular aneurysm occlusion. The study aims to evaluate functional outcomes and bleeding complications to establish the efficacy and safety of LDIVH [24].
5-Fluorouracil, capecitabine and vasospasm: a scoping review of pathogenesis, management options and future research considerations
Published in Acta Cardiologica, 2022
Eleftherios Teperikidis, Aristi Boulmpou, Panagiotis Charalampidis, Chalil Tsavousoglou, George Giannakoulas, Christodoulos E. Papadopoulos, Vassilios Vassilikos
Prevention strategies with CCB and nitrates have not been effective. Vitamin E, statins and magnesium seemed effective in treating vasospasm in some reports, but the level of evidence is rather low. Nevertheless, their favourable safety profile could make these agents candidates for future prevention strategies. More importantly, the role of L-arginine in preventing 5-FU related vasospasm should be explored further in a clinical trial setting. As described above, 5-FU seems to interfere with RNA synthesis, resulting in a reduction of NOS production by endothelial cells. Administration of L-arginine could provide additional fuel for NO synthesis and could therefore prove to be a valuable addition in prevention strategies, both prior to initiation of treatment as well as in cases of re-challenging.
Related Knowledge Centers
- Brain Ischemia
- Meninges
- Endothelium
- Subarachnoid Hemorrhage
- Ischemia
- Artery
- Atherosclerosis
- Vasoconstriction
- Spasm
- Variant Angina