Introduction to Cardiovascular Physiology

Cherng, Tom W.; Jackson‐Weaver, Olan; Kanagy, Nancy L.

doi:10.1016/b978-0-12-801238-3.02015-8

Cited by 3 publications

(3 citation statements)

References 197 publications

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“…Although the dose of PAG used in that study was lower than in our study, both suggest CSE participates more in blood flow control in conscious than in unconscious rats, perhaps because of higher activity of the sympathetic nervous system in regulating blood flow. This supposition is based on our observations that dilation to the H 2 S donor NaHS is ~40% when arteries are pressurized to 60 mmHg (12), but 100% when arteries are pressurized to 75 mmHg (20). Thus decreased vascular tone has a very profound impact on the response to H 2 S.…”

Section: Map and Hr Responses To Chronic Cse Inhibition In Conscious Ratsmentioning

confidence: 93%

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Hydrogen sulfide regulation of renal and mesenteric blood flow

Morales-Loredo

Barrera

Garcia

et al. 2019

American Journal of Physiology-Heart and Circulatory Physiology

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Hydrogen sulfide (H2S) dilates isolated arteries, and knockout of the H2S-synthesizing enzyme cystathionine γ-lyase (CSE) increases blood pressure. However, the contributions of endogenously produced H2S to blood flow regulation in specific vascular beds are unknown. Published studies in isolated arteries show that CSE production of H2S influences vascular tone more in small mesenteric arteries than in renal arteries or the aorta. Therefore, the goal of this study was to evaluate H2S regulation of blood pressure, vascular resistance, and regional blood flows using chronically instrumented rats. We hypothesized that during whole animal CSE inhibition, vascular resistance would increase more in the mesenteric than the renal circulation. Under anesthesia, CSE inhibition [β-cyanoalanine (BCA), 30 mg/kg bolus + 5 mg·kg−1·min−1 for 20 min iv) rapidly increased mean arterial pressure (MAP) more than saline administration (%Δ: saline −1.4 ± 0.75 vs. BCA 7.1 ± 1.69, P < 0.05) but did not change resistance (MAP/flow) in either the mesenteric or renal circulation. In conscious rats, BCA infusion similarly increased MAP (%Δ: saline −0.8 ± 1.18 vs. BCA 8.2 ± 2.6, P < 0.05, n = 7) and significantly increased mesenteric resistance (saline 0.9 ± 3.1 vs. BCA 15.6 ± 6.5, P < 0.05, n = 12). The H2S donor Na2S (50 mg/kg) decreased blood pressure and mesenteric resistance ,but the fall in resistance was not significant. Inhibiting CSE for multiple days with dl-proparglycine (PAG, 50 mg·kg−1·min−1 iv bolus for 5 days) significantly increased vascular resistance in both mesenteric (ratio of day 1: saline 0.86 ± 0.033 vs. PAG 1.79 ± 0.38) and renal circulations (ratio of day 1: saline 1.26 ± 0.22 vs. 1.98 ± 0.14 PAG). These results support our hypothesis that CSE-derived H2S is an important regulator of blood pressure and vascular resistance in both mesenteric and renal circulations. Furthermore, inhalation anesthesia diminishes the effect of CSE inhibition on vascular tone. NEW & NOTEWORTHY These results suggest that CSE-derived H2S has a prominent role in regulating blood pressure and blood flow under physiological conditions, which may have been underestimated in prior studies in anesthetized subjects. Therefore, enhancing substrate availability or enzyme activity or dosing with H2S donors could be a novel therapeutic approach to treat cardiovascular diseases.

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Section: Map and Hr Responses To Chronic Cse Inhibition In Conscious Ratsmentioning

confidence: 93%

“…H2S AND BLOOD FLOW in arteries at 60 mmHg (12,29), diminished basal vascular tone would limit H 2 S-dependent dilation.…”

Section: H1159mentioning

confidence: 99%

Hydrogen sulfide regulation of renal and mesenteric blood flow

Morales-Loredo

Barrera

Garcia

et al. 2019

American Journal of Physiology-Heart and Circulatory Physiology

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“…The cerebral artery, like other systemic arteries is composed of the tunica intima, tunica media, and the adventitia [ 5 ]. The tunica intima is the innermost layer and is lined with endothelial cells.…”

Section: Structure Of the Cerebral Arterymentioning

confidence: 99%

New Pathophysiological Considerations on Cerebral Aneurysms

Jung

2018

Neurointervention

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Cerebral aneurysm is a common cerebrovascular disease that is sometimes complicated by rupture or an enlarged mass. We are now aggressively evaluating and managing unruptured cerebral aneurysms based on a significant concern for the high morbidity and mortality related to its associated complications. However, the actual rupture rate is very low and the diagnostic and treatment modalities are expensive and invasive, which may lead to unnecessary costs and potential medical complications. This disproportionate situation is related to a poor understanding of the natural course and pathophysiology of cerebral aneurysms. In consideration of the concept that not all cerebral aneurysms must be removed, we need to examine their course and progression more accurately. Cerebral aneurysms may follow a variety of pathophysiological scenarios over their lifetime, from formation to growth and rupture. The disease course and the final outcome can differ depending on the timing and intensity of the pathological signals acting on the cerebral vessel wall. We should delineate a method of predicting the stability and risk of rupture of the lesion based on a comprehensive knowledge of the vessel wall integrity. This review deals with the basic knowledge and advanced concepts underlying the pathophysiology of cerebral aneurysms.

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