The mucosal microcirculation in innervated and denervated small intestine was studied using anesthetized rats. Denervation did not cause significant (P greater than 0.05) diameter changes in the precapillary vasculature; however, venules did constrict significantly. These results indicate minimum neural control in the precapillary vasculature during the resting state. The innervated precapillary vasculature constricted during both the carotid occlusion reflex and hemorrhagic hypotension. The diameter of the denervated precapillary vasculature was unchanged during the carotid occlusion reflex and dilated during hemorrhage. The responses of innervated and denervated precapillary vasculatures were attributed to increased neural activity and autoregulatory mechanisms, respectively. Neither innervated nor denervated venules responded during the carotid occlusion reflex. During hemorrhage, however, innervated venules constricted and denervated vessels dilated. The vasoconstriction of the innervated vasculature during hemorrhage contributed to a stoppage of blood and epithelial detachment; these responses did not occur in the dilated, denervated vasculature. Therefore, neural vasoconstriction, qualitatively similar to that in normal animals during the baroreceptor reflex, is a contributing cause to the vascular and tissue impairment in the intestinal mucosa during hemorrhage.
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http://dx.doi.org/10.1152/ajplegacy.1975.229.5.1159 | DOI Listing |
Cardiovasc Diagn Ther
December 2024
Clinic for Diagnostic and Interventional Radiology, Heidelberg University Hospital, Heidelberg, Germany.
Background: Computed tomography pulmonary angiography (CTPA) is frequently performed in patients with pulmonary hypertension (PH) and may aid non-invasive estimation of pulmonary hemodynamics. We, therefore, investigated automated volumetry of intrapulmonary vasculature on CTPA, separated into core and peel fractions of the lung volume and its potential to differentially reflect pulmonary hemodynamics in patients with pre- and postcapillary PH.
Methods: A retrospective case-control study of 72 consecutive patients with PH according to the 2022 joint guidelines of the European Society of Cardiology and the European Respiratory Society who underwent right heart catheterization (RHC) and CTPA within 7 days between August 2013 and February 2016 at Thoraxklinik at Heidelberg University Hospital (Heidelberg, Germany) was conducted.
bioRxiv
October 2024
Electrical Engineering and Computer Science Department, Florida Atlantic University, Boca Raton, FL, USA.
Autoregulation and neurogliavascular coupling are key mechanisms that modulate myogenic tone (MT) in vessels to regulate cerebral blood flow (CBF) during resting state and periods of increased neural activity, respectively. To determine relative contributions of distinct vascular zones across different cortical depths in CBF regulation, we developed a simplified yet detailed and computationally efficient model of the mouse cerebrovasculature. The model integrates multiple simplifications and generalizations regarding vascular morphology, the hierarchical organization of mural cells, and potentiation/inhibition of MT in vessels.
View Article and Find Full Text PDFDiagnostics (Basel)
July 2024
Department of Ophthalmology, Military Institute of Aviation Medicine, 01-755 Warsaw, Poland.
Purtscher retinopathy is a rare but severe sight-threatening eye condition that mostly occurs in middle-aged men after chest compression or head injury. In cases such as acute pancreatitis, connective tissue disorders, kidney failure or COVID-19 infection with similar ocular findings but no history of trauma, a diagnosis of Purtscher-like retinopathy is made. We present a case of a 72-year-old female with typical symptoms of Purtscher retinopathy in both eyes after a car crash accident.
View Article and Find Full Text PDFJ Am Heart Assoc
July 2024
INSERM UMR_S 999 Pulmonary Hypertension: Pathophysiology and Novel Therapies Le Plessis Robinson France.
Background: The primary genetic risk factor for heritable pulmonary arterial hypertension is the presence of monoallelic mutations in the gene. The incomplete penetrance of mutations implies that additional triggers are necessary for pulmonary arterial hypertension occurrence. Pulmonary artery stenosis directly raises pulmonary artery pressure, and the redirection of blood flow to unobstructed arteries leads to endothelial dysfunction and vascular remodeling.
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