Background: The effects of vasoconstriction on cardiac stroke volume (SV) and indices of peripheral and intestinal perfusion are insufficiently described.
Methods: In a non-randomized clinical study, 30 patients undergoing elective rectal surgery were exposed to modulation of preload. The primary endpoint was intestinal perfusion (flux), measured by single-point laser Doppler flowmetry. Secondary endpoints were central cardiovascular variables obtained by the LiDCO rapid monitor, the peripheral perfusion index (PPI) derived from the pulse oximetry signal and muscle (StO ) and cerebral oxygenation (ScO ) determined by near-infrared spectroscopy.
Results: For the whole cohort (n = 30), administration of Phenylephrine during HUT induced a median [IQR] increase in SV by 22% [14-41], p = .003 and in mean arterial pressure (MAP) by 54% [31-62], p < .001, with no change in PPI, StO and ScO or flux. In patients who were preload dependent during HUT (stroke volume variation; SSV >10%; n = 23), administration of phenylephrine increased SV by 29% [12-43], p = .01 and MAP by 54% [33-63], p < .001, followed by an increase in intestinal perfusion flux by 60% [15-289], p = .05, while PPI, StO and ScO remained unchanged. For non-preload dependent patients (SSV <10%; n = 7), no changes in hemodynamic indices were seen besides an increase in MAP by 54% [33-58], p = .002.
Conclusion: The reflection of vasoconstrictive modulation of preload in systemic cardiovascular variables and indices of perfusion was dependent on preload responsiveness. Administration of phenylephrine to increase preload did not appear to compromise organ perfusion.
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Pharmaceuticals (Basel)
November 2024
Department of Pharmaceutical Technology, Faculty of Pharmacy, Tanta University, Tanta 31527, Egypt.
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Sci Rep
January 2025
Laboratory of Veterinary Pharmacology, Department of Veterinary Medicine, Faculty of Agriculture, Tokyo University of Agriculture and Technology, 3-5-8 Saiwai-cho, Fuchu , Tokyo, 183-8509, Japan.
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View Article and Find Full Text PDFFood Chem Toxicol
December 2024
National Engineering Research Center for Bioengineering Drugs and the Technologies, Institute of Translational Medicine, Jiangxi Medical College, Nanchang University, Nanchang, 330031, China; School of Pharmacy, Jiangxi Medical College, Nanchang University, Nanchang, 330031, Jiangxi, China. Electronic address:
The highly toxic aflatoxin B1 (AFB1) is considered one of the primary risk factors for hepatocellular carcinoma, while effective measures after AFB1 exposure remain to be optimized. This study utilized cell-surface-display technique to construct an engineered S. cerevisiae-pYD1-ScFv-AFB1 (S.
View Article and Find Full Text PDFClin Transl Med
January 2025
Outcomes Research Consortium®, Houston, Texas, USA.
The gastrointestinal tract can be deranged by ailments including sepsis, trauma and haemorrhage. Ischaemic injury provokes a common constellation of microscopic and macroscopic changes that, together with the paradoxical exacerbation of cellular dysfunction and death following restoration of blood flow, are collectively known as ischaemia-reperfusion injury (IRI). Although much of the gastrointestinal tract is normally hypoxemic, intestinal IRI results when there is inadequate oxygen availability due to poor supply (pathological hypoxia) or abnormal tissue oxygen use and metabolism (dysoxia).
View Article and Find Full Text PDFInflamm Bowel Dis
December 2024
Department of Gastroenterology, Hepatology, Infectious Diseases and Endocrinology, Hannover Medical School, Hannover, Germany.
Background: Defects in SLC26A3, the major colonic Cl-/HCO3- exchanger, result in chloride-rich diarrhea, a reduction in short-chain fatty acid (SCFA)-producing bacteria, and a high incidence of inflammatory bowel disease in humans and in mice. Slc26a3-/- mice are, therefore, an interesting animal model for spontaneous but mild colonic inflammation and for testing strategies to reverse or prevent the inflammation. This study investigates the effect of Escherichia coli Nissle (EcN) application on the microbiome, SCFA production, barrier integrity, and mucosal inflammation in slc26a3-/- mice.
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