Articles: vasodilation-physiology.
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J. Cardiothorac. Vasc. Anesth. · Oct 2015
Multicenter Study Observational StudyIs Preoperative Endothelial Dysfunction a Potentially Modifiable Risk Factor for Renal Injury Associated With Noncardiac Surgery?
To determine whether preoperative endothelial dysfunction provides risk stratification for perioperative renal injury in patients undergoing noncardiac surgery. The relationship between perioperative renal injury and myocardial injury after noncardiac surgery (MINS) was explored secondarily. ⋯ For patients undergoing noncardiac surgery, preoperative endothelial function assessed by noninvasive peripheral arterial tonometry was not associated with perioperative AKI. Perioperative renal injury was associated strongly with MINS, and this may represent a mechanism by which AKI increases adverse outcomes.
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It is unknown how endothelial-dependent flow-mediated dilation (FMD) stimulated by a sustained, exercise-induced increase in shear stress (EX-FMD) is affected by a simultaneous sympathoexcitatory painful stimulus. The purpose of this study was to examine the impact of a cold pressor test (CPT) on brachial artery EX-FMD elicited by a handgrip exercise-induced increase in shear stress. Participants were healthy males (age 21±2 years) (n=28; 16 Experimental group, 12 Control). ⋯ The shear rate stimulus did not differ between groups (p=0.823) or trials (p=0.726) (group × trial interaction: p=0.646) (average exercise shear rate (mean ± SD): 67.6±6.2 s(-1)). The CPT (experienced during EX-FMD trial 2 in the Experimental group) increased mean arterial pressure (p<0.001) and heart rate (p=0.002) relative to the Control group. %EX-FMD was not different between groups (p=0.508) or trials (p=0.592) (group × trial interaction: p=0.879) (EX-FMD: Experimental group trial 1: 5.4±3.4%, trial 2: 5.6±2.6%; Control group trial 1: 6.0±3.7%, trial 2: 6.4±2.2%). In conclusion, the CPT did not impact concurrent EX-FMD, and this indicates that an acute painful stimulus does not interfere with conduit artery FMD responses during exercise in young healthy men.
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Paediatric anaesthesia · Aug 2015
Continuous minimally invasive cardiac output monitoring with the COstatus in a neonatal swine model: recalibration is necessary during vasoconstriction and vasodilation.
The COstatus monitor measures cardiac output via the transpulmonary ultrasound dilution method (COTPUD ) after injection of normal saline, and can calculate continuous cardiac output (CCO) from the arterial pressure waveform. The relationship between arterial waveform and COTPUD however, might be degraded during vasoconstriction/vasodilation. ⋯ Continuous cardiac output (CO) measured with the COstatus monitor requires recalibration during vasoconstriction and vasodilation, even if changes in COTPUD or SVR are not substantial.
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Transcranial Direct Current Stimulation and Cerebral Vasomotor Reserve: A Study in Healthy Subjects.
Cerebral vasomotor reserve (VMR) is the capability of cerebral arterioles to change their diameter in response to various stimuli, such hypercapnia. Changes of VMR due to transcranial direct current stimulation (tDCS) have been poorly studied. ⋯ Our study confirms that tDCS induces a modification of bilateral VMR with a polarity-specific effect; based on this bilateral MFV and BHI modifications, we can speculate an involvement of the SNS in the VMR regulation.
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Journal of neurotrauma · May 2015
Endothelial nitric oxide synthase mediates arteriolar vasodilatation after traumatic brain injury in mice.
Brain edema and increased cerebral blood volume (CBV) contribute to intracranial hypertension and hence to unfavorable outcome after traumatic brain injury (TBI). The increased post-traumatic CBV may be caused in part by arterial vasodilatation. The aim of the current study was to uncover the largely unknown mechanisms of post-traumatic arteriolar vasodilatation. ⋯ The diameter of pial veins was not affected. Our results suggest that arteriolar vasodilatation after TBI is largely mediated by excess production of endothelial nitric oxide. Accordingly, our data may explain the beneficial effects of the NOS inhibitor VAS203 in the early phase after TBI and suggest that inhibition of excess endothelial nitric oxide production may represent a novel therapeutic strategy following TBI.