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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: BACKGROUND, METHODS, RESULTS. Meshes: Adult, Arteries, Diagnostic Techniques, Cardiovascular, Hemodynamics, Humans, Hypothermia, Induced, Male, Smoking, Time Factors, Tobacco Use Disorder, Ventricular Function, Left.
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Are peripheral and central arterial haemodynamic interactions early abnormalities in young male cigarette smokers? Context: smoking, result in endothelial dysfunction and this affects systemic and local haemodynamics. The aim was to assess interactions of the left ventricle and arterial system of smokers at baseline and after a physiological stimulus--the cold pressor test (CPT) which causes a sympathetically driven vasoconstriction that counteracts the normal endothelial dependent vasodilatation. male smokers and controls were compared using applanation tonometry. Parameters included systolic and diastolic blood pressure, ejection duration, heart rate, aortic augmentation index (AAI), and sub-endocardial viability ratio (SEVR). The CPT was performed at 1 and 3 min following immersion of the hand in ice. smokers have abnormal baseline cardiac timing (heart rate and ejection duration), systolic and diastolic blood pressures which are due to increased peripheral wave reflection (AAI) and thus affect the SEVR. Following CPT, the pressure wave differential, dP/dt, was significantly increased in smokers compared to non-smokers who had a decrease at 1 min in ice. Mean systolic and diastolic pressure was significantly increased in both groups at 1 and 3 min as was end systolic pressure in non-smokers.
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baseline ventriculo-vascular dynamics, are abnormal as was the evoked response to CPT. The blunted blood pressure increase of smokers compared to controls following CPT, may represent altered nitric oxide production in the macro and microcirculation through differential upregulation of endothelial nitric oxide synthase (eNOS) and inducible NOS respectively. The potential for therapeutic intervention and prevention of ongoing endothelial injury, requires further investigation. Final Decision: yes