Diastolic Arterial Pressure Variability Research Articles

Exercise training ameliorates adrenergic control in spontaneously hypertensive rats

ABSTRACT The goal of this study was to examine vascular control after sympathetic stimulation by tyramine infusion in hypertensive rats submitted to swimming training. To this end, male rats were assigned to the following groups: sedentary (SN) and trained normotensive (TN), sedentary (SH) and trained hypertensive (TH). Arterial pressure (AP), heart rate (HR), HR variability (HRV), AP variability (APV), and cardiac autonomic function were recorded. Following, infusion of tyramine was administrated. The TN and TH showed a lower resting HR compared with their respective sedentary groups (p < .05). Pressure levels were less in TH than SH (p < .05). The TH showed a higher HRV together with a lower APV in comparison to SH (p < .05). The sympathetic modulation of HRV and APV was lower in TH than in SH (p < .05). Both trained groups presented an increased parasympathetic modulation of HRV compared with their respective sedentary groups (p < .05). The TN and TH groups had a higher vagal effect in comparison with their respective sedentary groups (p < .001). The sympathetic effect was lower in TH than in SH (p < .001). Pressor and HR responses to tyramine in different doses were attenuated in TH (p < .001). Further analysis showed a significant association between infusion of tyramine and normalized LF component of HRV (r = 0.84, p < .001), systolic APV (r = 0.58, p < .001) and diastolic APV (r = 0.49, p < .001). In conclusion, exercise training provokes less pressor response variation by tyramine infusion in hypertensive animals suggesting sympathetic nerve endings adjustments and decrease of the vasoconstrictor effect attenuates injury caused by hypertension improving cardiovascular autonomic dysfunction, which can be associated with sympathetic attenuation.

Baroreflex Sensitivity and Blood Pressure Variability can Help in Understanding the Different Response to Therapy During Acute Phase of Septic Shock.

ABSTRACTBackground:Mean values of hemodynamic variables are poorly effective in evaluating an actual recovery of the short-term autonomic mechanisms for blood pressure (BP) and heart rate (HR) regulation. The aim of this work is to analyze the response to therapy in the early phase of septic shock to verify possible associations between BP recovery and BP autonomic control.Methods:This is an ancillary study from the multicenter prospective observational trial Shockomics (NCT02141607). A total of 21 septic shock patients were studied at two time points during the acute phase of shock and were classified according to changes in SOFA score. Time series of BP components and HR were analyzed in time and frequency domain. Baroreflex sensitivity (BRS) was assessed, and a mathematical model for the decomposition of diastolic arterial pressure (DAP) oscillations was used to understand the different contributions of BRS and HR on peripheral vascular resistance control.Results:Only those patients, who significantly improved organ function (responders, R), showed an increase of mean value and low frequency (LF) power in BP time series. Fluid accumulation was higher in the non-responders (NR). BRS increased in NR and the model of DAP variability showed that the contribution of HR was highly reduced in NR.Conclusions:Although patients reached the mean BP target of 65 mmHg, our analyses highlighted important differences in terms of autonomic nervous system control. BP variability, HR variability and baroreflex trends can add information to individual vital sign measure such as mean BP, and can help in understanding the responsiveness to the combination of symphatomimetic drugs and fluid therapy.

Blood pressure variability in patients with atrial fibrillation.

The highly irregular ventricular rate during atrial fibrillation (AF) represents a unique and physiological experimental model to eliminate the influence of rhythmical components of RR variability on arterial pressure variability for investigating the origin of low frequency (LF) component in arterial pressure. Surface ECG, blood pressure and respiratory signals were recorded in thirty patients with persistent AF, at rest and during a passive orthostatic stimulus ("tilt test"). Short-term systolic (SAP) and diastolic arterial pressure (DAP) variability was estimated by autoregressive method. In 15 patients (group A), SAP significantly increased during tilt (from 98±16 to 114±18mmHg, p<0.001 rest vs. tilt), whereas in the remaining patients (group B) SAP remained almost unchanged (from 108±16 to 104±17mmHg, p=0.05, rest vs. tilt). No clinical differences were found between group A and B. When analyzing group A, a significant increase in the LF power in SAP and DAP variability was observed during tilt (SAP: 2.24±2.75 vs. 6.60±5.11mmHg(2), p<0.05, rest vs. tilt; DAP: 3.54±1.95 vs. 4.38±3.21mmHg(2), p<0.05, rest vs. tilt). No significant differences were found in group B. In AF patients, changes of arterial pressure variability during tilt were not uniform. Vascular regulatory mechanisms appeared to be still efficient only in the subgroup of patients who responded to a sympathetic stimulus with an increased SAP. In these subjects tilt increased the LF component in arterial pressure variability, thus mimicking the physiological response observed in subjects with sinus rhythm.

Central cholinergic modulation of blood pressure short-term variability

The role of neurally born acetylcholine in the central modulation of cardiovascular short-term variability was assessed using a pharmacological probe physostigmine, a cholinesterase inhibitor that can act centrally also. Experiments were performed in instrumented conscious rats. Equidistant sampling at 20 Hz of systolic arterial pressure (SAP), diastolic arterial pressure (DAP) and heart rate (HR) allowed direct spectral analysis. Spectra were analysed in the whole, very-low frequency (VLF), low-frequency (LF) and high-frequency (HF) domains. Physostigmine, but not neostigmine, increased SAP, LF SAP and HF SAP variability while neostigmine, but not physostigmine, decreased HR without affecting HR variability. Atropine methyl nitrate prevented neostigmine-induced bradycardia and potentiated the effects of physostigmine on DAP, LF DAP and HF DAP variability. Atropine sulphate, hexamethonium, phentolamine and metoprolol inhibited physostigmine-induced increase of SAP and LF SAP. Pre-treatment of rats by quinapril prevented physostigmine-induced increase of SAP, but not of LF SAP, while the V 1a antagonist prevented the increase of HF SAP. The results suggest that central cholinergic neurons facilitate but do not create LF SAP and HF SAP variability. The effect of physostigmine on LF SAP seems to be mediated via central muscarinic sites and the peripheral sympathetic system, while non-muscarinic central sites and vasopressin pathways subserve the increase of HF SAP.