scholarly journals Mitigating Initial Orthostatic Hypotension: Mechanistic Roles of Muscle Contraction Versus Sympathetic Activation

Author(s):  
Nasia Sheikh ◽  
Aaron A. Phillips ◽  
Shaun Ranada ◽  
Matthew Lloyd ◽  
Karolina Kogut ◽  
...  

Background: Initial orthostatic hypotension (IOH) is defined by a large drop in blood pressure (BP) within 15 s of standing. IOH often presents during an active stand, but not with a passive tilt, suggesting that a muscle activation reflex involving lower body muscles plays an important role. To our knowledge, there is no literature exploring how sympathetic activation affects IOH. We hypothesized involuntary muscle contractions before standing would significantly reduce the drop in BP seen in IOH while increasing sympathetic activity would not. Methods: Study participants performed 4 sit-to-stand maneuvers including a mental stress test (serial 7 mental arithmetic stress test), cold pressor test, electrical stimulation, and no intervention. Continuous heart rate and beat-to-beat BP were measured. Cardiac output and systemic vascular resistance were estimated from these waveforms. Data are presented as mean±SD. Results: A total of 23 female IOH participants (31±8 years) completed the study. The drops in systolic BP following the serial 7 mental arithmetic stress test (−26±12 mm Hg; P =0.004), cold pressor test (−20±15 mm Hg; P <0.001), and electrical stimulation (−28±12 mm Hg; P =0.01) were significantly reduced compared with no intervention (−34±11 mm Hg). The drops in systemic vascular resistance following the serial 7 mental arithmetic stress test (−391±206 dyne×s/cm 5 ; P =0.006) and cold pressor test (−386±179 dyne×s/cm 5 ; P =0.011) were significantly reduced compared with no intervention (−488±173 dyne×s/cm 5 ). Cardiac output was significantly increased upon standing (7±2 L/min) compared with during the sit (6±1 L/min; P <0.001) for electrical stimulation. Conclusion: Sympathetic activation mitigates the BP response in IOH, while involuntary muscle contraction mitigates the BP response and reduces symptoms. Active muscle contractions may induce both of these mechanisms of action in their pretreatment of IOH. Registration: URL: https://www.clinicaltrials.gov ; Unique identifier: NCT03970551.

1994 ◽  
Vol 267 (4) ◽  
pp. H1368-H1376 ◽  
Author(s):  
P. Boutouyrie ◽  
P. Lacolley ◽  
X. Girerd ◽  
L. Beck ◽  
M. Safar ◽  
...  

This study used a precise noninvasive method in normotensive humans to determine the effects of sympathetic activation on arterial compliance. A recently developed, high-resolution echo-tracking system capable of measuring systolic/diastolic variations of arterial diameter was coupled to a Finapres system and used to calculate instantaneous systolic/diastolic pressure-diameter and compliance-pressure curves for a muscular medium-sized artery, the radial artery. Two standardized tests of sympathetic system activation, a cold pressor test (2 min) and a mental stress test (2 min of mental arithmetic), were performed at an interval of 8 days in random order in nine healthy volunteers [30 +/- 9 (SD) yr]. Radial arterial parameters were recorded every 30 s for 9 min, which included 2 min of cold pressor test or mental stress test. During both tests, radial arterial mean diameter did not change despite t he increase in mean arterial pressure (P < 0.001); stroke change in diameter decreased (P < 0.01), whereas pulse pressure increased (P < 0.01). Arterial compliance, calculated for the instantaneous level of mean arterial pressure, decreased significantly (P < 0.01). Compliance (C) calculated at 100 mmHg (C100) was arbitrarily chosen as a reference point for comparing compliance among the different periods of the test. C100 decreased significant (P < 0.05) during both tests (from 2.93 +/- 1.27 to 2.04 +/- 0.94 and from 3.29 +/- 1.73 to 2.63 +/- 1.55 mm2.mmHg-1.10(-3) during mental stress and the cold pressor test, respectively). These results indicate that sympathetic activation is able to decrease radial arterial compliance in healthy subjects. The reduction in arterial compliance probably resulted from complex interactions between changes in distending blood pressure and changes in radial arterial smooth muscle tone.


1994 ◽  
Vol 16 (3) ◽  
pp. 163-167 ◽  
Author(s):  
Giuseppe Micieli ◽  
Cristina Tassorelli ◽  
Daniele Bosone ◽  
Anna Cavallini ◽  
Elena Viotti ◽  
...  

1999 ◽  
Vol 26 (10) ◽  
pp. 774-778 ◽  
Author(s):  
FRANCO LAGHI Pasini ◽  
PIER LEOPOLDO Capecchi ◽  
MARCELLA Colafati ◽  
PAOLA Randisi ◽  
LUCA Puccetti

1990 ◽  
Vol 79 (1) ◽  
pp. 43-50 ◽  
Author(s):  
I. Marriott ◽  
Janice M. Marshall ◽  
E. J. Johns

1. Laser Doppler flowmetry has been used to study changes in cutaneous erythrocyte flux produced in the hand (i) on successive immersion of the contralateral hand in water at 20°C (cold test) and then in water at 0–4°C (cold pressor test), and (ii) by mental arithmetic. 2. In 11 subjects, placing the right hand in water at 20°C for 2 min induced a significant decrease in cutaneous erythrocyte flux in the contralateral hand and a significant fall in mean arterial pressure. Cutaneous vascular resistance, calculated as arterial pressure/cutaneous erythrocyte flux, showed no significant change. Thus, the decrease in erythrocyte flux was apparently due to a fall in perfusion pressure. 3. Subsequent immersion of the right hand in water at 0–4°C for 2 min caused a significant decrease in erythrocyte flux in the contralateral hand and a significant rise in mean arterial pressure. It is concluded that the cold pressor response evoked from one hand elicited a substantial reflex vasoconstriction in the skin of the other hand; accordingly, calculated cutaneous vascular resistance increased significantly. 4. Eight subjects performed mental arithmetic for two periods of 2 min separated by a rest period of 2 min. By the end of the second minute of each period of mental arithmetic there was a significant decrease in erythrocyte flux. Mean arterial pressure increased significantly in the first period only, but calculated cutaneous vascular resistance increased in both periods, consistent with cutaneous vasoconstriction. 5. The cold pressor test and mental arithmetic are aversive stimuli that evoke the characteristic pattern of the alerting or defence response which includes splanchnic vasoconstriction and muscle vasodilatation. Previous studies on the cutaneous vascular component of this response have yielded equivocal results. The present study provides firm evidence that it includes cutaneous vasoconstriction, at least in the hand.


2000 ◽  
Vol 93 (2) ◽  
pp. 382-394 ◽  
Author(s):  
Thomas J. Ebert ◽  
Judith E. Hall ◽  
Jill A. Barney ◽  
Toni D. Uhrich ◽  
Maelynn D. Colinco

Background This study determined the responses to increasing plasma concentrations of dexmedetomidine in humans. Methods Ten healthy men (20-27 yr) provided informed consent and were monitored (underwent electrocardiography, measured arterial, central venous [CVP] and pulmonary artery [PAP] pressures, cardiac output, oxygen saturation, end-tidal carbon dioxide [ETCO2], respiration, blood gas, and catecholamines). Hemodynamic measurements, blood sampling, and psychometric, cold pressor, and baroreflex tests were performed at rest and during sequential 40-min intravenous target infusions of dexmedetomidine (0.5, 0.8, 1.2, 2.0, 3.2, 5.0, and 8.0 ng/ml; baroreflex testing only at 0.5 and 0.8 ng/ml). Results The initial dose of dexmedetomidine decreased catecholamines 45-76% and eliminated the norepinephrine increase that was seen during the cold pressor test. Catecholamine suppression persisted in subsequent infusions. The first two doses of dexmedetomidine increased sedation 38 and 65%, and lowered mean arterial pressure by 13%, but did not change central venous pressure or pulmonary artery pressure. Subsequent higher doses increased sedation, all pressures, and calculated vascular resistance, and resulted in significant decreases in heart rate, cardiac output, and stroke volume. Recall and recognition decreased at a dose of more than 0.7 ng/ml. The pain rating and mean arterial pressure increase to cold pressor test progressively diminished as the dexmedetomidine dose increased. The baroreflex heart rate slowing as a result of phenylephrine challenge was potentiated at both doses of dexmedetomidine. Respiratory variables were minimally changed during infusions, whereas acid-base was unchanged. Conclusions Increasing concentrations of dexmedetomidine in humans resulted in progressive increases in sedation and analgesia, decreases in heart rate, cardiac output, and memory. A biphasic (low, then high) dose-response relation for mean arterial pressure, pulmonary arterial pressure, and vascular resistances, and an attenuation of the cold pressor response also were observed.


2011 ◽  
Vol 163 (1-2) ◽  
pp. 74
Author(s):  
M.J. Falvo ◽  
M. Blatt ◽  
J.J. Jasien ◽  
B.M. Deegan ◽  
G. OLaighin ◽  
...  

2021 ◽  
Vol 12 ◽  
Author(s):  
Binbin Liu ◽  
Zhe Zhang ◽  
Xiaohui Di ◽  
Xiaoni Wang ◽  
Lin Xie ◽  
...  

Noninvasive assessment of autonomic nervous system (ANS) activity is of great importance, but the accuracy of the method used, which is primarily based on electrocardiogram-derived heart rate variability (HRV), has long been suspected. We investigated the feasibility of photoplethysmography (PPG) in ANS evaluation. Data of 32 healthy young men under four different ANS activation patterns were recorded: baseline, slow deep breathing (parasympathetic activation), cold pressor test (peripheral sympathetic activation), and mental arithmetic test (cardiac sympathetic activation). We extracted 110 PPG-based features to construct classification models for the four ANS activation patterns. Using interpretable models based on random forest, the main PPG features related to ANS activation were obtained. Results showed that pulse rate variability (PRV) exhibited similar changes to HRV across the different experiments. The four ANS patterns could be better classified using more PPG-based features compared with using HRV or PRV features, for which the classification accuracies were 0.80, 0.56, and 0.57, respectively. Sensitive features of parasympathetic activation included features of nonlinear (sample entropy), frequency, and time domains of PRV. Sensitive features of sympathetic activation were features of the amplitude and frequency domain of PRV of the PPG derivatives. Subsequently, these sensitive PPG-based features were used to fit the improved HRV parameters. The fitting results were acceptable (p &lt; 0.01), which might provide a better method of evaluating ANS activity using PPG.


2011 ◽  
Vol 110 (6) ◽  
pp. 1526-1533 ◽  
Author(s):  
Silvestro Roatta ◽  
Dario Farina

A positive inotropic action by the sympathetic nervous system on skeletal muscles has been observed and investigated in animal and in vitro studies. This action provided a theoretical basis for the putative ergogenic action of catecholamines and adrenergic agonists, although there is no clear evidence of this effect in humans. The aim of this study was to investigate the occurrence of inotropic effects associated to physiological sympathetic activation in healthy subjects. The muscle force capacity was investigated in the tibialis anterior ( n = 9 subjects) and in the soleus ( n = 9) muscles electrically stimulated with single pulses and double pulses with variable interspike interval (4–1,000 ms) and short pulse trains (frequency: 5–14 Hz) before, during, and after sympathetic activation by the cold pressor test (CPT). CPT significantly decreased by 10.4 ± 7.2 and 10.6 ± 4.4% the force produced by single and double pulse stimulation, respectively, and produced smaller decreases in the force obtained by train stimulation in the tibialis anterior, while no significant changes were observed in either type of contraction in the soleus muscle. CPT failed to induce any increase in the force capacity of the investigated muscles. The prevalent decrease in force evidenced in this study supports the concept that the weakening sympathetic action on type I fiber, already shown to occur in humans, prevails over the putative potentiating action.


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