scholarly journals Face cooling increases blood pressure during central hypovolemia

2017 ◽  
Vol 313 (5) ◽  
pp. R594-R600 ◽  
Author(s):  
Blair D. Johnson ◽  
James R. Sackett ◽  
Suman Sarker ◽  
Zachary J. Schlader
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Vascular Resistance ◽  
Lower Body Negative Pressure ◽  
Lower Body ◽  
Plastic Bag ◽  
Ice Water ◽  
Face Cooling ◽  
Healthy Participants ◽  
Cutaneous Vascular Resistance

A reduction in central blood volume can lead to cardiovascular decompensation (i.e., failure to maintain blood pressure). Cooling the forehead and cheeks using ice water raises blood pressure. Therefore, face cooling (FC) could be used to mitigate decreases in blood pressure during central hypovolemia. We tested the hypothesis that FC during central hypovolemia induced by lower-body negative pressure (LBNP) would increase blood pressure. Ten healthy participants (22 ± 2 yr, three women, seven men) completed two randomized LBNP trials on separate days. Trials began with 30 mmHg of LBNP for 6 min. Then, a 2.5-liter plastic bag of ice water (0 ± 0°C) (LBNP+FC) or thermoneutral water (34 ± 1°C) (LBNP+Sham) was placed on the forehead, eyes, and cheeks during 15 min of LBNP at 30 mmHg. Forehead temperature was lower during LBNP+FC than LBNP+Sham, with the greatest difference at 21 min of LBNP (11.1 ± 1.6 vs. 33.9 ± 1.4°C, P < 0.001). Mean arterial pressure was greater during LBNP+FC than LBNP+Sham, with the greatest difference at 8 min of LBNP (98 ± 15 vs. 80 ± 8 mmHg, P < 0.001). Cardiac output was higher during LBNP+FC than LBNP+Sham with the greatest difference at 18 min of LBNP (5.9 ± 1.4 vs. 4.9 ± 1.0 liter/min, P = 0.005). Forearm cutaneous vascular resistance was greater during LBNP+FC than LBNP+Sham, with the greatest difference at 15 min of LBNP (7.2 ± 3.4 vs. 4.9 ± 2.7 mmHg/perfusion units (PU), P < 0.001). Face cooling during LBNP increases blood pressure through increases in cardiac output and vascular resistance.

Sympathoadrenal-circulatory regulation of arterial pressure during orthostatic stress in young and older men

1992 ◽  
Vol 263 (5) ◽  
pp. R1147-R1155 ◽  
Author(s):  
J. A. Taylor ◽  
G. A. Hand ◽  
D. G. Johnson ◽  
D. R. Seals
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Systemic Vascular Resistance ◽  
Arterial Blood Pressure ◽  
Vascular Resistance ◽  
Older Men ◽  
Orthostatic Stress ◽  
Plasma Norepinephrine ◽  
Lower Body ◽  
Arterial Blood

Our purpose was to test the hypothesis that human aging alters sympathoadrenal-circulatory control of arterial blood pressure during orthostasis. Plasma catecholamine and hemodynamic adjustments to two different forms of orthostatic stress, lower body suction (-10 to -50 mmHg) and standing, were determined in 14 young (26 +/- 1 yr) and 13 older (64 +/- 1) healthy, normally active men. During quiet supine rest, cardiac output tended to be lower and systemic vascular resistance higher in the older men, but no other differences were observed. On average, arterial blood pressure was well maintained during both forms of orthostasis in the two groups; the older men actually demonstrated better maintenance of pressure (P < 0.05) and a lesser incidence of orthostatic hypotension than the young men during lower body suction. Despite a blunted reflex tachycardia during orthostatic stress (P < 0.05), cardiac output tended to decrease less in the older men because of a smaller decline in stroke volume (P < 0.05, suction only), whereas the reflex increases in systemic vascular resistance were not different in the two groups. The whole forearm vasoconstrictor response tended to be attenuated in the older men during lower body suction, but was identical in the two groups with standing. Forearm skin vascular resistance was unaltered during lower body suction in both groups. Orthostasis-evoked increases in antecubital venous plasma norepinephrine concentrations were similar in the young and older men, whereas little or no increases in plasma epinephrine concentrations were observed in either group.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Validity of auscultatory and Penaz blood pressure measurements during profound heat stress alone and with an orthostatic challenge

2011 ◽  
Vol 301 (5) ◽  
pp. R1510-R1516 ◽  
Author(s):  
Matthew S. Ganio ◽  
R. Matthew Brothers ◽  
Rebekah A. I. Lucas ◽  
Jeffrey L. Hastings ◽  
Craig G. Crandall
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Heat Stress ◽  
Brachial Artery ◽  
Lower Body Negative Pressure ◽  
Peripheral Resistance ◽  
Pressure Measurements ◽  
Lower Body ◽  
Dynamic Changes ◽  
Orthostatic Challenge

Despite frequent reporting of blood pressure (BP) during profound passive heat stress, both with and without a hypotensive challenge, the method by which BP is measured often varies between laboratories. It is unknown whether auscultatory and finger BP measures accurately reflect intra-arterial BP during dynamic changes in cardiac output and peripheral resistance associated with the aforementioned conditions. The purpose of this investigation was to test the hypothesis that auscultatory BP measured at the brachial artery, and finger BP measured by the Penaz method, are valid measures of intra-arterial BP during a passive heat stress and a heat-stressed orthostatic challenge, via lower body negative pressure (LBNP). Absolute (specific aim 1) and the change in (specific aim 2) systolic (SBP), diastolic (DBP), and mean BPs (MBP) were compared at normothermia, after a core temperature increase of 1.47 ± 0.09°C, and during subsequent LBNP. Heat stress did not change auscultatory SBP (6 ± 11 mmHg; P = 0.16), but Penaz SBP (−22 ± 16 mmHg; P < 0.001) and intra-arterial SBP (−11 ± 13 mmHg P = 0.017) decreased. In contrast, DBP and MBP did not differ between methods throughout heat stress. Compared with BP before LBNP, the magnitude of the reduction in BP with all three methods was similar throughout LBNP ( P > 0.05). In conclusion, auscultatory SBP and Penaz SBP failed to track the decrease in intra-arterial SBP that occurred during the profound heat stress, while decreases in arterial BP during an orthostatic challenge are comparable between methodologies.

scholarly journals Sustained increases in blood pressure elicited by prolonged face cooling in humans

2016 ◽  
Vol 311 (4) ◽  
pp. R643-R648 ◽  
Author(s):  
Zachary J. Schlader ◽  
Gregory L. Coleman ◽  
James R. Sackett ◽  
Suman Sarker ◽  
Blair D. Johnson
Keyword(s):  
Blood Pressure ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Vascular Resistance ◽  
Dependent Variables ◽  
The Face ◽  
Cardiac Parasympathetic Activity ◽  
Ice Water ◽  
Face Cooling ◽  
Forearm Vascular Resistance

We tested the hypothesis that increases in blood pressure are sustained throughout 15 min of face cooling. Two independent trials were carried out. In the Face-Cooling Trial, 10 healthy adults underwent 15 min of face cooling where a 2.5-liter bag of ice water (0 ± 0°C) was placed over their cheeks, eyes, and forehead. The Sham Trial was identical except that the temperature of the water was 34 ± 1°C. Primary dependent variables were forehead temperature, mean arterial pressure, and forearm vascular resistance. The square root of the mean of successive differences in R-R interval (RMSSD) provided an index of cardiac parasympathetic activity. In the Face Cooling Trial, forehead temperature fell from 34.1 ± 0.9°C at baseline to 12.9 ± 3.3°C at the end of face cooling ( P < 0.01). Mean arterial pressure increased from 83 ± 9 mmHg at baseline to 106 ± 13 mmHg at the end of face cooling ( P < 0.01). RMSSD increased from 61 ± 40 ms at baseline to 165 ± 97 ms during the first 2 min of face cooling ( P ≤ 0.05), but returned to baseline levels thereafter (65 ± 49 ms, P ≥ 0.46). Forearm vascular resistance increased from 18.3 ± 4.4 mmHg·ml−1·100 g tissue−1·min at baseline to 26.6 ± 4.0 mmHg·ml−1·100 g tissue−1·min at the end of face cooling ( P < 0.01). There were no changes in the Sham Trial. These data indicate that increases in blood pressure are sustained throughout 15 min of face cooling, and face cooling elicits differential time-dependent parasympathetic and likely sympathetic activation.

Venous and arterial reflex responses to positive-pressure breathing and lower body negative pressure

1997 ◽  
Vol 82 (6) ◽  
pp. 1889-1896 ◽  
Author(s):  
Jochen K. Peters ◽  
George Lister ◽  
Ethan R. Nadel ◽  
Gary W. Mack
Keyword(s):  
Cardiac Output ◽  
Vascular Resistance ◽  
Negative Pressure ◽  
Lower Body Negative Pressure ◽  
Venous Pressure ◽  
Transmural Pressure ◽  
Right Atrial ◽  
Positive Pressure ◽  
Lower Body ◽  
Reflex Responses

Peters, Jochen K., George Lister, Ethan R. Nadel, and Gary W. Mack. Venous and arterial reflex responses to positive-pressure breathing and lower body negative pressure. J. Appl. Physiol. 82(6): 1889–1896, 1997.—We examined the relative importance of arteriolar and venous reflex responses during reductions in cardiac output provoked by conditions that increase [positive end-expiratory pressure (PEEP)] or decrease [lower body negative pressure (LBNP)] peripheral venous filling. Five healthy subjects were exposed to PEEP (10, 15, 20, and 25 cmH2O) and LBNP (−10, −15, −20, and −25 mmHg) to induce progressive but comparable reductions in right atrial transmural pressure (control to minimum): from 5.9 ± 0.4 to 1.8 ± 0.7 and from 6.5 ± 0.6 to 2.0 ± 0.2 mmHg with PEEP and LBNP, respectively. Cardiac output (impedance cardiography) fell less during PEEP than during LBNP (from 3.64 ± 0.21 to 2.81 ± 0.21 and from 3.39 ± 0.21 to 2.14 ± 0.24 l ⋅ min−1 ⋅ m−2with PEEP and LBNP, respectively), and mean arterial pressure increased. We observed sustained increases in forearm vascular resistance (i.e., forearm blood flow by venous occlusion plethysmography) and systemic vascular resistance that were greater during LBNP: from 19.7 ± 2.91 to 27.97 ± 5.46 and from 20.56 ± 2.48 to 50.25 ± 5.86 mmHg ⋅ ml−1 ⋅ 100 ml tissue−1 ⋅ min ( P < 0.05) during PEEP and LBNP, respectively. Venomotor responses (venous pressure in the hemodynamically isolated limb) were always transient, significant only with the greatest reduction in right atrial transmural pressure, and were similar for LBNP and PEEP. Thus arteriolar rather than venous responses are predominant in blood volume mobilization from skin and muscle, and venoconstriction is not intensified with venous engorgement during PEEP.

Noise-Enhanced Heart Rate and Sympathetic Nerve Responses to Oscillatory Lower Body Negative Pressure in Humans

2001 ◽  
Vol 86 (2) ◽  
pp. 559-564 ◽  
Author(s):  
Ichiro Hidaka ◽  
Shin-Ichi Ando ◽  
Hideaki Shigematsu ◽  
Koji Sakai ◽  
Soko Setoguchi ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Stochastic Resonance ◽  
Negative Pressure ◽  
Sympathetic Nerve ◽  
Carotid Sinus ◽  
Lower Body Negative Pressure ◽  
Arterial System ◽  
Lower Body ◽  
Cardiopulmonary Baroreceptors

By injecting noise into the carotid sinus baroreceptors, we previously showed that heart rate (HR) responses to weak oscillatory tilt were enhanced via a mechanism known as “stochastic resonance.” It remains unclear, however, whether the same responses would be observed when using oscillatory lower body negative pressure (LBNP), which would unload the cardiopulmonary baroreceptors with physically negligible effects on the arterial system. Also, the vasomotor sympathetic activity directly controlling peripheral resistance against hypotensive stimuli was not observed. We therefore investigated the effects of weak (0 to approximately −10 mmHg) oscillatory (0.03 Hz) LBNP on HR and muscle sympathetic nerve activity (MSNA) while adding incremental noise to the carotid sinus baroreceptors via a pneumatic neck chamber. The signal-to-noise ratio of HR, cardiac interbeat interval, and total MSNA were all significantly improved by increasing noise intensity, while there was no significant change in the arterial blood pressure in synchronized with the oscillatory LBNP. We conclude that the stochastic resonance, affecting both HR and MSNA, results from the interaction of noise with the signal in the brain stem, where the neuronal inputs from the arterial and cardiopulmonary baroreceptors first come together in the nucleus tractus solitarius. Also, these results indicate that the noise could induce functional improvement in human blood pressure regulatory system in overcoming given hypotensive stimuli.

scholarly journals Hemodynamic abnormalities during muscle metaboreflex activation in patients with type 2 diabetes mellitus

2019 ◽  
Vol 126 (2) ◽  
pp. 444-453 ◽  
Author(s):  
Silvana Roberto ◽  
Raffaele Milia ◽  
Azzurra Doneddu ◽  
Virginia Pinna ◽  
Girolamo Palazzolo ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Blood Pressure ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Cardiac Output ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Blood Pressure Response ◽  
Pressure Response

Metaboreflex is a reflex triggered during exercise or postexercise muscle ischemia (PEMI) by metaboreceptor stimulation. Typical features of metaboreflex are increased cardiac output (CO) and blood pressure. Patients suffering from metabolic syndrome display hemodynamic abnormalities, with an exaggerated systemic vascular resistance (SVR) and reduced CO response during PEMI-induced metaboreflex. Whether patients with type 2 diabetes mellitus (DM2) have similar hemodynamic abnormalities is unknown. Here we contrast the hemodynamic response to PEMI in 14 patients suffering from DM2 (age 62.7 ± 8.3 yr) and in 15 age-matched controls (CTLs). All participants underwent a control exercise recovery reference test and a PEMI test to obtain the metaboreflex response. Central hemodynamics were evaluated by unbiased operator-independent impedance cardiography. Although the blood pressure response to PEMI was not significantly different between the groups, we found that the SVR and CO responses were reversed in patients with DM2 as compared with the CTLs (SVR: 392.5 ± 549.6 and −14.8 ± 258.9 dyn·s−1·cm−5; CO: −0.25 ± 0.63 and 0.46 ± 0.50 l/m, respectively, in DM2 and in CTL groups, respectively; P < 0.05 for both). Of note, stroke volume (SV) increased during PEMI in the CTL group only. Failure to increase SV and CO was the consequence of reduced venous return, impaired cardiac performance, and augmented afterload in patients with DM2. We conclude that patients with DM2 have an exaggerated vasoconstriction in response to metaboreflex activation not accompanied by a concomitant increase in heart performance. Therefore, in these patients, blood pressure response to the metaboreflex relies more on SVR increases rather than on increases in SV and CO. NEW & NOTEWORTHY The main new finding of the present investigation is that subjects with type 2 diabetes mellitus have an exaggerated vasoconstriction in response to metaboreflex activation. In these patients, blood pressure response to the metaboreflex relies more on systemic vascular resistance than on cardiac output increments.

The effect of Trendelenburg and modified trendelenburg positions on cardiac output, blood pressure, and oxygenation: a preliminary study

1994 ◽  
Vol 3 (5) ◽  
pp. 382-386 ◽  
Author(s):  
CL Ostrow ◽  
E Hupp ◽  
D Topjian
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Critically Ill ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Critically Ill Patients ◽  
Hemodynamic Parameters ◽  
Trendelenburg Position ◽  
Dependent Variables ◽  
Preliminary Study

BACKGROUND: Although we have insufficient knowledge about the effects of Trendelenburg positions on various hemodynamic parameters, these positions are frequently used to influence cardiac output and blood pressure in critically ill patients. OBJECTIVES: To determine the effect of Trendelenburg and modified Trendelenburg positions on five dependent variables: cardiac output, cardiac index, mean arterial pressure, systemic vascular resistance, and oxygenation in critically ill patients. METHODS: In this preliminary study subjects were 23 cardiac surgery patients (mean age, 55; SD, 8.09) who had a pulmonary artery catheter for cardiac output determination and who were clinically stable, normovolemic and normotensive. Baseline measurements of the dependent variables were taken in the supine position. Patients were then placed in 10 degrees Trendelenburg or 30 degrees modified Trendelenburg position. The dependent variables were measured after 10 minutes in each position. A 2-period, 2-treatment crossover design with a preliminary baseline measurement was used. RESULTS: Five subjects were unable to tolerate Trendelenburg position because of nausea or pain in the sternal incision. In the 18 who were able to tolerate both position changes, no statistically significant changes were found in the five dependent variables. Changes in systemic vascular resistance over time approached statistical significance and warrant further study. CONCLUSIONS: This preliminary study does not provide support for Trendelenburg positions as a means to influence hemodynamic parameters such as cardiac output and blood pressure in normovolemic and normotensive patients.

L-propionylcarnitine increases postischemic blood flow but does not affect recovery of energy charge

1991 ◽  
Vol 261 (1) ◽  
pp. H172-H180 ◽  
Author(s):  
L. M. Sassen ◽  
K. Bezstarosti ◽  
W. J. Van der Giessen ◽  
J. M. Lamers ◽  
P. D. Verdouw
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Systemic Vascular Resistance ◽  
Arterial Blood Pressure ◽  
Vascular Resistance ◽  
Contractile Function ◽  
Energy Charge ◽  
Left Ventricular ◽  
Arterial Blood

Effects of pretreatment with L-propionylcarnitine (50 mg/kg, n = 9) or saline (n = 10) were studied in open-chest anesthetized pigs, in which ischemia was induced by decreasing left anterior descending coronary artery blood flow to 20% of baseline. After 60 min of ischemia, myocardium was reperfused for 2 h. In both groups, flow reduction abolished contractile function of the affected myocardium and caused similar decreases in ATP (by 55%) and energy charge [(ATP + 0.5ADP)/(ATP + ADP + AMP); decrease from 0.91 to 0.60], mean arterial blood pressure (by 10-24%), the maximum rate of rise in left ventricular pressure (by 26-32%), and cardiac output (by 20-30%). During reperfusion, “no-reflow” was attenuated by L-propionylcarnitine, because myocardial blood flow returned to 61 and 82% of baseline in the saline- and L-propionylcarnitine-treated animals, respectively. Cardiac output of the saline-treated animals further decreased (to 52% of baseline), and systemic vascular resistance increased from 46 +/- 3 to 61 +/- 9 mmHg.min.l-1, thereby maintaining arterial blood pressure. In L-propionylcarnitine-treated pigs, cardiac output remained at 75% of baseline, and systemic vascular resistance decreased from 42 +/- 3 to 38 +/- 4 mmHg.min.l-1. In both groups, energy charge but not the ATP level of the ischemic-reperfused myocardium tended to recover, whereas the creatine phosphate level showed significantly more recovery in saline-treated animals. We conclude that L-propionylcarnitine partially preserved vascular patency in ischemic-reperfused porcine myocardium but had no immediate effect on “myocardial stunning.” Potential markers for long-term recovery were not affected by L-propionylcarnitine.

Mechanism of circulatory responses to systemic hypoxia in the anesthetized dog

1965 ◽  
Vol 209 (2) ◽  
pp. 397-403 ◽  
Author(s):  
Hermes A. Kontos ◽  
H. Page Mauck ◽  
David W. Richardson ◽  
John L. Patterson
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Vascular Resistance ◽  
The Other ◽  
Arterial Flow ◽  
Arterial Blood ◽  
Systemic Hypoxia ◽  
Anesthetized Dogs ◽  
Spontaneously Breathing

The possibility that mechanisms secondary to the increased ventilation may contribute significantly to the circulatory responses to systemic hypoxia was explored in anesthetized dogs. In 14 spontaneously breathing dogs systemic hypoxia induced by breathing 7.5% oxygen in nitrogen increased cardiac output, heart rate, mean arterial blood pressure, and femoral arterial flow, and decreased systemic and hindlimb vascular resistances. In 14 dogs whose ventilation was kept constant by means of a respirator pump and intravenous decamethonium, systemic hypoxia did not change cardiac output, femoral arterial flow, or limb vascular resistance; it significantly decreased heart rate and significantly increased systemic vascular resistance. In seven spontaneously breathing dogs arterial blood pCO2 was maintained at the resting level during systemic hypoxia. The increase in heart rate was significantly less pronounced but the other circulatory findings were not different from those found during hypocapnic hypoxia. Thus, mechanisms secondary to increased ventilation contribute significantly to the circulatory responses to systemic hypoxia. Hypocapnia accounts partly for the increased heart rate, but not for the other circulatory responses.

Effect of K ATP + channel inhibition on total and regional vascular resistance in guinea pig pregnancy

1998 ◽  
Vol 275 (2) ◽  
pp. H680-H688 ◽  
Author(s):  
Linda Keyes ◽  
David M. Rodman ◽  
Douglas Curran-Everett ◽  
Kenneth Morris ◽  
Lorna G. Moore
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Guinea Pig ◽  
Vascular Resistance ◽  
Coronary Vascular Resistance ◽  
Ang Ii ◽  
Channel Activity ◽  
Vasoconstrictor Response ◽  
Regional Vascular Resistance

Decreased vascular resistance and vasoconstrictor response during pregnancy enables an increase in cardiac output and regional blood flow to the uterine circulation. We sought to determine whether inhibition of vascular smooth muscle ATP-sensitive potassium ([Formula: see text]) channel activity during pregnancy increased systemic and/or regional vascular resistance and resistance response to ANG II. A total of 32 catheterized, awake, pregnant or nonpregnant guinea pigs were treated with either the [Formula: see text]channel inhibitor glibenclamide (3.5 mg/kg) or vehicle (DMSO) ( n = 8/group). In nonpregnant and pregnant animals, glibenclamide raised blood pressure and systemic, uterine, and coronary vascular resistance, diminishing cardiac output and organ blood flow. Glibenclamide produced a greater rise in coronary vascular resistance in the pregnant than nonpregnant groups and increased renal and cerebral vascular resistance in the pregnant animals only. ANG II infusion raised blood pressure and systemic and renal vascular resistance and lowered cardiac output and renal blood flow in vehicle-treated animals. Glibenclamide augmented ANG II-induced systemic vasoconstriction in the nonpregnant and pregnant groups and the rise in uteroplacental vascular resistance in the pregnant animals. We concluded that [Formula: see text] channel activity likely modulates systemic, uterine, and coronary vascular resistance and opposes ANG II-induced systemic vasoconstriction in nonpregnant and pregnant guinea pigs. Pregnancy augments[Formula: see text] channel activity in the uterine, coronary, renal, and cerebral vascular beds and the uteroplacental circulation during ANG II infusion. Thus increased[Formula: see text] channel activity appears to influence regional control of vascular resistance during guinea pig pregnancy but cannot account for the characteristic decrease in systemic vascular resistance and ANG II-induced systemic vasoconstrictor response.

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