Postexercise hypotension is not explained by a prostaglandin-dependent peripheral vasodilation

2005 ◽  
Vol 98 (2) ◽  
pp. 447-453 ◽  
Author(s):  
Jennifer M. Lockwood ◽  
Mollie P. Pricher ◽  
Brad W. Wilkins ◽  
Lacy A. Holowatz ◽  
John R. Halliwill
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Potential Contribution ◽  
Vascular Conductance ◽  
Cyclooxygenase Inhibition ◽  
Peripheral Vasodilation ◽  
Arterial Blood ◽  
Single Bout ◽  
Oral Ibuprofen ◽  
Postexercise Hypotension

In normally active individuals, postexercise hypotension after a single bout of aerobic exercise occurs due to an unexplained peripheral vasodilation. Prostaglandin production has been suggested to contribute to the increases in blood flow during and after exercise; however, its potential contribution to postexercise hypotension has not been assessed. The purpose of this study was to determine the potential contribution of a prostaglandin-dependent vasodilation to changes in systemic vascular conductance underlying postexercise hypotension; this was done by inhibiting production of prostaglandins with the cyclooxygenase inhibitor ibuprofen. We studied 11 healthy normotensive men (aged 23.7 ± 4.2 yr) before and during the 90 min after a 60-min bout of cycling at 60% peak O2 uptake on a control and a cyclooxygenase inhibition day (randomized). Subjects received 10 mg/kg of oral ibuprofen on the cyclooxygenase inhibition day. On both study days, arterial blood pressure (automated auscultation) and cardiac output (acetylene uptake) were measured, and systemic vascular conductance was calculated. Inhibition of cyclooxygenase had no effect on baseline values of mean arterial pressure or systemic vascular conductance ( P > 0.2). After exercise on both days, mean arterial pressure was reduced (−2.2 ± 1.0 mmHg change with the control condition and −3.8 ± 1.5 mmHg change with the ibuprofen condition, both P < 0.05 vs. preexercise) and systemic vascular conductance was increased (5.2 ± 5.0% change with the control condition and 8.7 ± 4.1% change with the ibuprofen condition, both P < 0.05 vs. preexercise). There were no differences between study days ( P > 0.6). These data suggest that prostaglandin-dependent vasodilation does not contribute to the increased systemic vascular conductance underlying postexercise hypotension.

scholarly journals H2-receptor-mediated vasodilation contributes to postexercise hypotension

2006 ◽  
Vol 100 (1) ◽  
pp. 67-75 ◽  
Author(s):  
Jennifer L. McCord ◽  
Julie M. Beasley ◽  
John R. Halliwill
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Potential Contribution ◽  
Vascular Conductance ◽  
Men And Women ◽  
Femoral Blood Flow ◽  
Postexercise Hypotension ◽  
Femoral Blood ◽  
Randomized Control ◽  
Automated Auscultation

The early (∼30 min) postexercise hypotension response after a session of aerobic exercise is due in part to H1-receptor-mediated vasodilation. The purpose of this study was to determine the potential contribution of H2-receptor-mediated vasodilation to postexercise hypotension. We studied 10 healthy normotensive men and women (ages 23.7 ± 3.4 yr) before and through 90 min after a 60-min bout of cycling at 60% peak O2 uptake on randomized control and H2-receptor antagonist days (300 mg oral ranitidine). Arterial pressure (automated auscultation), cardiac output (acetylene washin) and femoral blood flow (Doppler ultrasound) were measured. Vascular conductance was calculated as flow/mean arterial pressure. Sixty minutes postexercise on the control day, femoral (Δ62.3 ± 15.6%, where Δ is change; P < 0.01) and systemic (Δ13.8 ± 5.3%; P = 0.01) vascular conductances were increased, whereas mean arterial pressure was reduced (Δ−6.7 ± 1.1 mmHg; P < 0.01). Conversely, 60 min postexercise with ranitidine, femoral (Δ9.4 ± 9.2%; P = 0.34) and systemic (Δ−2.8 ± 4.8%; P = 0.35) vascular conductances were not elevated and mean arterial pressure was not reduced (Δ−2.2 ± 1.3 mmHg; P = 0.12). Furthermore, postexercise femoral and systemic vascular conductances were lower ( P < 0.05) and mean arterial pressure was higher ( P = 0.01) on the ranitidine day compared with control. Ingestion of ranitidine markedly reduces vasodilation after exercise and blunts postexercise hypotension, suggesting H2-receptor-mediated vasodilation contributes to postexercise hypotension.

scholarly journals Plasticity in breathing and arterial blood pressure following acute intermittent hypercapnic hypoxia in infant rat pups with a partial loss of 5-HT neurons

2015 ◽  
Vol 309 (10) ◽  
pp. R1273-R1284 ◽  
Author(s):  
Jennifer Magnusson ◽  
Kevin J. Cummings
Keyword(s):  
Blood Pressure ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Arterial Blood Pressure ◽  
Cardiovascular Responses ◽  
Partial Loss ◽  
Rat Pups ◽  
Arterial Blood ◽  
Hypercapnic Hypoxia ◽  
Long Term Facilitation

The role of serotonin (5-HT) neurons in cardiovascular responses to acute intermittent hypoxia (AIH) has not been studied in the neonatal period. We hypothesized that a partial loss of 5-HT neurons would reduce arterial blood pressure (BP) at rest, increase the fall in BP during hypoxia, and reduce the long-term facilitation of breathing (vLTF) and BP following AIH. We exposed 2-wk-old, 5,7-dihydroxytryptamine-treated and controls to AIH (10% O2; n = 13 control, 14 treated), acute intermittent hypercapnia (5% CO2; n = 12 and 11), or acute intermittent hypercapnic hypoxia (AIHH; 10% O2, 5% CO2; n = 15 and 17). We gave five 5-min challenges of AIH and acute intermittent hypercapnia, and twenty ∼20-s challenges of AIHH to mimic sleep apnea. Systolic BP (sBP), diastolic BP, mean arterial pressure, heart rate (HR), ventilation (V̇e), and metabolic rate (V̇o2) were continuously monitored. 5,7-Dihydroxytryptamine induced an ∼35% loss of 5-HT neurons from the medullary raphe. Compared with controls, pups deficient in 5-HT neurons had reduced resting sBP (∼6 mmHg), mean arterial pressure (∼5 mmHg), and HR (56 beats/min), and experienced a reduced drop in BP during hypoxia. AIHH induced vLTF in both groups, reflected in increased V̇e and V̇e/V̇o2, and decreased arterial Pco2. The sBP of pups deficient in 5-HT neurons, but not controls, was increased 1 h following AIHH. Our data suggest that a relatively small loss of 5-HT neurons compromises resting BP and HR, but has no influence on ventilatory plasticity induced by AIHH. AIHH may be useful for reversing cardiorespiratory defects related to partial 5-HT system dysfunction.

Abstract 9934: High Mean Arterial Pressure Aggravates Cerebral Hemodynamics After Extracorporeal Resuscitation in Swine

Circulation ◽  
2021 ◽  
Vol 144 (Suppl_2) ◽  
Author(s):  
Yael Levy ◽  
Alice Hutin ◽  
Nicolas Polge ◽  
fanny lidouren ◽  
Matthias Kohlhauer ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiac Arrest ◽  
Oxygen Consumption ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Cerebral Hemodynamics ◽  
Reactivity Index ◽  
Extracorporeal Cardiopulmonary Resuscitation ◽  
Standard Map ◽  
Arterial Blood

Introduction: Extracorporeal cardiopulmonary resuscitation (E-CPR) is used for the treatment of refractory cardiac arrest but the optimal target to reach for mean arterial pressure (MAP) remains to be determined. Hypothesis: We hypothesized that MAP levels modify cerebral hemodynamics during E-CPR. Accordingly, we tested two MAP targets (65-75 vs 80-90 mmHg) in a porcine model of E-CPR. Methods: Pigs were anesthetized and instrumented for the evaluation of cerebral and systemic hemodynamics. They were submitted to 15 min of untreated ventricular fibrillation followed by 30 min of E-CPR. Electric attempts of defibrillation were then delivered until resumption of spontaneous circulation (ROSC). Extracorporeal circulation was initially set to an average flow of 40 ml/kg/min with a standardized volume expansion in both groups. The dose of epinephrine was set to reach either a standard or a high MAP target level (65-75 vs 80-90 mmHg, respectively). Animals were followed during 120 min after ROSC. Results: Six animals were included in both groups. After cardiac arrest, MAP was maintained at the expected level (Figure). During E-CPR, high MAP transiently improved carotid blood flow as compared to standard MAP. This blood flow progressively decreased after ROSC in high vs standard MAP, while intra-cranial pressure increased. Interestingly, this was associated with a significant decrease in cerebral oxygen consumption (26±8 vs 54±6 L O 2 /min/kg at 120 min after ROSC, respectively; p<0.01) (Figure). The pressure reactivity index (PRx), which is the correlation coefficient between arterial blood pressure and intracranial pressure, became positive in high MAP (0.47±0.02) vs standard MAP group (-0.16±0.10), demonstrating altered cerebral autoregulation with high MAP. Conclusion: Increasing MAP above 80 mmHg with epinephrine aggravates cerebral hemodynamics after E-CPR. Figure: Mean arterial pressure (MAP), cerebral blood flow and oxygen consumption (*, p<0.05)

Increased vascular resistance in paralyzed legs after spinal cord injury is reversible by training

2002 ◽  
Vol 93 (6) ◽  
pp. 1966-1972 ◽  
Author(s):  
Maria T. E. Hopman ◽  
Jan T. Groothuis ◽  
Marcel Flendrie ◽  
Karin H. L. Gerrits ◽  
Sibrand Houtman
Keyword(s):  
Blood Pressure ◽  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Vascular Resistance ◽  
Arterial Blood Flow ◽  
Arterial Blood ◽  
Cord Injury

The purpose of the present study was to determine the effect of a spinal cord injury (SCI) on resting vascular resistance in paralyzed legs in humans. To accomplish this goal, we measured blood pressure and resting flow above and below the lesion (by using venous occlusion plethysmography) in 11 patients with SCI and in 10 healthy controls (C). Relative vascular resistance was calculated as mean arterial pressure in millimeters of mercury divided by the arterial blood flow in milliliters per minute per 100 milliliters of tissue. Arterial blood flow in the sympathetically deprived and paralyzed legs of SCI was significantly lower than leg blood flow in C. Because mean arterial pressure showed no differences between both groups, leg vascular resistance in SCI was significantly higher than in C. Within the SCI group, arterial blood flow was significantly higher and vascular resistance significantly lower in the arms than in the legs. To distinguish between the effect of loss of central neural control vs. deconditioning, a group of nine SCI patients was trained for 6 wk and showed a 30% increase in leg blood flow with unchanged blood pressure levels, indicating a marked reduction in vascular resistance. In conclusion, vascular resistance is increased in the paralyzed legs of individuals with SCI and is reversible by training.

Increases in intramuscular pressure raise arterial blood pressure during dynamic exercise

2001 ◽  
Vol 91 (5) ◽  
pp. 2351-2358 ◽  
Author(s):  
K. M. Gallagher ◽  
P. J. Fadel ◽  
S. A. Smith ◽  
K. H. Norton ◽  
R. G. Querry ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Arterial Blood Pressure ◽  
Dynamic Exercise ◽  
Positive Pressure ◽  
Intramuscular Pressure ◽  
Arterial Blood ◽  
Exercise In Humans ◽  
Cuff Occlusion

This investigation was designed to determine the role of intramuscular pressure-sensitive mechanoreceptors and chemically sensitive metaboreceptors in affecting the blood pressure response to dynamic exercise in humans. Sixteen subjects performed incremental (20 W/min) cycle exercise to fatigue under four conditions: control, exercise with thigh cuff occlusion of 90 Torr (Cuff occlusion), exercise with lower body positive pressure (LBPP) of 45 Torr, and a combination of thigh cuff occlusion and LBPP (combination). Indexes of central command (heart rate, oxygen uptake, ratings of perceived exertion, and electromyographic activity), cardiac output, stroke volume, and total peripheral resistance were not significantly different between the four conditions. Mechanical stimulation during LBPP and combination conditions resulted in significant elevations in intramuscular pressure and mean arterial pressure from control at rest and throughout the incremental exercise protocol ( P < 0.05). Conversely, there existed no significant changes in mean arterial pressure when the metaboreflex was stimulated by cuff occlusion. These findings suggest that under normal conditions the mechanoreflex is tonically active and is the primary mediator of exercise pressor reflex-induced alterations in arterial blood pressure during submaximal dynamic exercise in humans.

Furosemide in the Intraoperative Reduction of Intracranial Pressure in the Patient with Subarachnoid Hemorrhage

Neurosurgery ◽  
1982 ◽  
Vol 10 (2) ◽  
pp. 167-169 ◽  
Author(s):  
Duke Samson ◽  
Chester W. Beyer
Keyword(s):  
Mean Arterial Pressure ◽  
Intracranial Pressure ◽  
Arterial Pressure ◽  
Blood Gases ◽  
Base Line ◽  
Arterial Pco2 ◽  
Arterial Blood ◽  
Ruptured Intracranial Aneurysm ◽  
Intracranial Lesions ◽  
Sequential Measurements

Abstract The effect of furosemide in the intraoperative reduction of intracranial pressure was measured in 25 patients undergoing the operative repair of a ruptured intracranial aneurysm. Seven patients with similar intracranial lesions served as controls. A single bolus of 80 mg of furosemide was administered intravenously after the induction of anesthesia, and sequential measurements were made of intracranial pressure, mean arterial pressure, and arterial blood gases. A mean decrease of intracranial pressure of 56% was measured in the furosemide-treated patients, whereas the control patients demonstrated a mean decline of subarachnoid pressures of 18%. These changes are significant at the P &lt; 0.005 confidence level, whereas changes in mean arterial pressure, mean arterial pCO2, and base line arterial pCO2 were statistically insignificant. This study suggests that intravenous furosemide is a quick, dependable, and effective mechanism for the intraoperative reduction of intracranial pressure in the postsubarachnoid hemorrhage aneurysm patient.

scholarly journals Role of endothelial nitric oxide in control of peripheral vascular conductance during muscle metaboreflex activation

2017 ◽  
Vol 313 (1) ◽  
pp. R29-R34
Author(s):  
Danielle Senador ◽  
Jasdeep Kaur ◽  
Alberto Alvarez ◽  
Hanna W. Hanna ◽  
Abhinav C. Krishnan ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Vascular Conductance ◽  
Muscle Metaboreflex ◽  
Peripheral Vasodilation ◽  
Dependent Flow ◽  
Flow Mediated Vasodilation ◽  
The Relationship

The muscle metaboreflex is a powerful pressor reflex induced by the activation of chemically sensitive muscle afferents as a result of metabolite accumulation. During submaximal dynamic exercise, the rise in arterial pressure is primarily due to increases in cardiac output, since there is little systemic vasoconstriction. Indeed, in normal animals, we have often shown a small, but significant, peripheral vasodilation during metaboreflex activation, which is mediated, at least in part, by release of epinephrine and activation of vascular β2-receptors. We tested whether this vasodilation is in part due to increased release of nitric oxide caused by the rise in cardiac output eliciting endothelium-dependent flow-mediated vasodilation. The muscle metaboreflex was activated via graded reductions in hindlimb blood flow during mild exercise with and without nitric oxide synthesis blockade [ NG-nitro-l-arginine methyl ester (l-NAME); 5 mg/kg]. We assessed the role of increased cardiac output in mediating peripheral vasodilation via the slope of the relationship between the rise in nonischemic vascular conductance (conductance of all vascular beds excluding hindlimbs) vs. the rise in cardiac output. l-NAME increased mean arterial pressure at rest and during exercise. The metaboreflex-induced increases in mean arterial pressure were unaltered by l-NAME, whereas the increases in cardiac output and nonischemic vascular conductance were attenuated. However, the slope of the relationship between nonischemic vascular conductance and cardiac output was not affected by l-NAME, indicating that the rise in cardiac output did not elicit vasodilation via increased release of nitric oxide. Thus, although nitric oxide is intrinsic to the vascular tonus, endothelial-dependent flow-mediated vasodilation plays little role in the small peripheral vasodilation observed during muscle metaboreflex activation.

scholarly journals Comparative study of intravenous hydralazine and labetalol in severe hypertensive disorders of pregnancy

2020 ◽  
Vol 9 (2) ◽  
pp. 675
Author(s):  
Anupma Kumari ◽  
Renu Rohatgi ◽  
Amrita Singh ◽  
Raj Kumar
Keyword(s):  
Blood Pressure ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Neonatal Morbidity ◽  
Medical Complications ◽  
Age Group ◽  
Efficacy And Safety ◽  
Hypertensive Disorders Of Pregnancy ◽  
Arterial Blood ◽  
Hypertensive Disorders

Background: Hypertensive disorders of pregnancy are among the most common medical complications of pregnancy and major cause of maternal, fetal and neonatal morbidity and mortality. The purpose of this study was to compare the efficacy and safety of intravenous hydralazine and labetalol for management of severe hypertensive disorders of pregnancy.Methods: This prospective study was conducted among 100 women admitted with SBP ≥ 160 or DBP ≥ 110 mmHg or both. Patients were divided into 2 groups randomly: labetalol and hydralazine group.Results: Majority of patients (38%) were in the age group of 21-25 years and primigravida (52%). There was more significant decrease in the systolic, diastolic and mean arterial blood pressure at the end of 15 and 30 minutes in labetalol group. Labetalol required fewer doses as compared to hydralazine to achieve the target blood pressure (average 1.95 versus 3.1). Total numbers of term deliveries were 19 (38%) in hydralazine group and 16 (32%) in labetalol group. Pre-term deliveries in hydralazine and labetalol group were 14 (28%) and 15 (30%) respectively. Headache was significantly more common in hydralazine treated patients than labetalol group.Conclusions: Both hydralazine and labetalol were effective and well-tolerated in the treatment of severe hypertensive disorders of pregnancy. Labetalol may be preferred because it was more effective in lowering the systolic blood pressure, diastolic blood pressure and mean arterial pressure to achieve target levels with less number of doses.

Is postexercise hypotension related to excess postexercise oxygen consumption through changes in leg blood flow?

2005 ◽  
Vol 98 (4) ◽  
pp. 1463-1468 ◽  
Author(s):  
Jay T. Williams ◽  
Mollie P. Pricher ◽  
John R. Halliwill
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Oxygen Consumption ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Muscle Blood Flow ◽  
Causal Link ◽  
Skeletal Muscle Blood Flow ◽  
Leg Blood Flow ◽  
Postexercise Hypotension

After a single bout of aerobic exercise, oxygen consumption remains elevated above preexercise levels [excess postexercise oxygen consumption (EPOC)]. Similarly, skeletal muscle blood flow remains elevated for an extended period of time. This results in a postexercise hypotension. The purpose of this study was to explore the possibility of a causal link between EPOC, postexercise hypotension, and postexercise elevations in skeletal muscle blood flow by comparing the magnitude and duration of these postexercise phenomena. Sixteen healthy, normotensive, moderately active subjects (7 men and 9 woman, age 20–31 yr) were studied before and through 135 min after a 60-min bout of upright cycling at 60% of peak oxygen consumption. Resting and recovery V̇o2 were measured with a custom-built dilution hood and mass spectrometer-based metabolic system. Mean arterial pressure was measured via an automated blood pressure cuff, and femoral blood flow was measured using ultrasound. During the first hour postexercise, V̇o2 was increased by 11 ± 2%, leg blood flow was increased by 51 ± 18%, leg vascular conductance was increased by 56 ± 19%, and mean arterial pressure was decreased by 2.2 ± 1.0 mmHg (all P < 0.05 vs. preexercise). At the end of the protocol, V̇o2 remained elevated by 4 ± 2% ( P < 0.05), whereas leg blood flow, leg vascular conductance, and mean arterial pressure returned to preexercise levels (all P > 0.7 vs. preexercise). Taken together, these data demonstrate that EPOC and the elevations in skeletal muscle blood flow underlying postexercise hypotension do not share a common time course. This suggests that there is no causal link between these two postexercise phenomena.

Association between Intraoperative Hypotension and Myocardial Injury after Vascular Surgery

2016 ◽  
Vol 124 (1) ◽  
pp. 35-44 ◽  
Author(s):  
Judith A. R. van Waes ◽  
Wilton A. van Klei ◽  
Duminda N. Wijeysundera ◽  
Leo van Wolfswinkel ◽  
Thomas F. Lindsay ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Vascular Surgery ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Myocardial Injury ◽  
Arterial Blood ◽  
Intraoperative Hypotension ◽  
Cumulative Duration

Abstract Background Postoperative myocardial injury occurs frequently after noncardiac surgery and is strongly associated with mortality. Intraoperative hypotension (IOH) is hypothesized to be a possible cause. The aim of this study was to determine the association between IOH and postoperative myocardial injury. Methods This cohort study included 890 consecutive patients aged 60 yr or older undergoing vascular surgery from two university centers. The occurrence of myocardial injury was assessed by troponin measurements as part of a postoperative care protocol. IOH was defined by four different thresholds using either relative or absolute values of the mean arterial blood pressure based on previous studies. Either invasive or noninvasive blood pressure measurements were used. Poisson regression analysis was used to determine the association between IOH and postoperative myocardial injury, adjusted for potential clinical confounders and multiple comparisons. Results Depending on the definition used, IOH occurred in 12 to 81% of the patients. Postoperative myocardial injury occurred in 131 (29%) patients with IOH as defined by a mean arterial pressure less than 60 mmHg, compared with 87 (20%) patients without IOH (P = 0.001). After adjustment for potential confounding factors including mean heart rates, a 40% decrease from the preinduction mean arterial blood pressure with a cumulative duration of more than 30 min was associated with postoperative myocardial injury (relative risk, 1.8; 99% CI, 1.2 to 2.6, P &lt; 0.001). Shorter cumulative durations (less than 30 min) were not associated with myocardial injury. Postoperative myocardial infarction and death within 30 days occurred in 26 (6%) and 17 (4%) patients with IOH as defined by a mean arterial pressure less than 60 mmHg, compared with 12 (3%; P = 0.08) and 15 (3%; P = 0.77) patients without IOH, respectively. Conclusions In elderly vascular surgery patients, IOH defined as a 40% decrease from the preinduction mean arterial blood pressure with a cumulative duration of more than 30 min was associated with postoperative myocardial injury.

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