Percent Change In Mean Arterial Pressure Research Articles

Abstract MP35: Blood Pressure Reductions Before Arrival at a Thrombectomy-Capable Hospital Are Associated With Neurologic Worsening in Patients With Large-Vessel Occlusion

Introduction: Decreases in blood pressure (BP) during thrombectomy are associated with infarct progression and worse outcomes. Many patients present first to a primary stroke center (PSC) and are later transferred to a comprehensive stroke center (CSC) to undergo thrombectomy. During this period, important BP variations might occur. We evaluated the association of BP reductions with neurological worsening and functional outcomes. Methods: We prospectively collected hemodynamic, clinical, and radiographic data on consecutive patients with LVO ischemic stroke who were transferred from a PSC for possible thrombectomy between 2018 and 2020. We assessed systolic BP (SBP) and mean arterial pressure (MAP) at five time points: earliest recorded, average pre-PSC, PSC admission, average PSC, and CSC admission. We measured neurologic worsening as a change in NIHSS (ΔNIHSS) from PSC to CSC >3 and functional outcome using the modified Rankin Scale (mRS) at discharge and 90 days. Relationships between variables of interest were evaluated using linear regression. Results: Of 91 patients (mean age 70±16 years, mean NIHSS 12) included, 13 (14%) experienced early neurologic deterioration (ΔNIHSS>3), and 34 (37%) achieved a good outcome at discharge (mRS<3). We found that patients with good outcome had significantly lower SBP at all five assessed time points compared to patients with poor outcome (Figure 1, p<0.05). Percent change in MAP from initial presentation to CSC arrival was independently associated with ΔNIHSS after adjusting for age, sex, and transfer time (p=0.03, β=0.27). Conclusions: Patients with poor outcomes have higher BP throughout the pre-CSC period, possibly reflecting an augmented hypertensive response. Reductions in SBP and MAP before arrival at the CSC are associated with neurologic worsening. These results suggest that BP management strategies in the pre-CSC period to avoid large reductions in BP may improve outcomes in patients affected by LVO stroke.

Hemodynamic effects of vasorelaxant compounds in mice lacking one, two or all three angiotensin II receptors

The renin-angiotensin system (RAS) has a vital role in regulating the cardiovascular system. The primary effector of the RAS is the octapeptide angiotensin (Ang) II, a potent regulator of blood pressure and water homeostasis. Ang II mediates its functions through the stimulation of two distinct receptors, AT(1) (two subtypes in rodents (AT(1a) and AT(1b))) and AT(2). It was shown that in addition to Ang II, shorter fragments of Ang are also biologically active. Ang-(1-7) came into focus because it opposes many of the detrimental effects of Ang II. However, it is still controversial whether Ang II receptors are involved in Ang-(1-7)-mediated signaling. To characterize the impacts of Ang II receptors on Ang-(1-7)-stimulated vascular relaxation, the effects of acute infusion of the three vasorelaxant compounds, that is, Ang-(1-7), bradykinin (BK) and acetylcholine (ACh), on heart rate (HR) and mean arterial pressure (MAP) were investigated in mice deficient for one, two or all three Ang II receptors. Ang-(1-7) and BK reduced MAP in wild-type, AT(1a)/AT(1b)-deficient and AT(2)-deficient mice. Although the change in absolute MAP values in the hypotensive triple knockouts (KO) could not be further reduced by both peptides, the percent change in MAP was comparable between the triple KO and wild-type mice. Both peptides did not alter the HR in all four genotypes. ACh significantly reduced absolute MAP values in all four genotypes with a similar percentage of reduction. In contrast to Ang-(1-7) and BK, ACh significantly reduced HR without genotypic differences. Our results generate proof that Ang-(1-7)-induced effects on MAP are mediated by a receptor that is independent of AT(1) and AT(2).

425 BOTULISM TOXIN TYPE A INJECTIONS IN THE NEUROGENIC BLADDER LESSONS THE SEVERITY OF AUTONOMIC DYSREFLEXIA IN THREE PERSONS WITH SCI DURING URODYNAMICS

You have accessJournal of UrologyBladder and Urethra: Anatomy, Physiology and Pharmacology1 Apr 2011425 BOTULISM TOXIN TYPE A INJECTIONS IN THE NEUROGENIC BLADDER LESSONS THE SEVERITY OF AUTONOMIC DYSREFLEXIA IN THREE PERSONS WITH SCI DURING URODYNAMICS Cynthia Trop, Christina Yen, Giuseppe Galea, Marinella Galea, William Bauman, and Jill Wecht Cynthia TropCynthia Trop Bronx, NY More articles by this author , Christina YenChristina Yen Bronx, NY More articles by this author , Giuseppe GaleaGiuseppe Galea Bronx, NY More articles by this author , Marinella GaleaMarinella Galea Bronx, NY More articles by this author , William BaumanWilliam Bauman Bronx, NY More articles by this author , and Jill WechtJill Wecht Bronx, NY More articles by this author View All Author Informationhttps://doi.org/10.1016/j.juro.2011.02.515AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookTwitterLinked InEmail INTRODUCTION AND OBJECTIVES Autonomic dysreflexia (AD) is caused by a massive sympathetic discharge triggered by a stimulus below the level of the spinal cord injury, commonly caused by bladder distention or irritation. It is assumed that treatment with botulism toxin A reduces the incidence of AD by reducing neurogenic detruser overactivity. The study objective was to compare changes in beat to beat mean arterial pressure (MAP) during clinical urodynamics, prior to and 6 weeks post botulism toxin A injections in three spinal cord injured individuals. METHODS Three individuals with chronic SCI (>1 yr), T3 and above had botulism toxin A injections during which three hundred units of botulism were injected under cystoscopic guidance into the bladder in 30 locations. Urodynamics were performed prior to treatment and 6 weeks post to evaluate for detrusor hyperreflexia, during which BP was monitored continuously. Data are reported as percent changes in MAP. DESIGN Interventional, prospective, observational. RESULTS All three subjects exhibited a reduction in the percent change in MAP from baseline to maximum cystometric capacity (MCC)(Table 1.0). There were no significant changes pre and post testing in volume infused or detrusor pressure at MCC. Although subjects 1 and 3 experienced AD during urodynamics both pre and post treatment, (change in MAP > 20%); the severity of the AD was greatly reduced post treatment in both cases. Subject 2 did not experience AD pre or post treatment, but change in MAP during post treatment urodynamics was reduced from change in MAP during pre treatment urodynamics. CONCLUSIONS Our preliminary findings suggest that intravesical botulism toxin A injections help alleviate elevations of blood pressure by decreasing detrusor muscle contractility. We suggest that by inhibiting acetylcholine release in the bladder membrane, botulinum toxin A injections help reduce the afferent discharge from the distended bladder, thus decreasing the incidence and severity of AD. © 2011 by American Urological Association Education and Research, Inc.FiguresReferencesRelatedDetails Volume 185Issue 4SApril 2011Page: e171-e172 Advertisement Copyright & Permissions© 2011 by American Urological Association Education and Research, Inc.MetricsAuthor Information Cynthia Trop Bronx, NY More articles by this author Christina Yen Bronx, NY More articles by this author Giuseppe Galea Bronx, NY More articles by this author Marinella Galea Bronx, NY More articles by this author William Bauman Bronx, NY More articles by this author Jill Wecht Bronx, NY More articles by this author Expand All Advertisement Advertisement PDF downloadLoading ...

Effect of hypotensive challenge on systemic hemodynamics and cerebral blood flow in persons with tetraplegia

Individuals with tetraplegia have impaired central control of sympathetic vascular modulation and blood pressure (BP); how this impairment affects cerebral blood flow (CBF) is unclear. To determine if persons with tetraplegia maintain CBF similarly to able-bodied controls after a hypotensive challenge. Seven individuals with chronic tetraplegia and seven age-matched, non-SCI control subjects underwent a hypotensive challenge consisting of angiotensin-converting enzyme (ACE) inhibition (1.25 mg enalaprilat) and 45 degrees head-up tilt (HUT). Heart rate (HR), low frequency systolic BP variability (LFsbp), brachial mean arterial pressure (MAP) and middle cerebral artery CBF were measured before and after the challenge. Group differences for the baseline (BL) to post-challenge response were determined by repeated measures ANOVA. HR did not differ between the groups in response to the hypotensive challenge. LFsbp response was significantly reduced in the tetra compared to the control group (-38 +/- 51 vs. 72 +/- 93%, respectively). MAP did not differ between the groups at BL but was significantly lower in the tetra compared to the control group post-challenge (55 +/- 13 vs. 71 +/- 9 mmHg, respectively); the percent change in MAP was significantly greater in the tetra than in the control group (-29 +/- 14.1 vs. -13 +/- 9%, respectively). However, CBF did not differ between the groups at baseline or post-challenge; the percent change in CBF post-challenge was not different between the tetra and control groups (-29 +/- 13.2 vs. -23 +/- 10.3%, respectively). Despite impaired sympathetic vasomotor and BP control, CBF in persons with tetraplegia was comparable to that of control subjects during a hypotensive challenge.

A POTENTIAL ROLE FOR IMMUNE ACTIVATION IN HEMODIALYSIS HYPOTENSION

The necessary exposure of blood to biomembranes during hemodialysis has been viewed by many as an immunogenic challenge leading to an acute phase response. In this study we examined the relationship between hemodialysis-induced immune activation and intradialytic hypotension, using the acute phase reactant serum C-reactive protein (CRP) as a surrogate for immunogenic activation. The maximum percent change in mean arterial pressure (MAP) was found to correlate significantly with CRP (r = 0.67, p < 0.05) in nine consecutive patients with a history of symptomatic hypotension during hemodialysis. In contrast, no correlation was found between CRP and maximum percent change in MAP in eight consecutive hemodialysis patients without intradialytic hypotension. Since interleukin-6 (IL-6) is a major regulator of CRP, the relationship between these two proteins was examined. Plasma IL-6 levels were found to correlate both with CRP (r = 0.67, p < 0.05) and with mean maximum percent change in MAP (r = 0.70, p < 0.05) in hemodialysis patients with a prior history of hypotension. IL-6 levels did not correlate with CRP or blood pressure in the hemodynamically stable patients. The results suggest that immune activation working through IL-6, CRP and other cytokines may play a role in the pathogenesis of hemodialysis hypotension in some patients.

Circadian blood pressure variation versus renal function

Several published reports describe an abnormal circadian blood pressure profile in chronic renal failure subjects. Factors other than renal failure, including age, diagnosis of diabetes mellitus, autonomic dysfunction, and race, also may affect circadian blood pressure profiles. To further elucidate the relationship between renal function and circadian blood pressure variation, we compared day/night circadian blood pressure changes in three groups of male veteran hypertensive patients: group A, creatinine clearance (CC) > 80 mL/min, n = 20; group B, CC 20 to 80 mL/min, n = 19; and group C, CC < 20 mL/min, n = 14. We use postural changes in catecholamines, renin, and aldosterone as a measure of autonomic function. No significant difference in day/night percent change in systolic, diastolic, mean arterial pressure (MAP), or heart rate was seen by renal function group. Regression analysis using age, diagnosis of diabetes mellitus, postural hormonal changes, and creatinine clearance found race to be the only significant predictor of the day/night percent change in MAP, ( P < 0.05). Compared with whites, black subjects had higher nocturnal heart rates ( P = 0.01); smaller day/night heart rate changes ( P = 0.03); significantly higher diastolic blood pressure ( P = 0.01); and a trend toward smaller day/night change in diastolic blood pressure ( P = 0.06). In conclusion, renal function level does not influence day/night blood pressure changes. The blunting or reversal of the normal circadian blood pressure pattern seen in some chronic renal failure hypertensive subjects may be attributable to the association between chronic renal failure and cofactors associated with abnormal circadian blood pressure, including black race and possibly severity of atherosclerosis.

Area postrema stimulation induces differential renal hemodynamics with two anesthetics.

The effect of area postrema stimulation (APS) on blood pressure, renal blood flow (RBF), and renal vascular resistance was compared in urethan-anesthetized and pentobarbital sodium-anesthetized Sprague-Dawley rats. Mean arterial pressure (MAP) increased in a frequency-dependent manner during APS in both urethan- and pentobarbital-anesthetized rats. Although no significant differences occurred in the maximum percent change in MAP between groups, marked differences occurred in RBF and calculated renal vascular resistance (RVR) changes. In urethan-anesthetized rats, RBF and MAP increased during APS, but RVR did not change. In contrast, APS significantly decreased RBF (-26.5 +/- 1.9%) while increasing RVR (+99.4 +/- 11.4%) in pentobarbital-anesthetized rats. The increase in RVR in the pentobarbital-anesthetized group during APS was eliminated by prior ganglionic blockade. It was concluded that the anesthetic agent employed can significantly alter the degree to which APS can activate renal vasomotion in the rat.

Interrelationship between plasma ionized calcium, plasma noradrenaline (NA) and pressor response to infused NA in patients with essential hypertension.

We evaluated the role of calcium metabolism on plasma noradrenaline concentration (pNA) and pressor response to infused noradrenaline (NA-R) in patients with mild-to-moderate essential hypertension (EHT). Mean arterial pressure (MAP), plasma ionized calcium (pCa2+), and NA-R were measured at the basal condition in 17 EHT and after the administration of calcium antagonist, nifedipine (60mg, t.i.d., for 4 weeks) in 9 EHT. Under basal condition, pCa2+ correlated positively with pNA and negatively with NA-R in EHT. Following nifedipine therapy, persistent reductions of MAP and NA-R, a transient increase in pNA and a sustained increase of urinary excretion of calcium were observed. On the other hand, no significant change in pCa2+ was found during the therapy. Percent change in MAP following 4 weeks of nifedipine administration correlated positively with pCa2+ and pNA before the therapy. In addition, change in NA-R by nifedipine therapy correlated positively with the basal values of pCa2+ and PNA and negatively with NA-R before the treatment. A significant negative correlation between NA-R and pNA was observed following nifedipine therapy as well as the basal state. However, the slope of the regression line between NA-R and pNA decreased significantly after the treatment as compared to the basal state. These results suggest that calcium metabolism relating sympathetic nerve activity and NA-R may contribute to the hypertensive mechanism in EHT. The hypotensive effects of nifedipine may be caused partly by the attenuation of sympathetic nerve activity and NA-R.