Involvement of circulating phospholipase A2 in the pathogenesis of the hemodynamic changes in endotoxin shock

1983 ◽  
Vol 61 (6) ◽  
pp. 561-566 ◽  
Author(s):  
Peter Vadas ◽  
John B. Hay
Keyword(s):  
Blood Pressure ◽  
Enzyme Activity ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Fold Increase ◽  
Hypotensive Effect ◽  
Systemic Circulation ◽  
Endotoxin Shock ◽  
Exogenous Enzyme ◽  
Arterial Blood

This study examined the role of plasma phospholipase A2 (PLA2) in the mediation of the hypotension associated with experimental endotoxin shock in rabbits. Endotoxin shock was induced in rabbits, and mean arterial blood pressure and plasma PLA2 levels were monitored. Serial plasma PLA2 determinations over 5 h showed an 11-fold increase in circulating enzyme activity, and the rise in circulating enzyme activity was directly related to the fall in mean arterial blood pressure. Pretreatment of rabbits with glucocorticoids abrogated the hypotensive effect of endotoxin, and also inhibited a rise in plasma PLA2 activity. To determine if the rise in PLA2 activity was simply a mechanistically unrelated epiphenomenon, the effect of infusion of exogenous PLA2 (purified from the blood of rabbits in endotoxin shock) was investigated. Infusion of the exogenous enzyme into normal rabbits caused a fall in mean arterial blood pressure, and the rate of fall of blood pressure paralleled that induced by endotoxin itself. Treatment of the PLA2-active fraction, prior to infusion with the PLA2 inhibitor, p-bromophenacyl bromide, protected against this hypotensive effect. These data are consistent with the postulate that the endotoxin-induced release of massive amounts of PLA2 into the systemic circulation in rabbits contributes significantly to the hypotension associated with septic shock.

Chronic regulation of arterial blood pressure by ANP: role of endogenous vasoactive endothelial factors

1998 ◽  
Vol 275 (5) ◽  
pp. H1826-H1833 ◽  
Author(s):  
L. G. Melo ◽  
A. T. Veress ◽  
U. Ackermann ◽  
H. Sonnenberg
Keyword(s):  
Blood Pressure ◽  
Enzyme Activity ◽  
Arterial Blood Pressure ◽  
Natriuretic Peptide ◽  
Peripheral Resistance ◽  
Cardiovascular Effects ◽  
Hypotensive Effect ◽  
Synthetic Activity ◽  
Arterial Blood

Atrial natriuretic peptide (ANP) exerts a chronic hypotensive effect due to a decrease in total peripheral resistance (TPR). This study examines if chronic ANP-dependent vasodilation is attributable to differences in the cardiovascular regulatory activity of vascular endothelium (VE), based on evidence that ANP affects synthesis/release and target cardiovascular effects of endothelin-1 (ET-1), C-type natriuretic peptide (CNP), and nitric oxide (NO). To determine if the synthetic activity of resistance vasculature VE is chronically altered by plasma ANP activity, we measured ET-1, CNP, and endothelial constitutive NO synthase (ecNOS) concentration and total NOS enzyme activity in homogenates of kidney, heart, lung, hindquarter skeletal muscle, and brain from hypotensive transgenic mice with elevated plasma ANP, hypertensive knockout mice (−/−) characterized by the absence of ANP, and the corresponding normotensive wild-type (NT, +/+) mice. Tissue distribution and abundance patterns of ET-1, CNP, ecNOS, and NOS enzyme activity were comparable between the different genotypes and did not differ significantly between mutant and control mice. Antagonism of ETA/B receptors in −/− and +/+ mice in vivo with SB-209670 reduced arterial blood pressure (ABP) significantly and comparably in both genotypes (−27 ± 4 and −25 ± 2% change for −/− and +/+ mice, respectively) independent of any significant changes in heart rate (HR) (−6 ± 8 and −4 ± 4% change for −/− and +/+ mice, respectively). Immunoneutralization of CNP-specific guanylate cyclase-linked receptors (GC-B) with monoclonal antibodies (3G12) increased ABP slightly, but not significantly, by similar relative amounts in both −/− (10 ± 6% change) and +/+ mice (8 ± 3% change), without changing HR significantly (4 ± 1% change for both +/+ and −/− mice). Inhibition of NOS activity (by N G-nitro-l-arginine methyl ester) significantly increased ABP, but the changes were comparable between −/− (53 ± 5% change) and +/+ mice (50 ± 6% change) and occurred in the absence of significant changes in HR (−1 ± 5 and 7 ± 5% change for −/− and +/+ mice, respectively). We conclude that the differences in ABP associated with chronic variations in endogenous ANP activity are not due to alterations in synthesis or responsiveness of the cardiovascular system to the effects of ET-1, CNP, or NO.

Peripheral Resistance Changes and Blood Pooling After Endotoxin in Eviscerated Dogs

1958 ◽  
Vol 195 (3) ◽  
pp. 631-634 ◽  
Author(s):  
Lerner B. Hinshaw ◽  
Robert P. Gilbert ◽  
Hiroshi Kuida ◽  
Maurice B. Visscher
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Endotoxin Shock ◽  
E Coli ◽  
Arterial Blood ◽  
Later Phase

Studies were performed on eviscerated dogs maintained with a constant cardiac inflow with and without injections of lethal amounts of E. coli endotoxin. Continuous recordings of mean arterial blood pressure and total venous return permitted determination of changes in total peripheral resistance and extent of vascular pooling. A significant fall in mean arterial blood pressure occurs within 30 minutes after endotoxin in the eviscerated dog with constant cardiac inflow. There is therefore a decrease in total peripheral resistance. There is also a small but significant increase in vascular pooling exceeding that seen without endotoxin but much reduced from that observed in noneviscerated animals given endotoxin. It is concluded that a decrease in vascular tone occurs after endotoxin and that it probably plays a significant role in the later phase of endotoxin shock in the dog.

Cardiovascular effects of atrial extracts in anesthetized rats

1984 ◽  
Vol 62 (7) ◽  
pp. 819-826 ◽  
Author(s):  
Uwe Ackermann ◽  
Terumi G. Irizawa ◽  
Susan Milojevic ◽  
Harald Sonnenberg
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Cardiovascular Effects ◽  
Hypotensive Effect ◽  
Vagal Afferents ◽  
Sprague Dawley ◽  
Direct Stimulation ◽  
Arterial Blood ◽  
Cardiopulmonary Receptors

Tissue extracts derived from atria or ventricles of Sprague–Dawley rats were injected into Inactin-anesthetized assay rats. Compared with ventricular extracts, atrial extracts produced a 20 mmHg (1 mmHg = 133.322 Pa) fall in mean arterial blood pressure. This fall resulted from failure to increase cardiac output in compensation for peripheral vasodilation. Two factors were responsible: depression of heart rate (by 25 beats/min) and failure to increase cardiac performance. The time patterns and magnitudes of changes in cardiovascular parameters after cardiac extracts were not changed by prior atropinization. However, assay rats that were vagotomized showed no cardiac slowing after atrial extract and showed a significantly smaller decrease in mean arterial blood pressure than did sham-vagotomized or intact rats. Another group of assay rats was vagotomized as well as carotid-sinus-denervated before extract injection. In these rats the degree of hypotension caused by atrial extract was significantly greater than that observed after vagotomy alone and was not significantly different from that observed in rats with intact innervation. The results suggest that the hypotension that is caused by atrial extract, but not by ventricular extracts, results in part from the reflex effects of direct stimulation of chemosensitive cardiopulmonary receptors with vagal afferents and partly from the reflex effects of baroreceptor unloading. Ventricular extract had no hypotensive effect in any group of assay rats.

scholarly journals Butyric acid, a gut bacteria metabolite, lowers arterial blood pressure via colon-vagus nerve signaling and GPR41/43 receptors

2019 ◽  
Vol 471 (11-12) ◽  
pp. 1441-1453 ◽  
Author(s):  
Maksymilian Onyszkiewicz ◽  
Marta Gawrys-Kopczynska ◽  
Piotr Konopelski ◽  
Marta Aleksandrowicz ◽  
Aneta Sawicka ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Vagus Nerve ◽  
Arterial Blood Pressure ◽  
Butyric Acid ◽  
Ex Vivo ◽  
Fold Increase ◽  
Hypotensive Effect ◽  
Gut Bacteria ◽  
Nitric Oxide Synthase Inhibitor ◽  
Arterial Blood

AbstractButyric acid (BA) is a short-chain fatty acid (SCFA) produced by gut bacteria in the colon. We hypothesized that colon-derived BA may affect hemodynamics. Arterial blood pressure (BP) and heart rate (HR) were recorded in anesthetized, male, 14-week-old Wistar rats. A vehicle, BA, or 3-hydroxybutyrate, an antagonist of SCFA receptors GPR41/43 (ANT) were administered intravenously (IV) or into the colon (IC). Reactivity of mesenteric (MA) and gracilis muscle (GMA) arteries was tested ex vivo. The concentration of BA in stools, urine, portal, and systemic blood was measured with liquid chromatography coupled with mass spectrometry. BA administered IV decreased BP with no significant effect on HR. The ANT reduced, whereas L-NAME, a nitric oxide synthase inhibitor, did not affect the hypotensive effect of BA. In comparison to BA administered intravenously, BA administered into the colon produced a significantly longer decrease in BP and a decrease in HR, which was associated with a 2–3-fold increase in BA colon content. Subphrenic vagotomy and IC pretreatment with the ANT significantly reduced the hypotensive effect. Ex vivo, BA dilated MA and GMA. In conclusion, an increase in the concentration of BA in the colon produces a significant hypotensive effect which depends on the afferent colonic vagus nerve signaling and GPR41/43 receptors. BA seems to be one of mediators between gut microbiota and the circulatory system.

Cerebral autoregulation in premature infants during the first 96 hours of life and relationship to adverse outcomes

2018 ◽  
Vol 104 (5) ◽  
pp. F473-F479 ◽  
Author(s):  
Suma B Hoffman ◽  
Yun-Ju Cheng ◽  
Laurence S Magder ◽  
Narendra Shet ◽  
Rose M Viscardi
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Premature Infants ◽  
Mean Arterial Blood Pressure ◽  
Cerebral Autoregulation ◽  
Blood Pressure Monitoring ◽  
Intraventricular Haemorrhage ◽  
Fold Increase ◽  
Adverse Outcomes ◽  
Arterial Blood

ObjectiveTo test the hypothesis that impaired cerebral autoregulation (ICA) increases the susceptibility of premature infants to adverse outcomes, we determined the relationship of ICA and cerebral reactivity (CR) measured in the first 96 hours of life to the outcome of grade 3 or 4 intraventricular haemorrhage (IVH) and/or death within 1 month.SettingSingle-centre level IV neonatal intensive care unit.PatientsNeonates 24–29 weeks’ gestation less than 12 hours old with invasive blood pressure monitoring.DesignCerebral saturations and mean arterial blood pressure were recorded every 30 s for 96 hours. For each 10 min epoch, the correlation coefficient (r) was calculated for mean arterial blood pressure versus cerebral saturations. The epoch was considered to have ICA if r>0.5 and CR if r<0.ResultsSixty-one subjects were included. During the first 96 hours, ICA occurred 17.6% and CR occurred 41% of recorded time. In those without adverse outcomes, ICA decreased and CR increased by postnatal day (p<0.05). Adjusted for birth weight and gestational age, those with IVH and those who died spent more time with ICA and less time with CR (p<0.05) over the entire recording period. Those with IVH had 1.5-fold increase in time with ICA on day 2 (p=0.021), and decrease in time with CR on day 3 (p=0.036). Compared with survivors, non-survivors spent more time with ICA on days 3 and 4 (p<0.005), and less with CR on day 3 (p=0.032).ConclusionICA and CR vary by postnatal day and these patterns are associated with adverse outcomes.

Liberal vs. conservative vasopressor use to maintain mean arterial blood pressure during resuscitation of septic shock: an observational study

2007 ◽  
Vol 34 (1) ◽  
pp. 157-162 ◽  
Author(s):  
Sanjay Subramanian ◽  
Murat Yilmaz ◽  
Ahmer Rehman ◽  
Rolf D. Hubmayr ◽  
Bekele Afessa ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Septic Shock ◽  
Observational Study ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Arterial Blood ◽  
Vasopressor Use

Cerebral hemorrhage and edema following brain biopsy in rats: significance of mean arterial blood pressure

2000 ◽  
Vol 92 (1) ◽  
pp. 100-107 ◽  
Author(s):  
Helene Benveniste ◽  
Katie R. Kim ◽  
Laurence W. Hedlund ◽  
John W. Kim ◽  
Allan H. Friedman
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Neurosurgical Procedures ◽  
Shr Rats ◽  
Mr Microscopy ◽  
Content Type ◽  
Wky Rats ◽  
Arterial Blood ◽  
Fine Print

Object. It is taken for granted that patients with hypertension are at greater risk for intracerebral hemorrhage during neurosurgical procedures than patients with normal blood pressure. The anesthesiologist, therefore, maintains mean arterial blood pressure (MABP) near the lower end of the autoregulation curve, which in patients with preexisting hypertension can be as high as 110 to 130 mm Hg. Whether patients with long-standing hypertension experience more hemorrhage than normotensive patients after brain surgery if their blood pressure is maintained at the presurgical hypertensive level is currently unknown. The authors tested this hypothesis experimentally in a rodent model.Methods. Hemorrhage and edema in the brain after needle biopsy was measured in vivo by using three-dimensional magnetic resonance (MR) microscopy in the following groups: WKY rats, acutely hypertensive WKY rats, spontaneously hypertensive rats (SHR strain), and SHR rats treated with either sodium nitroprusside or nicardipine. Group differences were compared using Tukey's studentized range test followed by individual pairwise comparisons of groups and adjusted for multiple comparisons.There were no differences in PaCO2, pH, and body temperature among the groups. The findings in this study indicated that only acutely hypertensive WKY rats had larger volumes of hemorrhage. Chronically hypertensive SHR rats with MABPs of 130 mm Hg did not have larger hemorrhages than normotensive rats. There were no differences in edema volumes among groups.Conclusions. The brains of SHR rats with elevated systemic MABPs are probably protected against excessive hemorrhage during surgery because of greater resistance in the larger cerebral arteries and, thus, reduced cerebral intravascular pressures.

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