scholarly journals Sympathetic innervation of the splanchnic region mediates the beneficial hemodynamic effects of 8-OH-DPAT in hemorrhagic shock

2012 ◽  
Vol 303 (5) ◽  
pp. R527-R538 ◽  
Author(s):  
Ruslan Tiniakov ◽  
Kalipada Pahan ◽  
Karie E. Scrogin
Keyword(s):  
Blood Pressure ◽  
Hemorrhagic Shock ◽  
Arterial Blood Pressure ◽  
Sympathetic Innervation ◽  
Hypovolemic Shock ◽  
Pressor Effect ◽  
Venous Tone ◽  
Blood Withdrawal ◽  
Arterial Blood ◽  
Splanchnic Nerves

Administration of the 5-HT1A receptor agonist, 8-OH-DPAT, improves cardiovascular hemodynamics and tissue oxygenation in conscious rats subjected to hypovolemic shock. This effect is mediated by sympathetic-dependent increases in venous tone. To determine the role of splanchnic nerves in this response, effects of 8-OH-DPAT (30 nmol/kg iv) were measured following fixed-arterial blood pressure hemorrhagic shock (i.e., maintenance of 50 mmHg arterial pressure for 25 min) in rats subjected to bilateral splanchnic nerve denervation (SD). Splanchnic denervation decreased baseline venous tone as measured by mean circulatory filling pressure (MCFP) and accelerated the onset of hypotension during blood loss. Splanchnic denervation did not affect the immediate pressor effect of 8-OH-DPAT but did reverse the drug's lasting pressor effect, as well as its ability to increase MCFP and improve metabolic acidosis. Like SD, adrenal demedullation (ADMX) lowered baseline MCFP and accelerated the hypotensive response to blood withdrawal but also reduced the volume of blood withdrawal required to maintain arterial blood pressure at 50 mmHg. 8-OH-DPAT raised MCFP early after administration in ADMX rats, but the response did not persist throughout the posthemorrhage period. In a fixed-volume hemorrhage model, 8-OH-DPAT continued to raise blood pressure in ADMX rats. However, it produced only a transient and variable rise in MCFP compared with sham-operated animals. The data indicate that 8-OH-DPAT increases venoconstriction and improves acid-base balance in hypovolemic rats through activation of splanchnic nerves. This effect is due, in part, to activation of the adrenal medulla.

Corticosteroids for reversal of hemorrhagic shock in rats

1965 ◽  
Vol 209 (4) ◽  
pp. 815-818 ◽  
Author(s):  
Max Harry Weil ◽  
Howard Whigham
Keyword(s):  
Blood Pressure ◽  
Hemorrhagic Shock ◽  
Arterial Blood Pressure ◽  
Adrenal Glands ◽  
Pharmacological Action ◽  
Therapeutic Benefit ◽  
Dosage Range ◽  
Arterial Blood ◽  
Adrenalectomized Animal ◽  
Adrenocortical Hormone

Corticosteroids administered in amounts more than 100 times those required to sustain a fully adrenalectomized animal were highly effective in increasing survival following hemorrhagic shock. In rats with intact adrenal glands, hemorrhagic shock was produced by maintaining arterial blood pressure at 35 mm Hg for 240 min. Glucocorticoids and aldosterone were administered only after blood was reinfused. The therapeutic benefit is due to a pharmacological action of the adrenocortical hormone. Aldosterone had a lesser and relatively narrow dosage range of effectiveness.

Adrenal catecholamines in E. coli endotoxin shock

1961 ◽  
Vol 16 (2) ◽  
pp. 348-350 ◽  
Author(s):  
Florian Nykiel ◽  
Vincent V. Glaviano
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Arterial Blood Pressure ◽  
Venous Blood ◽  
Endotoxin Shock ◽  
Mean Blood Pressure ◽  
E Coli ◽  
Arterial Blood ◽  
Splanchnic Nerves

In dogs with left adrenal cannulation, administration of 1 mg/kg of purified E. coli endotoxin resulted in a decrease in mean blood pressure and adrenal blood flow. These changes were accompanied by significant increases in levels of epinephrine in adrenal venous blood. Release of epinephrine by the adrenals in endotoxin shock was due to a neurogenic mechanism, since sectioning of the splanchnic nerves prevented secretion of epinephrine. The rise in epinephrine output from an intact adrenal was noted to occur only in the presence of a significant decrease in arterial blood pressure; therefore endotoxin causes adrenal stimulation from reflexes initiated by the hypothalamus or peripheral baroreceptors. Submitted on September 20, 1960

Humoral factor depletion and reticuloendothelial depression during hemorrhagic shock

1977 ◽  
Vol 232 (3) ◽  
pp. H283-H287
Author(s):  
D. J. Loegering
Keyword(s):  
Blood Pressure ◽  
Hemorrhagic Shock ◽  
Arterial Blood Pressure ◽  
Liver Slice ◽  
Phagocytic Index ◽  
Phagocytic Function ◽  
Opsonic Activity ◽  
Shed Blood ◽  
Arterial Blood

Circulating opsonic activity and reticuloendothelial system (RES) phagocytic function were determined in anesthetized rats subjected to hemorrhagic shock. Animals were hemorrhaged to and maintained at 40 mmHg arterial blood pressure until they spontaneously took back 5% or 40% of the maximum bled volume. The phagocytic index, as determined by colloid clearance kinetics, was decreased in both groups following reinfusion of the shed blood. The reduction in phagocytic index was associated with decreased liver, unchanged spleen, and increased lung test colloid localization. Plasma opsonic activity, as determined by liver slice bioassay, was decreased 50-60% at 5% and 40% uptake of the maximum shed volume, decreased further 15 min after reinfusion in both groups, and tended to recover 1 h after reinfusion in the 5% uptake group. In vitro hepatic phagocytic activity of liver slices from shocked animals in the presence of normal rat plasma was decreased only in the 40% uptake animals after reinfusion when the arterial blood pressure had decreased to 50 mmHg. These data indicate that the depression of RES phagocytic function during hemorrhagic shock is associated with and may be mediated, in part, by decreased circulating opsonic activity.

Cardiovascular actions of trout urotensin II in the conscious trout, Oncorhynchus mykiss

1996 ◽  
Vol 271 (5) ◽  
pp. R1335-R1343 ◽  
Author(s):  
J. C. Le Mevel ◽  
K. R. Olson ◽  
D. Conklin ◽  
D. Waugh ◽  
D. D. Smith ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Cardiovascular Effects ◽  
Pressor Effect ◽  
Urotensin Ii ◽  
Cardinal Vein ◽  
Vascular Rings ◽  
Arterial Blood ◽  
Dose Dependent

The central and peripheral cardiovascular effects of synthetic trout urotensin II (UII) were investigated in the conscious rainbow trout. Intracerebroventricular injection of 50 pmol UII produced a slight (3%) but significant (P < 0.05) increase in heart rate but had no effect on mean arterial blood pressure. Injection of 500 pmol UII icv produced a significant (P < 0.05) rise (8%) in blood pressure with no change in heart rate. In contrast to the weak pressor effect of centrally administered UII, intra-arterial injection of UII produced a dose-dependent increase in arterial blood pressure and decrease in heart rate with significant (P < 0.05) effects on both parameters observed at a dose of 25 pmol. Higher doses of the peptide produced a sustained decrease in cardiac output that accompanied the bradycardia and rise in arterial blood pressure. The UII-induced bradycardia, but not the increase in pressure, was abolished by pretreatment with phentolamine. Trout UII produced a sustained and dose-dependent contraction of isolated vascular rings prepared from trout efferent branchial [-log 50% of the concentration producing maximal contraction (pD2) = 8.30] and celiacomesenteric (pD2 = 8.22) arteries but was without effects on vascular rings from the anterior cardinal vein. The data indicate that the pressor effect of UII in trout is mediated predominantly, if not exclusively, by an increase in systemic vascular resistance. The UII-induced hypertensive response does not seem to involve release of catecholamines, but the bradycardia may arise from adrenergic-mediated activation of cardioinhibitory baroreflexes.

Cortical NOS inhibition raises the lower limit of cerebral blood flow-arterial pressure autoregulation

1999 ◽  
Vol 276 (4) ◽  
pp. H1253-H1262 ◽  
Author(s):  
Stephen C. Jones ◽  
Carol R. Radinsky ◽  
Anthony J. Furlan ◽  
Douglas Chyatte ◽  
Alejandro D. Perez-Trepichio
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Arterial Pressure ◽  
Arterial Blood Pressure ◽  
Lower Limit ◽  
Blood Withdrawal ◽  
Arterial Blood ◽  
Pressure Autoregulation

The maintenance of constant cerebral blood flow (CBF) as arterial blood pressure is reduced, commonly referred to as CBF-pressure autoregulation, is typically characterized by a plateau until the vasodilatory capacity is exhausted at the lower limit, after which flow falls linearly with pressure. We investigated the effect of cortical, as opposed to systemic, nitric oxide synthase (NOS) inhibition on the lower limit of CBF-pressure autoregulation. Forty-four Sprague-Dawley rats were anesthetized with halothane and N2O in O2. With a closed cranial window placed the previous day in a ventilated and physiologically stable preparation, we determined the CBF using laser-Doppler flowmetry. Animals with low reactivity to inhaled CO2 and suffused ADP or ACh were excluded. Five arterial pressures from 100 to 40 mmHg were obtained with controlled hemorrhagic hypotension under cortical suffusion with artificial cerebrospinal fluid (aCSF) and then again after suffusion for 35 ( n = 5) and 105 min ( n = 10) with aCSF, 10−3 M N ω-nitro-l-arginine (l-NNA; n = 12), or 10−3 M N ω-nitro-d-arginine (d-NNA; n = 5). An additional group ( n = 7) was studied after a 105-min suffusion of l-NNA followed by a single blood withdrawal procedure. The lower limit of autoregulation was identified visually by four blinded reviewers as a change in the slope of the five-point plot of CBF vs. mean arterial blood pressure. The lower limit of 90 ± 4.3 mmHg after 105 min of 1 mMl-NNA suffusion was increased compared with the value in the time-control group of 75 ± 5.3 mmHg ( P < 0.01; ANOVA) and the initial value of 67 ± 3.7 mmHg ( P < 0.001). The lower limit of 84 ± 5.9 mmHg in seven animals with 105 min of suffusion of 1 mM l-NNA without previous blood withdrawal was significantly increased ( P < 0.01) in comparison with 70 ± 1.9 mmHg from those with just aCSF suffusion ( n = 37). No changes in lower limit for the other agents or conditions, including 105 or 35 min of aCSF or 35 min of l-NNA suffusion, were detected. The lack of effect on the lower limit withd-NNA suffusion suggests an enzymatic mechanism, and the lengthyl-NNA exposure of 105 min, but not 35 min, suggests inhibition of a diffusionally distant NOS source that mediates autoregulation. Thus cortical suffusion ofl-NNA raises the lower limit of autoregulation, strongly suggesting that nitric oxide is at least one of the vasodilators active during hypotension as arterial pressure is reduced from normal.

Effect of Varying the Hematocrit Ratio on the Susceptibility to Hemorrhagic Shock

1957 ◽  
Vol 192 (1) ◽  
pp. 171-174 ◽  
Author(s):  
Jack W. Crowell ◽  
Sara H. Bounds ◽  
W. W. Johnson
Keyword(s):  
Blood Pressure ◽  
Hemorrhagic Shock ◽  
Arterial Blood Pressure ◽  
Natural Variation ◽  
Time Lapse ◽  
Arterial Blood ◽  
Time Required

By the use of a) acetyl phenylhydrazine, b) hemorrhage, c) transfusion, and d) natural variation, 67 dogs with hematocrit ratios varying from 12 to 56 were obtained. These dogs were subjected to hemorrhagic shock by lowering their arterial blood pressure to 30 mm Hg, and the time lapse between the initial production of hypotension and the beginning deterioration of the animal determined. This time lapse is a measure of the resistance of the animal to the development of irreversible shock. A graph of initial hematocrit versus the time required for the development of irreversible shock shows that an increase in the hematocrit ratio from 12 to 35 increases the resistance of the animals by a factor of approximately 5; however, increasing the hematocrit ratio above 35 decreases the resistance of the animal to the development of irreversible shock.

Renovascular reactivity measured by near-infrared spectroscopy

2012 ◽  
Vol 113 (2) ◽  
pp. 307-314 ◽  
Author(s):  
Christopher J. Rhee ◽  
Kathleen K. Kibler ◽  
R. Blaine Easley ◽  
Dean B. Andropoulos ◽  
Marek Czosnyka ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Infrared Spectroscopy ◽  
Hemorrhagic Shock ◽  
Renal Blood Flow ◽  
Arterial Blood Pressure ◽  
Near Infrared Spectroscopy ◽  
Near Infrared ◽  
Laser Doppler ◽  
Arterial Blood

Hypotension and shock are risk factors for death, renal insufficiency, and stroke in preterm neonates. Goal-directed neonatal hemodynamic management lacks end-organ monitoring strategies to assess the adequacy of perfusion. Our aim is to develop a clinically viable, continuous metric of renovascular reactivity to gauge renal perfusion during shock. We present the renovascular reactivity index (RVx), which quantifies passivity of renal blood volume to spontaneous changes in arterial blood pressure. We tested the ability of the RVx to detect reductions in renal blood flow. Hemorrhagic shock was induced in 10 piglets. The RVx was monitored as a correlation between slow waves of arterial blood pressure and relative total hemoglobin (rTHb) obtained with reflectance near-infrared spectroscopy (NIRS) over the kidney. The RVx was compared with laser-Doppler measurements of red blood cell flux, and renal laser-Doppler measurements were compared with cerebral laser-Doppler measurements. Renal blood flow decreased to 75%, 50%, and 25% of baseline at perfusion pressures of 60, 45, and 40 mmHg, respectively, whereas in the brain these decrements occurred at pressures of 30, 25, and 15 mmHg, respectively. The RVx compared favorably to the renal laser-Doppler data. Areas under the receiver operator characteristic curves using renal blood flow thresholds of 50% and 25% of baseline were 0.85 (95% CI, 0.83–0.87) and 0.90 (95% CI, 0.88–0.92). Renovascular autoregulation can be monitored and is impaired in advance of cerebrovascular autoregulation during hemorrhagic shock.

scholarly journals Exceptional Cause of Hemorrhagic Shock in Intensive Care by Arterial Blood Pressure Catheter Disconnection

2021 ◽  
Vol 7 (4) ◽  
pp. 168-169
Author(s):  
  A. Elmoqaddem ◽  
N. Mrani Alaoui ◽  
T. Cherrad ◽  
M. Hmidi ◽  
F. Choumi ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Intensive Care ◽  
Hemorrhagic Shock ◽  
Arterial Blood Pressure ◽  
Arterial Blood ◽  
Pressure Catheter
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