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.

Fluid resuscitation with O2 vs. non-O2 carriers after 2 h of hemorrhagic shock in conscious hamsters

1997 ◽  
Vol 272 (1) ◽  
pp. H525-H537 ◽  
Author(s):  
H. Kerger ◽  
A. G. Tsai ◽  
D. J. Saltzman ◽  
R. M. Winslow ◽  
M. Intaglietta
Keyword(s):  
Blood Pressure ◽  
Hemorrhagic Shock ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Whole Blood ◽  
Shed Blood ◽  
Arterial Blood ◽  
Dextran 70 ◽  
Autologous Whole Blood ◽  
Tissue Po2

Efficacy of a cell-free o-raffinose cross-linked and oligomerized hemoglobin (Hemo-link) solution in restoring macro- and microcirculatory conditions after 2 h of hemorrhagic shock (40 mmHg) was compared with conventional treatment with autologous whole blood, Ringer lactate (RL), and Dextran 70. Studies were conducted in the dorsal skinfold microcirculation of conscious hamsters. Initial infusion was equivalent to shed blood volume (SBV) for RL and 50% of SBV for remaining solutions. After 2 h all animals received blood at 50% of SBV. Vessel diameter, functional capillary density, microvascular red blood cell velocity, and flow were measured. Arteriolar, venular, and tissue PO2 were determined by phosphorescence decay. Systemic parameters included mean arterial blood pressure, heart rate, arterial blood gases, pH, and base excess. Autologous whole blood and Hemolink, but not Dextran 70 and RL, restored mean arterial blood pressure, systemic blood gas, and metabolic parameters. Tissue PO2 recovered to 40–50% with blood and Hemolink but remained significantly lower (10-15% of control) with Dextran 70 and RL. Initial volume replacement after shock with blood or Hemolink yields equivalent macro- and microhemodynamic improvements not attainable with non-O2-carrying plasma expanders.

Cardiovascular Effects of Micromeria graeca (L.) Benth. ex Rchb in Normotensive and Hypertensive Rats

2020 ◽  
Vol 20 (8) ◽  
pp. 1253-1261
Author(s):  
Mourad Akdad ◽  
Mohamed Eddouks
Keyword(s):  
Blood Pressure ◽  
Cardiovascular System ◽  
Arterial Blood Pressure ◽  
Antihypertensive Activity ◽  
Computer Assisted ◽  
Hypertensive Rats ◽  
Vasorelaxant Effect ◽  
Arterial Blood

Aims: The present study was performed in order to analyze the antihypertensive activity of Micromeria graeca (L.) Benth. ex Rchb. Background: Micromeria graeca (L.) Benth. ex Rchb is an aromatic and medicinal plant belonging to the Lamiaceae family. This herb is used to treat various pathologies such as cardiovascular disorders. Meanwhile, its pharmacological effects on the cardiovascular system have not been studied. Objective: The present study aimed to evaluate the effect of aqueous extract of aerial parts of Micromeria graeca (AEMG) on the cardiovascular system in normotensive and hypertensive rats. Methods: In this study, the cardiovascular effect of AEMG was evaluated using in vivo and in vitro investigations. In order to assess the acute effect of AEMG on the cardiovascular system, anesthetized L-NAME-hypertensive and normotensive rats received AEMG (100 mg/kg) orally and arterial blood pressure parameters were monitored during six hours. In the sub-chronic study, rats were orally treated for one week, followed by blood pressure assessment during one week of treatment. Blood pressure was measured using a tail-cuff and a computer-assisted monitoring device. In the second experiment, isolated rat aortic ring pre-contracted with Epinephrine (EP) or KCl was used to assess the vasorelaxant effect of AEMG. Results: Oral administration of AEMG (100 mg/kg) provoked a decrease of arterial blood pressure parameters in hypertensive rats. In addition, AEMG induced a vasorelaxant effect in thoracic aortic rings pre-contracted with EP (10 μM) or KCl (80 mM). This effect was attenuated in the presence of propranolol and methylene blue. While in the presence of glibenclamide, L-NAME, nifedipine or Indomethacin, the vasorelaxant effect was not affected. Conclusion: This study showed that Micromeria graeca possesses a potent antihypertensive effect and relaxes the vascular smooth muscle through β-adrenergic and cGMP pathways.

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.

scholarly journals Cerebral Blood Flow Changes during Cortical Spreading Depression are Not Altered by Inhibition of Nitric Oxide Synthesis

1994 ◽  
Vol 14 (6) ◽  
pp. 939-943 ◽  
Author(s):  
Zheng Gang Zhang ◽  
Michael Chopp ◽  
Kenneth I. Maynard ◽  
Michael A. Moskowitz
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Cortical Spreading Depression ◽  
Spreading Depression ◽  
Arterial Blood ◽  
Nos Inhibitors ◽  
Before And After ◽  
Male Wistar Rats

CBF increases concomitantly with cortical spreading depression (CSD). We tested the hypothesis that CBF changes during CSD are mediated by nitric oxide (NO). Male Wistar rats (n = 23) were subjected to KCl-induced CSD before and after administration of nitric oxide synthase (NOS) inhibitors N-nitro-l-arginine (L-NNA) or N-nitro-l-arginine methyl ester (L-NAME) and in nontreated animals. CBF, CSD, and mean arterial blood pressure were recorded. Brain NOS activity was measured in vitro in control, L-NNA, and L-NAME-treated rats by the conversion of [3H]arginine to [3H]citrulline. Our data show that the NOS inhibitors did not significantly change regional CBF (rCBF) during CSD, even though cortical NOS activity was profoundly depressed and systemic arterial blood pressure was significantly increased. Our data suggest that rCBF during CSD in rats is not regulated by NO.

PROSTACYCLIN (PGI2) FORMATION IN RELATION TO ANAPHYLATOXIN C5a GENERATION DURING RABBIT ENDOTOXIN SHOCK

1987 ◽  
Author(s):  
M Rampart ◽  
H Bult ◽  
A G Herman ◽  
P J Jose ◽  
T J Williams
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Endotoxin Shock ◽  
Rabbit Serum ◽  
Classical Pathway ◽  
E Coli ◽  
Arterial Blood ◽  
Anaphylatoxin C5a

Injection of endotoxin (LPS) in animals, a model for gram-negative septic shock, leads to intravascular activation of the complement system, and is one of the few conditions in which 6-oxo-PGF]CX and thromboxane (TX) B2 (non-enzymic metabolites of PGI2 and TXA2) can be detected in arterial blood. Previously we reported associations between complement activation, PGI2 biosynthesis and LPS-induced hypotension in rabbits. As C5a and C5adesArg trigger endothelial PGI2 formation in vitro, we have now measured the plasma levels of immunoreactive (ir) C5a in relation to generation of PGI2 and changes in arterial blood pressure in LPS shock. Pentobarbitone anaesthethized rabbits received LPS (E. coli 0111:B4, 0.5 mg/kg) or saline via the marginal ear vein. A catheter in the left carotid artery was used to collect blood and to monitor mean arterial blood pressure (MABP). Platelet and leukocyte numbers, haemolytic complement titre (CH50), and plasma ir6-oxo-PGFioc , irTXB2 and irC5a were measured 15 min before and at different times after saline or LPS injection. LPS caused a dose- and time-dependent formation of irC5a in rabbit serum in vitro, predominantly via the classical pathway. LPS also activated complement in vivo, as indicated by about 20 % reduction of CH50 titre (measured after 3h) and a marked increase of arterial irC5a (20-120 ng/ml) in the first 2 to 5 min. After 30 min, irC5a had returned to baseline levels (< 2-5 ng/ml) and remained so up to 3h after injection of LPS. This irC5a peak correlated with a shortlasting initiation of PGI2 release (from < 20 pg/ml up to 550 pg/ml) and a drop in MABP (from about 95 mmHg to 50 mmHg) 2-5 min after LPS. None of these changes occurred after saline injection.In conclusion, LPS activates complement in vivo with concomitant formation of C5a. This peptide may trigger -either directly or after phagocyte activation - endothelial PGI2 biosynthesis, leading to arterial hypotension. This is supported by the suppression of the initial rise of arterial ir6-oxo-PGF1α and hypotension in complement-depleted rabbits. Inhibition of C5a formation or activity may prove to be a meaningful approach to the treatment of septic circulatory shock.

Reticuloendothelial system blockade-induced humoral factor depletion and susceptibility to hemorrhagic shock

1978 ◽  
Vol 56 (6) ◽  
pp. 1055-1057 ◽  
Author(s):  
Daniel J. Loegering ◽  
Marlowe J. Schneidkraut
Keyword(s):  
Hemorrhagic Shock ◽  
Host Defense ◽  
Lipid Emulsion ◽  
Reticuloendothelial System ◽  
Humoral Factor ◽  
Phagocytic Index ◽  
Phagocytic Function ◽  
Opsonic Activity ◽  
Circulating Levels ◽  
Increased Susceptibility

This study was carried out to determine if reticuloendothelial system (RES) Mockade-induced depletion of circulating alpha-2-glycoprotein opsonic activity resulted in increased susceptibility to hemorrhagic shock. RES blockade induced by the injection of gelatinized lipid emulsion was associated with a 45.9% decrease in phagocytic index and a 85.7% decrease in plasma alpha-2-glycoprotein opsonic activity. Animals subjected to RES blockade 30 min prior to hemorrhagic shock showed a decrease in time to decompensation and a decrease in maximum shed volume. These results are consistent with the concept that circulating levels of this opsonic protein are important in modulating RES phagocytic function and in host defense to shock.

IN VIVO SELECTIVITY BETWEEN HYPOTENSIVE AND PLATELET ANTIAGGREGATING ACTIONS OF ILOPROST AND PGI2 IN BEAGLE DOGS

1987 ◽  
Author(s):  
F Hermán ◽  
P Hadházy ◽  
K Magyar
Keyword(s):  
Blood Pressure ◽  
Platelet Aggregation ◽  
Arterial Blood Pressure ◽  
Bolus Administration ◽  
Beagle Dogs ◽  
Duration Of Action ◽  
Arterial Blood ◽  
Level Of Significance

Iloprost (Schering A.G.) is a chemically stable derivative of prostacyclin. We compared the hypotensive and antiaggregatory effects of PGI2 and Iloprost. The concentration producing 50% inhibition (IC50) of ADP-induced platelet aggregation in vitro was 0.35±0.15 nmol/1 for PGI2 and 0.56±0.2 nmol/1 for Iloprost (n=5). The in vivo antiaggregatory activity was measured with a modified filtration pressure technique (F.Hermán et al.Thromb. Res.44 /1986/, 575) in anaesthetized beagle dogs; the change in arterial blood pressure was recorded simultaneously. Using this technique, the dose-response relationship and the duration of action of prostacyclin and Iloprost following bolus administration have been determined. PGI2 was equipotent with Iloprost in inhibiting platelet aggregation in vivo (ED25: 0.25±0.04 nmol/kg; 0.28±0.05 respectively). At the same time PGI2 was two times as potent as Iloprost in decreasing the mean arterial blood pressure (ED25: 0.41±0.12 nmol/kg; 0.87±0.14 nmol/kg respectively). The antiaggregatory and hypotensive effects of Iloprost last longer in each experiment than that of PGI2, but did not reach the level of significance probably due to the considerable interindividual differences. The in vivo selectivity ratios (hypotensive potency/antiaggregatory potency) of Iloprost and PGI2 were 0.32 and 0.6 respectively. These results show that in anesthetized beagles Iloprost is somewhat more selective than PGI2 in inhibiting platelet aggregation.

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.

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