Role of AVP in maintenance of circulatory homeostasis during hemorrhagic shock

1984 ◽  
Vol 246 (2) ◽  
pp. H174-H179 ◽  
Author(s):  
C. E. Hock ◽  
J. Y. Su ◽  
A. M. Lefer
Keyword(s):  
Hemorrhagic Shock ◽  
Cathepsin D ◽  
Mesenteric Artery ◽  
The Other ◽  
Arterial Blood ◽  
Neurohypophyseal Hormone ◽  
Specific Antagonist ◽  
Plasma Arginine ◽  
Artery Flow

Hemorrhagic hypotension produces significantly increased plasma arginine vasopression (AVP) concentrations. We have utilized a specific antagonist (AVP-A) of the pressor effects of endogenous AVP to investigate the role of this neurohypophyseal hormone on the pathogenesis of hemorrhagic shock. Infusion of the AVP-A (2 micrograms/kg bolus + 2 micrograms X kg-1 X h-1 infusion) into sham-shocked animals produced no significant changes in any of the observed experimental variables. Cats subjected to hemorrhagic shock given AVP-A had final superior mesenteric artery flow (SMAF) values significantly (P less than 0.05) higher than shock cats given vehicle (7.7 +/- 1.1 vs. 4.5 +/- 0.8 ml X kg-1 X min-1, respectively). Increases in postreinfusion plasma cathepsin D activities were significantly blunted in hemorrhaged animals treated with AVP-A (10.4 +/- 2.0 vs. 24.8 +/- 5.5 U/mg protein; P less than 0.05). Plasma proteolysis as well as the plasma accumulation of myocardial depressant factor (MDF) were also significantly modulated by AVP-A treatment in hemorrhaged animals. MDF activities were 75 +/- 6 and 53 +/- 4 U/ml (P less than 0.02) for shock cats given vehicle or AVP-A, respectively. However, these beneficial actions were not reflected in any significant improvement in postreinfusion mean arterial blood pressure (MABP). These findings suggest that endogenous AVP functions not only as a potent splanchnic vasoconstrictor but also as a key humoral factor in the maintenance of postreinfusion MABP, a profile that is different from the role of angiotensin II, the other major splanchnic vasoconstrictor, in shock.

Platelet-activating factor mediates gastric damage induced by hemorrhagic shock

1990 ◽  
Vol 259 (1) ◽  
pp. G140-G146 ◽  
Author(s):  
J. L. Wallace ◽  
C. M. Hogaboam ◽  
G. W. McKnight
Keyword(s):  
Hemorrhagic Shock ◽  
Marked Decrease ◽  
Ex Vivo ◽  
Platelet Activating Factor ◽  
Gastric Damage ◽  
Doppler Flowmetry ◽  
Shed Blood ◽  
Arterial Blood ◽  
Gastric Lumen

The role of platelet-activating factor (PAF) as a mediator of the gastric damage associated with hemorrhagic shock was investigated using a rat model. With use of an ex vivo gastric chamber preparation, the gastric mucosa was bathed with 0.1 M HCl for 90 min. At minute 10 the systemic arterial blood pressure (BP) was reduced to 25 mmHg by bleeding from the femoral artery. BP was maintained at this level for 15 min, then the shed blood was reinfused. In control rats subjected to this protocol, extensive gastric damage developed during and after the shock period and involved an average of 50 +/- 8% of the total area of glandular mucosa. A marked decrease in transmucosal potential difference (PD) was observed during shock, with little recovery thereafter. Also, significant appearance of protein and hemoglobin (Hb) in the gastric lumen was detected after induction of shock. Oral pretreatment of the rats with the PAF antagonist WEB 2086 (0.5-20 mg/kg) dose dependently reduced the extent of macroscopically visible gastric damage, the decrease in transmucosal PD, and the appearance in the lumen of protein and Hb. A similar protective effect was observed with another PAF antagonist, BN 52021 (10 mg/kg). With use of laser-Doppler flowmetry, changes in gastric blood flow were determined before, during, and after induction of shock.(ABSTRACT TRUNCATED AT 250 WORDS)

Modulatory role of a constitutively active population of α1D-adrenoceptors in conductance arteries

2002 ◽  
Vol 282 (2) ◽  
pp. H475-H481 ◽  
Author(s):  
Khalid Ziani ◽  
Regina Gisbert ◽  
Maria Antonia Noguera ◽  
Maria Dolores Ivorra ◽  
Pilar D'Ocon
Keyword(s):  
Mesenteric Artery ◽  
Functional Role ◽  
Mesenteric Arteries ◽  
The Other ◽  
Active Population ◽  
Abrupt Changes ◽  
Resting Tone ◽  
Constitutively Active

A constitutively active population of α1D-adrenoceptors in iliac and proximal, distal, and small mesenteric rat arteries was studied. The increase in resting tone (IRT) that evidences it was observed only in iliac and proximal mesenteric and was inhibited by prazosin (pIC50 = 9.57), 5-methylurapidil (pIC50 = 7.61), and BMY 7378 (pIC50 = 8.77). Chloroethylchlonidine (100 μmol/l) did not affect IRT, but when added before the other antagonists it blocked their effect. The potency shown by BMY 7378 confirms the α1D-subtype as responsible for IRT. BMY 7378 displayed greater inhibition of adrenergic responses in iliac (pIC50 = 7.57 ± 0.11) and proximal mesenteric arteries (pIC50 = 8.05 ± 0.2) than in distal (pIC50 = 6.94 ± 0.13) or small mesenteric arteries (pIC50 = 6.30 ± 0.14), which confirms the functional role of the α1D-adrenoceptor in iliac and proximal mesenteric arteries. This subtype prevents abrupt changes in iliac and proximal mesenteric artery caliber when the agonist disappears, and this modulatory role is evidenced by the slower decay in the response to norepinephrine after removal.

Release of prostaglandin F2alpha during splanchnic artery occlusion shock

1976 ◽  
Vol 230 (3) ◽  
pp. 684-690 ◽  
Author(s):  
JT Flynn ◽  
GA Bridenbaugh ◽  
AM Lefer
Keyword(s):  
Cathepsin D ◽  
Amino Nitrogen ◽  
Artery Occlusion ◽  
Prostaglandin F2alpha ◽  
Arterial Blood ◽  
Nitrogen Concentrations ◽  
Splanchnic Artery ◽  
Hepatic Portal ◽  
Cathepsin D Activity

Prostaglandin F2alpha concentrations were determined in hepatic portal venous plasma of dogs during splanchnic artery occlusion (SAO) shock and in nonshock control dogs. Dogs subjected to SAO shock exhibited a dramatic decrease in mean arterial blood pressure and significant increases in portal venous PGF2alpha and amino-nitrogen concentrations, as well as in cathepsin D and MDF activities. Dogs treated with indomethacin prior to SAO shock did not exhibit a significant increase in portal venous PGF2alpha. Indomethacin had no effect on the increase of plasma amino-nitrogen and only slightly reduced portal venous cathepsin D activity during SAO shock. Nevertheless, indomethacin significantly attenuated the severity of the postrelease hypotension observed in SAO shock and diminished the plasma accumulation of MDF. These studies indicate that prostaglandins are released from the splanchnic region during SAO shock and that this release can be prevented by pretreatment with indomethacin. The role of endogenously released prostaglandins in SAO shock is not clear, but the magnitude of the increase warrants further study.

Epinephrine-induced hepatic potassium movements before and after adrenergic blockade

1976 ◽  
Vol 54 (3) ◽  
pp. 347-356 ◽  
Author(s):  
Stephen D. Guthrie ◽  
Quillian R. Murphy
Keyword(s):  
Portal Vein ◽  
Superior Mesenteric Artery ◽  
Adrenergic Receptors ◽  
Mesenteric Artery ◽  
Adrenergic Blockade ◽  
Blood Flows ◽  
Arterial Blood ◽  
Before And After ◽  
Anesthetized Dogs ◽  
Artery Flow

The epinephrine-induced loss and subsequent uptake of K+ by the liver was studied by measuring hepatic arterio–venous K+ differences and splanchnic blood flows in anesthetized dogs with chronically implanted portal vein catheters and celiac and superior mesenteric artery flow probes. When epinephrine was administered intraportally, neither α- nor β-adrenergic blockade, singly or in combination, had significant effects upon the hyper-kalemic or the hypokalemic phases in either hepatic venous or systemic arterial blood. It was concluded that the movements of K+ into and out of the liver caused by epinephrine are not mediated by the classical adrenergic receptors as defined by inhibition by specific blocking agents.

scholarly journals Role of Doppler ultrasonography evaluation of superior mesenteric artery flow volume in the assessment of Crohn's disease activity

2013 ◽  
Vol 46 (5) ◽  
pp. 279-283 ◽  
Author(s):  
Fabiana Paiva Martins ◽  
Eduardo Garcia Vilela ◽  
Maria de Lourdes Abreu Ferrari ◽  
Henrique Osvaldo da Gama Torres ◽  
Juliana Brovini Leite ◽  
...  
Keyword(s):  
Crohn’S Disease ◽  
Crohn's Disease ◽  
Disease Activity ◽  
Superior Mesenteric Artery ◽  
Mesenteric Artery ◽  
Doppler Ultrasonography ◽  
Flow Volume ◽  
Crohn’S Disease Activity ◽  
Artery Flow

scholarly journals Comparison of Malated Ringer’s with Two Other Balanced Crystalloid Solutions in Resuscitation of Both Severe and Moderate Hemorrhagic Shock in Rats

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Judith Keitel ◽  
Bjoern Hussmann ◽  
Sven Lendemans ◽  
Herbert de Groot ◽  
Ricarda Rohrig
Keyword(s):  
Hemorrhagic Shock ◽  
Wistar Rats ◽  
The Other ◽  
Adverse Impact ◽  
Positive Effects ◽  
Arterial Blood ◽  
Preclinical Treatment ◽  
Male Wistar Rats ◽  
Crystalloid Solutions ◽  
Balanced Crystalloid

In preclinical treatment of polytraumatized patients crystalloids are preferentially used. To avoid metabolic acidosis, metabolizable anions like lactate or acetate are used to replace chloride in these solutions. We here studied the effects of malated Ringer’s in resuscitation of both shock severities in comparison to lactated and acetated Ringer’s. Male Wistar rats underwent severe (mean arterial blood pressure (MAP) of 25–30 mmHg) or moderate (MAP 40–45 mmHg) hemorrhagic shock. Adjacent to the shock period animals were resuscitated with acetated (AR), lactated (LR), or malated Ringer’s (MR) and observed for 150 min. MR improved survival compared with LR and AR in severe hemorrhagic shock whereas it was equally effective to LR and superior to AR in moderate hemorrhagic shock. In all other parameters tested, MR was also effective similar to the other solutions under these conditions. We conclude that MR is preferable to AR and LR in resuscitation of hemorrhagic shock independent of shock depth. The positive effects of MR may stem from the absence of any adverse impact on energy metabolism under both conditions.

Arterial Inflow Into the Mesenteric and Hepatic Vascular Circuits During Hemorrhagic Shock

1956 ◽  
Vol 185 (2) ◽  
pp. 365-371 ◽  
Author(s):  
Theodore E. Cull ◽  
Mario P. Scibetta ◽  
Ewald E. Selkurt
Keyword(s):  
Hemorrhagic Shock ◽  
Hepatic Artery ◽  
Vascular Resistance ◽  
Mesenteric Artery ◽  
Venous Pressure ◽  
Portal Pressure ◽  
Outflow Resistance ◽  
Arterial Inflow ◽  
Flow Changes ◽  
Artery Flow

Mesenteric artery and hepatic artery flows were studied in dogs during a standardized hemorrhagic shock procedure. Both flows decreased in response to hemorrhage, with development of greater vascular resistance in the hepatic artery circulation. Toward the end of the hypotensive period vascular resistance in the mesenteric artery often entered a declining phase, correlated with an increase in portal venous pressure, but hepatic artery resistance increased somewhat further. On transfusion, mesenteric artery flow increased rapidly, often exceeding the control values. Portal pressure doubled, and mesenteric resistance decreased to values less than control for about 30 minutes. This may represent a phase of pooling and trapping of blood in the capillaries and venules of the mesenteric circulation favored by reduced inflow resistance, and increased outflow resistance. This was followed by a phase of increased mesenteric resistance which often persisted until the demise of the animal, although it decreased in some animals during the terminal stage. Following transfusion, hepatic artery flow increased more gradually than mesenteric artery flow and reached a peak about 1 1/2 hours post-transfusion, at a time when flow in the mesenteric artery was markedly reduced and its resistance was maximal. The mechanism of this reciprocity of flow and resistance is discussed and its relevance to the interpretation of the hepatic artery flow changes in shock is considered.

Levels of plasma-bound iron in experimental shock in the rabbit and dog

1960 ◽  
Vol 198 (6) ◽  
pp. 1161-1165 ◽  
Author(s):  
Aaron Janoff ◽  
Benjamin W. Zweifach ◽  
Lawrence R. Shapiro
Keyword(s):  
Hemorrhagic Shock ◽  
Mesenteric Artery ◽  
Oxygen Supply ◽  
Tissue Oxygen ◽  
Plasma Iron ◽  
Hemorrhagic Hypotension ◽  
Experimental Shock ◽  
Tissue Oxygen Supply ◽  
Lethal Doses

In order to determine whether plasma iron becomes elevated in other forms of experimental shock as it does in hemorrhagic shock, plasma iron was measured in rabbits subjected to lethal doses of endotoxin or infused with lethal amounts of catecholamines, and in dogs in superior mesenteric artery (SMA) occlusion shock. Patterns obtained from these animals were compared with those obtained from rabbits and dogs shocked by hemorrhagic hypotension. In both species hemorrhagic hypotension caused marked elevations in plasma iron, while iron levels were depressed in rabbits treated with endotoxin or lethal infusions of catecholamines and in dogs in shock following SMA-occlusion. The implications of these observations are discussed with respect to differences in tissue oxygen supply in normovolemic and hypovolemic forms of shock and with respect to the presumed role of hyperferremia in the vasculotoxic sequelae of the shock syndrome.

Oxygen transport in hemorrhagic shock as a function of the hematocrit ratio

1959 ◽  
Vol 196 (5) ◽  
pp. 1033-1038 ◽  
Author(s):  
Jack W. Crowell ◽  
Robert G. Ford ◽  
Virginia M. Lewis
Keyword(s):  
Cardiac Output ◽  
Oxygen Consumption ◽  
Hemorrhagic Shock ◽  
Oxygen Transport ◽  
Peripheral Resistance ◽  
Oxygen Deficit ◽  
Oxygen Transport Capacity ◽  
Arterial Blood ◽  
Blood Ph

The oxygen consumption, arterial and venous oxygen concentration, and the arterial blood pH were measured, and the cardiac output, peripheral resistance and maximum oxygen transport capacity determined in 75 dogs with different hematocrit ratios in which the blood pressure had been maintained at 30 mm Hg for 15 minutes. The O2 consumption increased as the hematocrit ratio increased until the hematocrit ratio reached 42. However, an increase in the hematocrit ratio above 42 caused a decrease in O2 consumption. This optimal hematocrit ratio occurs because of the dual role of the hematocrit ratio in determining O2 content of blood and blood viscosity. A curve obtained by multiplying cardiac output times arterial O2 showed that when the hematocrit ratio is 42 the O2 transport is maximal. The oxygen consumed by the animal was determined by the oxygen available. Arterial blood pH was highest in those dogs with the greatest oxygen consumption, but the pH was below limits compatible with life in the anemic animals. Total peripheral resistance increased greatly as the hematocrit ratio increased. Analysis of the data showed that the rate of maximum resistance to hemorrhagic shock coincides with the hematocrit ratio range of maximum O2 transport. Also, the rate of development of an oxygen debt determines how long the animals can remain hypotensive without developing irreversible shock and indicates that, regardless of the hematocrit ratio, a fixed oxygen deficit must occur before irreversible shock develops.

Plasma Levels of Protein S, Protein C, and Factor X: Effects of Sex, Hormonal State and Age

1995 ◽  
Vol 74 (05) ◽  
pp. 1271-1275 ◽  
Author(s):  
C M A Henkens ◽  
V J J Bom ◽  
W van der Schaaf ◽  
P M Pelsma ◽  
C Th Smit Sibinga ◽  
...  
Keyword(s):  
Regression Analysis ◽  
Postmenopausal Women ◽  
Protein C ◽  
Blood Donors ◽  
Premenopausal Women ◽  
Protein S ◽  
The Other ◽  
Factor X ◽  
Normal Ranges

SummaryWe measured total and free protein S (PS), protein C (PC) and factor X (FX) in 393 healthy blood donors to assess differences in relation to sex, hormonal state and age. All measured proteins were lower in women as compared to men, as were levels in premenopausal women as compared to postmenopausal women. Multiple regression analysis showed that both age and subgroup (men, pre- and postmenopausal women) were of significance for the levels of total and free PS and PC, the subgroup effect being caused by the differences between the premenopausal women and the other groups. This indicates a role of sex-hormones, most likely estrogens, in the regulation of levels of pro- and anticoagulant factors under physiologic conditions. These differences should be taken into account in daily clinical practice and may necessitate different normal ranges for men, pre- and postmenopausal women.

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