Mechanism of histamine release in endotoxin shock

1961 ◽  
Vol 200 (5) ◽  
pp. 987-989 ◽  
Author(s):  
Lerner B. Hinshaw ◽  
Margaret M. Jordan ◽  
James A. Vick
Keyword(s):  
Histamine Release ◽  
Active Role ◽  
Endotoxin Shock ◽  
Hemodynamic Changes ◽  
Endotoxin Administration ◽  
E Coli ◽  
Anesthetized Dogs ◽  
Blood Histamine ◽  
Lethal Doses

Reports from this laboratory have dealt with hemodynamic changes after injection of endotoxin and the role of histamine in endotoxin shock. This study relates to the mechanism of histamine release. Anesthetized dogs were administered lethal doses of E. coli endotoxin. During the course of the subsequent hypotension, simultaneous increases of blood histamine, histamine-histidine ratio(H/Hd), and circulating hematocrit were observed. Results suggest that a conversion from histidine to histamine occurs at an accelerated rate following endotoxin administration. These findings give further evidence for the active role of histamine in endotoxin shock and support a hypothesis recently proposed by Schayer.

Increased myocardial contractility during endotoxin shock in dogs

1985 ◽  
Vol 249 (4) ◽  
pp. H715-H722 ◽  
Author(s):  
P. M. Kober ◽  
J. X. Thomas ◽  
R. M. Raymond
Keyword(s):  
Myocardial Contractility ◽  
Salmonella Enteritidis ◽  
Systolic Pressure ◽  
Systemic Arterial Pressure ◽  
Endotoxin Shock ◽  
Left Ventricular ◽  
Terminal Phase ◽  
Endotoxin Administration ◽  
Before And After ◽  
Anesthetized Dogs

The slope of the left ventricular (LV) end-systolic pressure-diameter relationship (Ees) was analyzed in open-chest, pentobarbital-anesthetized dogs before and after endotoxin administration. A lead II electrocardiogram, systemic arterial pressure, LV pressure, LV dP/dt, and LV minor axis diameter were measured. After control measurements were taken, dogs were given either 1 mg/kg Salmonella enteritidis endotoxin (n = 5) or an equivalent volume of saline (n = 4). Control dogs were followed for 240 min. Endotoxic dogs were monitored until death (246 +/- 44 min). There were no significant changes in Ees in control dogs (17 +/- 3 mmHg/mm), which were hemodynamically stable for 4 h. Ees was significantly increased in endotoxic dogs even into the late stages of shock (41 +/- 11 mmHg/mm, P less than 0.01). Only during the terminal phase did Ees fall significantly below control (11 +/- 2 mmHg/mm, P less than 0.05). End-diastolic diameter decreased following endotoxin administration (P less than 0.05) but returned toward control by the terminal stage. Peak + LV dP/dt was depressed following endotoxin injection. Myocardial contractility was not depressed except as a terminal event. Early depression of cardiovascular performance in endotoxic dogs was therefore due to decreased preload and not cardiac dysfunction.

scholarly journals Alterations of Plasmin Activity, Plasminogen Levels and Activity of Anti-Plasmins During Endotoxin Shock in Dogs

1977 ◽  
Author(s):  
A. O. Aasen ◽  
M. J. Gallimore ◽  
K. Ohlsson ◽  
E. Amundsen
Keyword(s):  
Intravenous Infusion ◽  
Lethal Dose ◽  
Endotoxin Shock ◽  
Time Dependent ◽  
Plasmin Activity ◽  
Endotoxin Infusion ◽  
E Coli ◽  
Research Division ◽  
Late Stages

Endotoxin shock was induced in dogs by intravenous infusion of a lethal dose of E. coli endotoxin over a period of 3 hours. Typical changes of cardiovascular parameters were found and evidence of an intravascular clotting process was observed. Spontaneous plasmin activity and “immediate” and “time dependent” antiplasmin activities were determined by means of assays utilizing the chromogenic tripeptide derivative S-2251(Kabi Peptide Research Division, Mölndal, Sweden). Levels of plasminogen, α2-macrolobulin (α2-M) , and ai-antitrypsin(α1-AT) were determined immunochemically. During shock, gradually decreasing values of “immediate” antiplasmin and α2M were observed. During the late stages of shock “immediate” antiplasmin was found to be reduced by up to 89 per cent and α2M up to 50 per cent of pre endotoxin infusion values. A less marked lowering of “time dependent” antiplasmin and α1-AT also occurred during shock. These changes of plasma antiplasmins were accompanied by decreasing values of plasminogen and evidence of plasmin activity. These findings indicate that plasminogen is converted to plasmin during endotoxin shock and emphasize the role of antiplasmins in the pathophysiology of endotoxin shock.

Changes in glycerol kinetics after E. coli endotoxin administration in dogs

1984 ◽  
Vol 246 (3) ◽  
pp. R325-R330
Author(s):  
O. P. McGuinness ◽  
J. J. Spitzer
Keyword(s):  
Steady State ◽  
Infusion Rate ◽  
Volume Of Distribution ◽  
Constant Infusion ◽  
Metabolic Clearance ◽  
Glycerol Concentration ◽  
Endotoxin Administration ◽  
E Coli ◽  
The Face ◽  
Anesthetized Dogs

The metabolic clearance rate (MCR) and maximal rate of glycerol removal (Rd max) were determined in anesthetized dogs at two time periods after the intravenous administration of either Escherichia coli endotoxin or saline. The nonisotopic method employed in these studies to determine the MCR of glycerol consisted of a constant infusion of glycerol at three different infusion rates. At each infusion rate a steady-state glycerol concentration was obtained. The reciprocal of the slope of the linear relationship between the glycerol infusion rate and the change in the steady-state arterial glycerol concentration was equal to the MCR of glycerol. Administration of endotoxin significantly decreased the MCR of glycerol, whereas the volume of distribution of glycerol was not altered significantly. The arterial glycerol turnover remained unaltered, whereas arterial glycerol concentration increased after endotoxin administration. The studies demonstrate that the elevated arterial glycerol concentration maintained the rate of glycerol turnover in the face of decreased efficiency of glycerol removal after endotoxin administration.

Effect of lethal doses of bacterial endotoxin (E. coli) on sympathetic neurohormones in the rabbit

1960 ◽  
Vol 198 (6) ◽  
pp. 1307-1311 ◽  
Author(s):  
Melvin H. Heiffer ◽  
Roy L. Mundy ◽  
Benjamin Mehlman
Keyword(s):  
Blood Pressure ◽  
Catecholamine Level ◽  
Endotoxin Administration ◽  
E Coli ◽  
Blood Pressure Fall ◽  
Late Stages ◽  
Sympathetic Discharge ◽  
Lethal Doses ◽  
Gland Content ◽  
Pressure Fall

Lethal doses of E. coli endotoxin, administered intravenously, produced an immediate, precipitous fall in blood pressure, which returned to near normal levels over the next hour. Approximately 1 hour after endotoxin administration the blood pressure began to fall gradually and continued to fall until the death of the animal. During the period of immediate blood pressure fall there was no significant increase in the circulating catecholamines and no decrease in the adrenal content of these hormones. This suggests that the sympathetic nervous system may be depressed during the initial phases of endotoxin poisoning so that the sympathetic discharge which is seen during hypotension, produced by other means, is inoperative. When the pressure returned to near normal levels, the circulating catecholamine concentrations were elevated and the adrenal gland content of these materials was decreased. When the pressure dropped to levels below 60 mm Hg, 4–6 hours after endotoxin administration, the circulating catecholamine level was still statistically elevated and the adrenal content of catecholamines was further depressed. These experiments demonstrate that the blood pressure levels, during endotoxin administration, do not parallel expected peripheral catecholamine concentrations. During the late stages of endotoxin poisoning there is evidence that the animal becomes refractive to increased endogenous epinephrine and norepinephrine.

Carotid sinus baroceptor modifications associated with endotoxin shock

1962 ◽  
Vol 202 (5) ◽  
pp. 971-977 ◽  
Author(s):  
John W. Trank ◽  
Maurice B. Visscher
Keyword(s):  
Carotid Sinus ◽  
Endotoxin Shock ◽  
Compensatory Response ◽  
Endotoxin Administration ◽  
E Coli ◽  
Reflex Modification ◽  
Before And After ◽  
Profound Hypotension ◽  
The Relationship ◽  
Nerve Discharge

Carotid sinus baroceptor responses were studied in dogs before and after administration of shock-producing quantities of E. coli endotoxin. Responses were characterized as the relationship between intrasinusal stimulus pressure and baroceptor nerve discharge frequency. Both constant and pulsating pressure stimuli were used. After endotoxin administration and the onset of endotoxin shock it was found that postendotoxin discharge frequencies exceeded control discharge frequencies for most pressures. These response shifts result in a resetting of the hemoregulatory barostatic mechanism to regulate blood pressure to a new and hypotensive level. It is concluded that in the later phases of endotoxin shock, the reflex modification may play the predominant role in maintaining hypotension and that barostatic resetting partially explains the poor compensatory response to the initial profound hypotension after endotoxin administration.

Protection by histamine and metabolites in anaphylaxis, scalds, and endotoxin shock

1962 ◽  
Vol 202 (1) ◽  
pp. 111-113 ◽  
Author(s):  
Charles L. Fox ◽  
Sigmund E. Lasker
Keyword(s):  
Horse Serum ◽  
Lethal Factor ◽  
Lethal Dose ◽  
Active Role ◽  
Endotoxin Shock ◽  
E Coli ◽  
Thermal Burns ◽  
Scald Injury ◽  
Toxic Factors

The release of toxic factors has been implicated in the mechanism of shock from various forms of trauma. If histamine (H) released after anaphylaxis, endotoxin shock, or thermal burns is a lethal factor in mice, priming with (H) before injury would presumably enhance mortality. Mice were pretreated with (H) or certain metabolites prior to inducing shock via horse serum anaphylaxis, scald injury, or lethal dose of E. coli endotoxin. Large doses of (H) did not enhance mortality; actually, mortality from these three forms of shock was lowered by pretreatment with (H) or imidazoleacetic acid, but not by other metabolites tested. The data, while unexplained, do not appear to support hypotheses assigning an active role to (H) release in these three forms of shock in mice.

Glucose utilization and role of blood in endotoxin shock.

1977 ◽  
Vol 233 (2) ◽  
pp. E71
Author(s):  
L B Hinshaw ◽  
L T Archer ◽  
B K Beller ◽  
G L White ◽  
T M Schroeder ◽  
...  
Keyword(s):  
Glucose Uptake ◽  
Glucose Utilization ◽  
Lactic Acid Production ◽  
White Blood Cells ◽  
Endotoxin Shock ◽  
E Coli ◽  
Predicted Values

The present study was conducted to explore influences modifying glucose uptake in canine blood administered LD100 E. coli endotoxin. Particular emphasis was given to assay the role of the white blood cell (WBC) in glucose utilization. Significant increases in glucose uptake and lactic acid production, attributed to increased activity of the WBC, were observed 1-3 h after endotoxin was added to blood in vitro. Although a net increase in glucose utilization was noted, endotoxin simultaneously exerted adverse effects by depressing glucose uptake below predicted values (Q10 = 2.12 with LD100 endotoxin vs. 2.78 in saline controls) and increasing WBC mortality rate. Blood from dogs pretreated with sublethal doses of endotoxin in vivo utilized glucose at an accelerated rate when subjected to endotoxin in vitro. Excess glucose was consumed because of elevated numbers of white blood cells although additional glucose requirements after endotoxin were independent of temperature between the ranges of 34-41 degrees C. All animals pretreated with daily sublethal injections of endotoxin for 3 days survived superlethal doses of endotoxin.

Role of spectrin in membrane fusion and in shape change of human erythrocyte ghost

1978 ◽  
Vol 36 (2) ◽  
pp. 328-329
Author(s):  
Hideo Hayashi ◽  
Yoshikazu Hirai ◽  
John T. Penniston
Keyword(s):  
Conformational Changes ◽  
Human Erythrocyte ◽  
Shape Change ◽  
Membrane Surface ◽  
Slight Modification ◽  
Active Role ◽  
Main Role ◽  
Bank Blood ◽  
Human Erythrocyte Ghost

Spectrin is a membrane associated protein most of which properties have been tentatively elucidated. A main role of the protein has been assumed to give a supporting structure to inside of the membrane. As reported previously, however, the isolated spectrin molecule underwent self assemble to form such as fibrous, meshwork, dispersed or aggregated arrangements depending upon the buffer suspended and was suggested to play an active role in the membrane conformational changes. In this study, the role of spectrin and actin was examined in terms of the molecular arrangements on the erythrocyte membrane surface with correlation to the functional states of the ghosts.Human erythrocyte ghosts were prepared from either freshly drawn or stocked bank blood by the method of Dodge et al with a slight modification as described before. Anti-spectrin antibody was raised against rabbit by injection of purified spectrin and partially purified.

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