Effects of Anti-inflammatory Drugs in Shock Caused by Injection of Living E. coli Cells

Culp, Jerilyn; Erdös, E. G.; Hinshaw, Lerner B.; Holmes, D. D.

doi:10.3181/00379727-137-35548

Cited by 15 publications

(8 citation statements)

References 5 publications

(5 reference statements)

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“…Cardiac output and systolic ejection time were still reduced and there was a substantial metabolic acidosis, with marked lactate production. It was of interest, however, that the decrease in arterial blood pH was significantly delayed in the indomethacintreated cats; this was also observed by Erdos et al (1967) and by Culp et al (1971) in dogs. In our experiments there was no clear relationship between arterial pH and lactate levels following endotoxin and this is apparent from Figure 2.…”

Section: The Effect Of Indomethacin On the Cardiovascular And Metabolsupporting

confidence: 61%

“…In the dog, the predominant acute effect of endotoxin consists of hepatic arterial and venous constriction, elevation of portal venous pressure and subsequent hepatic pooling. Since this effect is also prevented or reduced by aspirin (Solomon & Hinshaw, 1968) and by indomethacin (Erdos et al, 1967;Culp, Erdos, Hinshaw & Holmes, 1971) this may point to a common mediator (or mediators) in both species. Of the possible candidates, histamine would seem the most likely.…”

Section: The Effect Of Indomethacin On the Cardiovascular And Metabolmentioning

confidence: 99%

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THE EFFECT OF INDOMETHACIN ON THE CARDIOVASCULAR AND METABOLIC RESPONSES TO E. coli ENDOTOXIN IN THE CAT

Parratt

Sturgess

1974

British J Pharmacology

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I The response of pentobarbitone-anaesthetized cats to the intravenous administration of E. coli endotoxin (2 mg/kg) consisted of acute pulmonary vasoconstriction (3-5 min after the injection) and a secondary shock phase characterized by delayed systemic hypotension, decreased central venous pressure and cardiac output, and metabolic acidosis with arterial lactate levels three to four times normal. Only one of 25 animals survived 6 hours. 2 Indomethacin (10 mg/kg), administered intravenously 30 min before the endotoxin, reduced both systemic arterial pressure and myocardial blood flow. It abolished the pulmonary vasoconstriction induced by endotoxin. 3 Indomethacin modified some of the characteristic features of the delayed, endotoxin shock phase. Systemic hypotension was not observed and the blood pressure in the indomethacintreated cats 1, 2 and 4 h after endotoxin was 30 mmHg higher than in those cats administered endotoxin alone. The decrease in arterial pH was also significantly delayed. Six out of 15 animals survived 6 hours. 4 It is suggested that indomethacin may abolish the initial pulmonary hypertension and oedema by antagonizing the release, or vasoconstrictor effect, of histamine and that part of its action during the shock phase is due to inhibition of prostaglandin release.

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Section: The Effect Of Indomethacin On the Cardiovascular And Metabolsupporting

confidence: 61%

Section: The Effect Of Indomethacin On the Cardiovascular And Metabolmentioning

confidence: 99%

THE EFFECT OF INDOMETHACIN ON THE CARDIOVASCULAR AND METABOLIC RESPONSES TO E. coli ENDOTOXIN IN THE CAT

Parratt

Sturgess

1974

British J Pharmacology

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“…They showed that the administration of anti-inflammatory drugs either before or after endotoxin resulted in improved circulatory function. Others (Hinshaw et al, 1967;Greenway & Murthy, 1971;Culp et al, 1971;Parratt & Sturgess, 1974;1975a,b,c; have demonstrated improved haemodynamic function as well as increased survival by pretreatment with antiinflammatory drugs. In contrast, Hinshaw et al (1967) and Parratt & Sturgess (1975d) were unable to show increased survival when analgesic-antipyretic drugs were administered only after endotoxin.…”

Section: Discussionmentioning

confidence: 99%

“…Non-steroidal anti-inflammatory drugs decrease the haemodynamic responses in endotoxin shock and enhance survival (Northover & Subramanian, 1962;Hinshaw, Soloman, Erdos, Reins & Gunter, 1967;Culp, Erdos, Hinshaw & Holmes, 1971;Greenway & Murthy, 1971;Hall, Hodge, Irvine, Katic & Middleton, 1972;Parratt & Sturgess, 1974;1975a,b,c;Anderson, Jubiz, Tsagaris & Kuida, 1975a,b;Fletcher, Ramwell & Herman, 1976). …”

Section: Introductionmentioning

confidence: 99%

MODIFICATION, BY ASPIRIN AND INDOMETHACIN, OF THE HAEMODYNAMIC AND PROSTAGLANDIN RELEASING EFFECTS OF E. coli ENDOTOXIN IN THE DOG

Fletcher

Ramwell

1977

British J Pharmacology

100

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Dogs treated with aspirin (10 mg/kg) or indomethacin (1.5 mg/kg) 45 min before, and 3 h after, an LD50 dose (1 mg/kg) of E. coli endotoxin were alive 72 h later. Although all dogs in both treated groups survived, only those treated with indomethacin were protected against the fall in blood pressure 1–2 min following endotoxin. Endotoxin increased the level of prostaglandin F2α in both the mixed venous and arterial blood. No increase was observed in the aspirin and indomethacin‐treated groups. Aspirin and indomethacin treatment did not modify thrombocytopaenia or blood coagulation parameters following endotoxin.

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“…It has been also indicated, that endotoxin may cause damage to tissues and the release of subcellular constituents such as lysosomal enzymes (5,6). The aggregation of platelets is also frequently encountered in septic and other forms of shock ( 7 , 8, 9 ) .…”

mentioning

confidence: 99%

Effect of Prostaglandin E1 on the Pulmonary Vascular Response to Endotoxin

Sorrells

Erdös

1972

Experimental Biology and Medicine

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Effects of Anti-inflammatory Drugs in Shock Caused by Injection of Living E. coli Cells

Cited by 15 publications

References 5 publications

THE EFFECT OF INDOMETHACIN ON THE CARDIOVASCULAR AND METABOLIC RESPONSES TO E. coli ENDOTOXIN IN THE CAT

THE EFFECT OF INDOMETHACIN ON THE CARDIOVASCULAR AND METABOLIC RESPONSES TO E. coli ENDOTOXIN IN THE CAT

MODIFICATION, BY ASPIRIN AND INDOMETHACIN, OF THE HAEMODYNAMIC AND PROSTAGLANDIN RELEASING EFFECTS OF E. coli ENDOTOXIN IN THE DOG

Effect of Prostaglandin E1 on the Pulmonary Vascular Response to Endotoxin

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