Systemic arterial blood pressure and pulse rate in chronically restrained rhesus monkeys

Rp, Forsyth; Baireuther, R

doi:10.1152/ajplegacy.1967.212.6.1461

Cited by 27 publications

(8 citation statements)

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“…Mean control values ±SD for a number of variables are included in Tables 2 and 3. These data agree with normal values found by others (10,11), except that our monkeys had a higher heart rate and lower hematocrit.…”

Section: Cardiovascular Alterations--the Monkeyssupporting

confidence: 93%

Contribution of Kinins to Endotoxin Shock in Unanesthetized Rhesus Monkeys

Nies

Forsyth

Williams

et al. 1968

Circulation Research

135

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The effects of endotoxin (Escherichia colt and Pseudomonas pseudomallei) were studied in 18 unanesthetized rhesus monkeys restrained in primate chairs. Indwelling arterial and venous catheters were used for hemodynamic measurements and blood sampling. Whole blood kinin, plasma kininogen, lysosomal enzymes, complete blood counts, and blood gas tensions were measured. Within an hour of beginning the infusion of the endotoxin, the mean arterial pressure and systemic peripheral resistance decreased significantly in the 18 experimental monkeys compared to 13 control monkeys. These early changes were associated with significant elevation in whole blood kinin concentration and a decrease in plasma kininogen. All of these early changes were most marked in the animals that died. Granulocytopenia occurred within 15 minutes, and the concentration of free lysosomal enzyme in the plasma rose 2 hours after endotoxin infusion. The pretenninal phase of shock was characterized by a low peripheral vascular resistance and decreasing cardiac output without elevation of kinin levels. These findings support the hypothesis that kinins play a pathogenetic role in the early phase of endotoxin-induced shock and that the severity of the early phase may influence the animal's survival. The relation of kinins to other vasoactive substances released after endotoxin-induced shock is unknown.

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Section: Cardiovascular Alterations--the Monkeyssupporting

confidence: 93%

Contribution of Kinins to Endotoxin Shock in Unanesthetized Rhesus Monkeys

Nies

Forsyth

Williams

et al. 1968

Circulation Research

135

View full text Add to dashboard Cite

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“…All experiments were performed a minimum of 7-10 days postoperatively to avoid the cardiovascular effects of recent surgical procedures and anesthesia. Monkeys have been shown to remain stable for several months under these conditions (14). Details of this preparation have been reported previously (15).…”

Section: Methodsmentioning

confidence: 90%

Cardiovascular and Metabolic Effects of Whole or Fractionated Gram-Negative Bacterial Endotoxin in the Unanesthetized Rhesus Monkey

Reichgott

Melmon

Forsyth

et al. 1973

Circulation Research

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Rhesus monkeys were infused with endotoxin lipopolysaccharide (LPS) (10 mg/kg [LPS 10 ] or 2.5 mg/kg {LPS 28 ]) or with fractions of LPS containing 6.3% lipid (PSJ or 0.5% lipid (PS 2 ) (2.5 mg/kg). Systemic and regional hemodynamics, leukocyte counts, blood gases, pH, and plasma bradykinin concentration were measured. Monkeys receiving LPS 10 , LPS 2 5 , or PS t became hypotensive (mean blood pressure -37 ± 10 mm Hg) and had decreased peripheral vascular resistance (-10% to -24% of the base line), compensated metabolic acidosis, and elevated plasma bradykinin concentrations (14 ± 6 ng/ml) 2 hours after infusion. Vasodilation occurred in coronary, hepatic, and splanchnic vasculature; vasoconstriction occurred in the spleen. Cardiac output was diverted from muscle to viscera. Monkeys receiving PS 2 were normotensive with elevated peripheral vascular resistance (+46%) and no measurable plasma bradykinin concentration. By 6 hours, marked elevation of peripheral vascular resistance developed in monkeys given LPS 10 ( + 113%) and LPS 2S (+57%). Monkeys receiving PS X returned to base-line values, but monkeys receiving PS 2 remained unchanged. Leukopenia (-50% to -65%) was persistent only in monkeys receiving LPS or PS V Toxicity of LPS apparently depends on the lipid portions of the molecule. Vasodilation and bradykinin generation are correlated with persistent granuloeytopenia. Late toxicity may be independent of early cardiovascular events. KEY WORDS lipopolysaccharidebradykinin microspheres cardiac output polysaccharides granuloeytopenia regional blood flow• Gram-negative bacterial endotoxin, a complex lipopolysaccharide, causes species-specific effects (1). Primates, both human and subhuman, develop vasodilation, granuloeytopenia, and elevated plasma concentrations of bradykinin as the initial response to endotoxemia (2-4). Although granuloeytopenia is common, vasodilation does not occur in other species exposed to endotoxin (1), and bradykinin does not participate in the endotoxinshock syndrome in these animals (5-6).Leukocyte kinin-generating capabilities differ between primates and other species (7-9), but plasma kinin-generating systems are similar (9-10). Leukocyte interactions with endotoxin depend on lipid portions of the bacterial preparation (11-12), although endotoxin-plasma interactions require only bacterial polysaccharide antigens (12).Therefore, the interaction of leukocytes with lipid portions of endotoxin may result in the generation of vasoactive substances which mediate the cardiovascular events of endotoxemia. Bradykinin may be an important mediator in the primate (3, 13). To test this hypothesis, lipid-containing and lipid-free preparations of bacterial endotoxin were infused into unanesthetized Rhesus monkeys. The results confirmed the importance of Iipids for both the generation of bradykinin and the development of hemodynamic effects. The results also supported the hypothesis that interaction of endotoxin with leukocytes is the primary pathogenetic mechanism. 346

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“…Baseline heart rate and blood pressure recorded for the remainder of the study (after the transiently observed decreases) were similar to those reported during controlled ventilation at 1 minimum alveolar concentration in halothane-and isoflurane-anesthetized monkeys 1,2 and lower than those reported for awake chronically instrumented monkeys. 13,14 Although significant changes were recorded, clinically relevant changes in ventilator-controlled breaths were minimal during the study. However, a progressive increase in spontaneous breathing was detected approximately 2 hours after FEN administration.…”

Section: Discussionmentioning

confidence: 99%