Plasma Concentration of Epinephrine and Norepinephrine in Hemorrhagic and Anaphylactic Shock

1957 ◽  
Vol 190 (2) ◽  
pp. 310-316 ◽  
Author(s):  
William M. Manger ◽  
Jesse L. Bollman ◽  
Frank T. Maher ◽  
Joseph Berkson

A fluorometric method was used to quantitate plasma epinephrine and norepinephrine during hemorrhagic and anaphylactic shock in healthy adult dogs anesthetized with pentobarbital. Arterial plasma was analyzed before and after hemorrhage in four dogs. Loss of approximately 18% of blood volume through rapid arterial bleeding caused no remarkable change in pressor amines. Loss of approximately one-third of the total blood volume decreased the mean arterial pressure by a range of 56–81% and invariably caused increased concentration of plasma pressor amines. The average concentration of epinephrine increased from 1.0 to 7.8 µg/1. of plasma, and that of norepinephrine increased from 2.5 to 3.6 µg. Additional bleeding caused further increase of plasma pressor amines. Seven dogs were given egg white intravenously to sensitize them. Subsequently, whenever a severe reaction (hypotension, bradycardia and respiratory depression) resulted from intravenous administration of egg white, venous plasma pressor amines increased. The average concentration of epinephrine increased from 0.7 to 7.7 µg/1. of plasma; norepinephrine increased in three dogs but remained unchanged or decreased in the remaining animals. Without a preceding ‘shock’ reaction, change in concentration of epinephrine-like substance was unremarkable. Intravenous administration of 1 mg of histamine base produced hypotension and usually slight increase of plasma pressor amines.

1984 ◽  
Vol 247 (3) ◽  
pp. E398-E404
Author(s):  
D. A. Bereiter ◽  
A. M. Zaid ◽  
D. S. Gann

To assess the early endocrine and physiological responses to rapid blood loss, adult cats anesthetized with chloralose-urethan sustained transient hemorrhage (H) of different magnitudes for a 3-min duration. The magnitude of H was expressed as a percentage of initial total blood volume after plasma volume determination by dye dilution or on a per unit body weight basis. Considerable variation in total blood volume was observed at all body weights (range, 44.5–80.2 mg/kg). Adrenocorticotropin (ACTH) in peripheral venous plasma was not significantly altered by 10% H but increased modestly after 20% H by 5 min (148 +/- 67 pg/ml) and rose promptly after 30% H by 2 min (541 +/- 155 pg/ml) with a peak at 5 min (579 +/- 171 pg/ml). Total change in ACTH during the 15-min sampling period was proportional to the magnitude of H (r = 0.730, P less than 0.001). Mean arterial pressure (MAP) decreased significantly to all magnitudes of H by 1 min with a graded recovery during the 3-min hypovolemic period that was well correlated (r = 0.602, P less than 0.005) with the percentage of blood volume removed. Mean plasma glucose concentration was not significantly changed by 10 or 20% H but increased after 30% H by 5 min (46.2 +/- 10.2 mg/dl). Total glucose change from prestimulus levels during the 15-min sampling period was correlated with the magnitude of H (r = 0.731, P less than 0.001). Plasma norepinephrine increased equally after 20 or 30% H or 10 ml/kg H but was not significantly elevated after 10% H.(ABSTRACT TRUNCATED AT 250 WORDS)


1996 ◽  
Vol 12 (5) ◽  
pp. 214-216 ◽  
Author(s):  
Noorizan Abdul Aziz ◽  
Zaitun Kamaruddin ◽  
Yahaya Hassan ◽  
Kamarudin Jaalam

Objective: To report a case of anaphylactic shock induced by the rapid intravenous administration of vitamin K1 in a patient in the intensive care unit (ICU). Case Summary: A 9-year-old Malay girl was admitted to the ICU and was diagnosed with Guillain-Barré syndrome. She developed an allergy to atropine that was manifested by a symmetric generalized transient macular rash over the trunk; it subsided 10 minutes after the drug was stopped. About 7 hours later, vitamin K1 10 mg iv was administered over 3 minutes due to the slight prolongation of prothrombin time and activated partial thromboplastin time. Immediately after the drug was administered, the patient developed a generalized transient macular rash, cyanosis, and shock. Her blood pressure and heart rate could not be detected. She responded well, however, after resuscitation. Discussion: Anaphylactic shock in this patient was most probably caused by the intravenous administration of vitamin K1, because this event occurred immediately after its administration. There have also been a few reported cases of severe reaction and death associated with intravenous administration of vitamin K1. The likelihood that the incident was drug-related could be classified as “probable” based on Naranjo's causal relationship algorithm. Conclusions: Rapid intravenous administration of vitamin K1 may induce anaphylactic shock in a critically ill patient with hemodynamic instability. If vitamin K1 is required, oral administration is preferred because it is rarely associated with severe reactions. Intravenous administration of vitamin K1 should be considered only in an emergency situation and the rate of administration should not exceed 1 mg/min.


1986 ◽  
Vol 250 (1) ◽  
pp. E18-E23
Author(s):  
D. A. Bereiter ◽  
D. S. Gann

The effect of prior blood loss on the plasma catecholamine response to acute hemorrhage (H) was assessed in alpha-chloralose-urethane anesthetized cats. Animals sustained an initial H period of 0 (samples only), 10, or 20% H total blood volume. Ninety minutes after reinfusion of the shed blood, all animals sustained a rapid 20% H. The catecholamine and arterial pressure responses to this second 20% H were assessed every 2 min for 20-min duration. Plasma norepinephrine increased modestly in the 0/20% group (+0.63 +/- 0.13 ng/ml) and 10/20% group (+0.66 +/- 0.07 ng/ml), whereas the 20/20% group showed a much larger (P less than 0.01) mean increase of 3.58 +/- 1.16 ng/ml. Plasma epinephrine did not increase after 0/20% (+0.05 +/- 0.02 ng/ml), increased slightly after 10/20% H (+0.10 +/- 0.05 ng/ml), and demonstrated a large significant increase after 20/20% H (+0.48 +/- 0.18 ng/ml). The differential effect of 20% H on catecholamine release, depending on the magnitude of prior blood loss, was not the result of altered mean arterial or pulse pressure responses to H. Correlation analyses revealed that the mean increases in epinephrine and norepinephrine during the post-H sampling period were well correlated in each animal (r = 0.864, P less than 0.001). The data indicate that the priming effect of prior blood loss on H evoked catecholamine release: requires an initial blood loss of 20% of total blood volume; occurs rapidly, as it is seen by 90 min after the initial H period; and affects epinephrine and norepinephrine similarly. We conclude that the immediate past secretory history of the sympathoadrenal system affects its responsiveness to subsequent blood loss.


1961 ◽  
Vol 1 (04) ◽  
pp. 353-379
Author(s):  
Jacques Lammerant ◽  
Norman Veall ◽  
Michel De Visscher

Summary1. The technique for the measurement of cardiac output by external recording of the intracardiac flow of 131I labelled human serum albumin has been extended to provide a measure of the mean circulation time from right to left heart and hence a new approach to the estimation of the pulmonary blood volume.2. Values for the basal cardiac output in normal subjects and its variations with age are in good agreement with the previously published data of other workers.3. The pulmonary blood volume in normal man in the basal state was found to be 28.2 ± 0.6% of the total blood volume.4. There was no correlation between cardiac output and pulmonary blood volume in a series of normal subjects in the basal state.5. The increase in cardiac output during digestion was associated with a decrease in pulmonary blood volume equal to 6.3 ± 1.2% of the total blood volume, that is, about 280 ml.6. The increase in cardiac output during exercise was associated with a decrease in pulmonary blood volume equal to 4.5 ± 1.0% of the total blood volume, that is, about 200 ml.7. The increase in cardiac output attributed to alarm is not associated with a decrease in pulmonary blood volume, the latter may in fact be increased.8. The total blood volume is advocated as a standard of reference for studies of this type in normal subjects in preference to body weight or surface area.9. The significance of these results and the validity of the method are discussed.


1986 ◽  
Vol 56 (03) ◽  
pp. 311-317 ◽  
Author(s):  
P A Barrett ◽  
K D Butler ◽  
R A Shand ◽  
R B Wallis

SummaryIntravenous administration of arachidonic acid to guinea-pigs caused a dose-related, rapid accumulation of 51Cr-labelled platelets in the thorax. Inhibitors of cyclooxygenase inhibited the platelet accumulation, induced by arachidonic acid (30 mg/kg), at doses which did not alter the thoracic blood volume (as measured by 131I-labelled human albumin). Thromboxane synthetase inhibitors had different effects on platelet accumulation depending on the dose. CGS 12970 (3 mg/kg) and N(1-carboxyheptyl) imidazole (100 mg/kg) reduced platelet accumulation. High doses of CGS 12970 and CGS 13080 caused an apparent enhancement of platelet accumulation which was associated with pooling of blood in the thorax, as measured by either 131I-labelled human albumin or 51Cr-labelled erythrocytes. This increase in thoracic blood volume was abolished if the guinea-pigs were also pretreated with diclofenac (1 mg/kg) in addition to the thromboxane synthetase inhibitor. Increases in thoracic blood volume were also obtained following infusions of PGI2 but not PGD2 or PGE2.


1990 ◽  
Vol 69 (3) ◽  
pp. 907-913 ◽  
Author(s):  
N. B. Hampson ◽  
E. M. Camporesi ◽  
B. W. Stolp ◽  
R. E. Moon ◽  
J. E. Shook ◽  
...  

The effects of mild hypoxia on brain oxyhemoglobin, cytochrome a,a3 redox status, and cerebral blood volume were studied using near-infrared spectroscopy in eight healthy volunteers. Incremental hypoxia reaching 70% arterial O2 saturation was produced in normocapnia [end-tidal PCO2 (PETCO2) 36.9 +/- 2.6 to 34.9 +/- 3.4 Torr] or hypocapnia (PETCO2 32.8 +/- 0.6 to 23.7 +/- 0.6 Torr) by an 8-min rebreathing technique and regulation of inspired CO2. Normocapnic hypoxia was characterized by progressive reductions in arterial PO2 (PaO2, 89.1 +/- 3.5 to 34.1 +/- 0.1 Torr) with stable PETCO2, arterial PCO2 (PaCO2), and arterial pH and resulted in increases in heart rate (35%) systolic blood pressure (14%), and minute ventilation (5-fold). Hypocapnic hypoxia resulted in progressively decreasing PaO2 (100.2 +/- 3.6 to 28.9 +/- 0.1 Torr), with progressive reduction in PaCO2 (39.0 +/- 1.6 to 27.3 +/- 1.9 Torr), and an increase in arterial pH (7.41 +/- 0.02 to 7.53 +/- 0.03), heart rate (61%), and ventilation (3-fold). In the brain, hypoxia resulted in a steady decline of cerebral oxyhemoglobin content and a decrease in oxidized cytochrome a,a3. Significantly greater loss of oxidized cytochrome a,a3 occurred for a given decrease in oxyhemoglobin during hypocapnic hypoxia relative to normocapnic hypoxia. Total blood volume response during hypoxia also was significantly attenuated by hypocapnia, because the increase in volume was only half that of normocapnic subjects. We conclude that cytochrome a,a3 oxidation level in vivo decreases at mild levels of hypoxia. PaCO is an important determinant of brain oxygenation, because it modulates ventilatory, cardiovascular, and cerebral O2 delivery responses to hypoxia.


1996 ◽  
Vol 81 (2) ◽  
pp. 895-904 ◽  
Author(s):  
M. F. Humer ◽  
P. T. Phang ◽  
B. P. Friesen ◽  
M. F. Allard ◽  
C. M. Goddard ◽  
...  

We tested the hypothesis that endotoxin increases the heterogeneity of gut capillary transit times and impairs oxygen extraction. The gut critical oxygen extraction ratio was determined by measuring multiple oxygen delivery-consumption points during progressive phlebotomy in eight control and eight endotoxin-infused anesthetized pigs. In multiple 1- to 2-g samples of small bowel, we measured blood volume (radiolabeled red blood cells) and flow (radiolabeled 15-microns microspheres) before and after critical oxygen extraction. Red blood cell transit time (= volume/flow) multiplied by morphologically determined capillary/total blood volume gave capillary transit time. During hemorrhage, capillary/total blood volume did not change in the endotoxin group (0.5 +/- 4.5%) but increased in the control group (17.6 +/- 2.5%; P < 0.05) due to a decrease in total gut blood volume. Flow decreased significantly in the endotoxin group (36 +/- 10%; P < 0.05) but not in the control group (12 +/- 10%). Capillary transit-time heterogeneity increased in the endotoxin group (12.3 +/- 4.9%) compared with the control group (-5.8 +/- 7.4%; P < 0.05), predicting a critical oxygen extraction ratio 0.14 lower in the endotoxin group than in the control group (K. R. Walley. J. Appl. Physiol. 81: 885–894, 1996). This matches the measured difference (endotoxin group, 0.60 +/- 0.04; control group, 0.74 +/- 0.03; P < 0.05). Increased heterogeneity of capillary transit times may be an important cause of impaired oxygen extraction.


2014 ◽  
Vol 7 (3) ◽  
pp. 193-198 ◽  
Author(s):  
Solange Ribeiro Peixoto ◽  
José Jurberg

Rhodnius stali Lent, Jurberg & Galvão vetor da Doença de Chagas domiciliado na região do Alto Beni, Bolívia é uma espécie com a biologia pouco conhecida. Com o objetivo de ampliar o conhecimento acerca de sua biologia, observamos parâmetros de seu ciclo de vida, nos estádios de ninfa, comparando-os com Rhodnius pictipes Stål, espécie morfologicamente semelhante e filogeneticamente próxima. Os seguintes parâmetros foram observados: tempo de eclosão dos ovos, ciclo biológico de ovo-adulto (em machos e fêmeas separadamente), taxa de mortalidade, idade do primeiro repasto sanguíneo e volume de sangue ingerido pelas ninfas. De maneira geral observou-se que as R. stali tem um ciclo de vida mais longo do que R. pictipes e, em ambas espécies, o tempo entre a eclosão do ovo até a fase adulta é menor em fêmeas. Curiosamente para R. stali, que é sabidamente capaz de colonizar domicílios, foi observada uma taxa de mortalidade das ninfas mais alta que em R. pictipes, algo inesperado para a espécie que coloniza estruturas artificiais e foi observada em ambiente artificial. Para R. stali, o primeiro repasto sanguíneo ocorreu, em média, quatro dias mais tarde do que em R. pictipes, espécie que ingeriu um volume total de sangue maior, possivelmente pelo fato de seu corpo ser maior. Conhecendo-se com profundidade os aspectos biológicos dessas espécies será possível direcionar o controle vetorial com mais precisão, principalmente em regiões onde colonizam casas, como no Alto Beni, Bolívia. Biology of Rhodnius stali Lent, Jurberg & Galvão and Rhodnius pictipes Stål (Hemiptera, Reduviidae, Triatiminae) in Laboratory Conditions Abstract. Rhodnius stali Lent, Jurberg & Galvão is a Chagas Disease vector that colonize houses in the Alto Beni region, Bolivia and its biology is poorly known. Aiming to enhance the understanding about their biology, we observed a few parameters of its life cycle, at nymphal stages, comparing them with Rhodnius pictipes Stål a morphologically similar and phylogenetically close species. The following parameters were observed: time of hatching, development time from egg to adult (male and female separately), mortality rate, age at first blood meal and blood volume ingested by nymphs. In general, it was observed that the R. stali has longer cycle than R. pictipes, and in both species, the time between hatching the egg to adult in females is lower. Interestingly for R. stali, which is known to be capable of colonizing households, the mortality rate of nymphs was higher than observed in R. pictipes, something unexpected for species that colonize artificial structures and was observed in artificial environment. For R. stali, the first blood meal was, on average, four days later than for R. pictipes, species that ingested a greater total blood volume, possibly because of its bigger size. By knowing in depth the biological aspects of these species it will be possible to direct vector control more accurately, especially in regions where they colonize houses, as in the Alto Beni, Bolivia.


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