Decrease in Blood Volume After Prolonged Hyperactivity of the Sympathetic Nervous System

Freeman, Norman E.

doi:10.1152/ajplegacy.1932.103.1.185

Cited by 84 publications

(16 citation statements)

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“…The blood pressure may be increased, but only at the expense of the blood flow. The observations that adrenalin can produce shock (21) and cause a reduction in blood volume (15) accord with the clinical opinion as to its therapeutic ineffectiveness. Where the lowered blood pressure is the result of a reduced volume of blood in the vascular bed, physiological treatment necessitates the administration of blood or some blood substitute.…”

Section: Resultssupporting

confidence: 65%

The Peripheral Blood Flow in Surgical Shock

Freeman

Shaw²,

Snyder³

1936

J. Clin. Invest.

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Patients in surgical shock present clinical evidence of a diminished peripheral circulation. The extremities are cold, the pulse is feeble, and the veins are empty of blood. An increase in the peripheral vascular resistance in experimental shock has been demonstrated by Erlanger, Gesell and Gasser (1). Quantitative measurements, however, on the reduction in circulation in human cases of shock have not been made. These studies were therefore undertaken to learn the extent of impairment in the distribution of blood to the peripheral tissues. In addition, the effect of traumatic stimuli on the volume flow of blood in normal individuals was studied under controlled conditions. METHODSThe subjects were patients and medical students at the Massachusetts General Hospital. The volume flow of blood through the hand at controlled temperatures was measured by the plethysmographic method previously described (2). In the observations on surgical shock the blood flow was determined with the hand at different temperatures. Then, at a constant temperature, the reactive hyperemia was measured 10 seconds after release of a tourniquet which had occluded the arterial inflow for 5 minutes. Samples of arterial and venous blood were taken when feasible for oxygen content, oxygen capacity and carbon dioxide content. The oxygen content, oxygen capacity and carbon dioxide content were determined in duplicate by the method of Van Slyke and Neill (3). Studies were carried out in the laboratory, in the operating amphitheatre, and on the wards. Notes were taken on the room temperature, clinical condition of the patient, and any incidental stimuli.The reactions of patients and students to the traumatic stimuli-cold, fear, pain and asphyxia-were studied.When the effect of cold was studied, the subject lay scantily clad on a bed for one-half hour with the temperature of the hand stabilized at 30°C. The window was then opened and the room temperature allowed to fall to between 15°and 180 C. After a short period of cold, the window was closed and the room temperature allowed to rise. Fear was produced by suggesting to the patient some painful or repulsive procedure which was to be carried out. The subject was unaware that his reactions were being noted.Pain was precipitated, with the consent of the subject, through faradic stimulation of the skin and other measures.Partial asphyxia was brought about by having the subject breathe gas with a reduced concentration of oxygen (between 7.1 and 15 volumes per cent) delivered from a Tissot spirometer. Rebreathing was avoided. After the experiment had been concluded, the oxygen content of the gas mixture was analyzed by the Haldane apparatus. In the experiments in which asphyxia was employed the temperature of the bath in which the hand was immersed was maintained between 320 and 340 C. The subject, after resting for half an hour, was connected to the spirometer tubing, but breathed room air for a period of 10 to 15 minutes while determinations of blood flow were being made. After a stable flow had been r...

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Section: Resultssupporting

confidence: 65%

The Peripheral Blood Flow in Surgical Shock

Freeman

Shaw²,

Snyder³

1936

J. Clin. Invest.

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“…The catecholamines have been implicated in the genesis of endotoxin shock for the following reasons: a) plasma concentrations and vascular sensitivity are altered during the early phase of endotoxemia (5-7, 11, 13); b) adrenergic blocking agents protect against certain effects of endotoxin (6,(35)(36); and c) both agents induce hepatic venoconstriction (1,37), splanchnic pooling (36,38), a diminished circulating blood volume (35,39), vasoconstriction-splanchnic (1,40), renal (41)(42)(43), and cutaneous (35,40), dilation of the circulation in the heart (44,45) and skeletal muscle (46), and an over-all reduction in total peripheral resistance (47,48). In our studies, however, systemic arterial pressure did not fall abruptly during catecholamine infusions, pretreatment with reserpine did not prevent usual responses to endotoxin, and pharmacological antagonists to catecholamines did not abolish all the hemodynamic responses to endotoxin (16).…”

Section: D) Sensitivity Experimentsmentioning

confidence: 99%

Vasoactive Mediators as the “Trigger Mechanism” of Endotoxin Shock*

Jacobson¹,

Mehlman²,

Kalas³

1964

J. Clin. Invest.

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The mechanisms by which endotoxin induces a profound shock state have not been clearly established. Several neurohumoral agents have been implicated as mediators of endotoxin shock. These include histamine (1-4), catecholamines (5-7), and serotonin (7-9).Inferences of the role played by any of these mediators have been derived from four types of evidence: a) the hemodynamic alterations observed in endotoxemia are simulated by vascular effects of the naturally occurring substance (4, 5), b) plasma concentrations of the neurohumoral agent undergo changes in endotoxin shock (7, 10-13), c) vascular reactivity to the agent is altered in endotoxemia (5,6,14), and d) pharmacological antagonists to the substance in question prevent certain responses to endotoxin (4,(15)(16)(17).That a primary role could be assigned to any single substance in endotoxin shock is doubtful, however, because of the complexity of endotoxemia and the frequently conflicting and occasionally inconclusive nature of the evidence (18). Our investigation was prompted by the uncertainties concerning the relative importance of several proposed intermediaries in the early phase of endotoxin shock. Experiments were designed to utilize some of the approaches mentioned above. MethodsStudies of endotoxin shock were performed in 71 dogs of both sexes weighing 10 to 20 kg each. All animals were anesthetized with pentobarbital sodium (30 mg per kg). These experiments may be divided into three types: a) those in which endotoxemia was induced in animals pretreated to deplete tissue supplies of histamine, catecholamines, or serotonin; b) studies in which the hemo-* Submitted for publication October 21, 1963; accepted January 23, 1964. Presented in part at the Midwestern Section Meeting of the American Federation for Clinical Research, Chicago, Ill., October 31, 1963. dynamic and chemical effects of infused histamine, catecholamines, acetylcholine, or serotonin were compared with the effects of endotoxin injection; and c) experiments in which vascular sensitivity to histamine, catecholamines, or serotonin was determined at various times before and after injecting endotoxin. The design of these experiments is outlined in Table I.Mean pressures in millimeters of Hc were monitored in arteries, veins, or perfusion circuits by pressure transducers and recorded on an oscillograph.1 Plasma concentrations of epinephrine and norepinephrine (micrograms per liter) were determined by the method of Weil-Malherbe and Bone (19) as modified in this laboratory (20). Platelet-free plasma concentrations of serotonin were determined by the method of Waalkes (21) using an interim wash with salt-saturated NaOH to remove residual traces of histidine. After the final acid extraction one sample was employed for the assay of serotonin; another sample was used for the fluorometric determination of histamine (22) Experiments and Results a) Control experimentsHeparin sodium (10 mg per kg) was administered to all dogs used for control (groups C and PV) and depletion (groups F and R) ex...

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“…Others have pointed out the vascular collapse which follows the hypersecretion of epinephrine of pheochromocytoma (10) and have shown that shock can be produced by epinephrine injection (11). One worker (12) believed that a reduction in plasma volume occurred as a result of epinephrine injection, but this finding was disputed by others (13). The amounts of epinephrine required to produce shock are far in excess of the physiologic range as measured (14), and the continuous injection in dogs, over a period of days to weeks, of the amount of epinephrine (3.0 jug.…”

Section: Resultsmentioning

confidence: 99%