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Shock, its mechanism and pathology
633
SELECTED ABSTRACTS
(2) and the ratio of systole to the interval of the pulse as well as the frequency of the pulse increases. From these two conclusions he draws the inference that a high degree of arterial sympathetic tone is associated or bound up with a high degree of vagal or parasympathetic tone. STEELE.
Moon, Virgil
H. : Shock, Its Mechanism
and Pathology.
Arch.
Path.
24:
794, 1937.
Shock is a circulatory deficiency, not cardiac and not vasomotor in origin, characterized by decreased total blood volume, decreased volume flow and by hemoconeentration. An imposing array of evidence from diverse sources supports the interpretation that substances absorbed from injured tissue produce progressive circulatory tleficienry by their efiects on the minute vessels in systemic areas. Under the influence of these substances, and of other agents, the capillaries and venules become ntonic and dilated, and their walls become abnormally permeable to the fluids of the blood. This results in stasis and leakage of fluid from the vessels. It also increases the volume capacity of the vascular system, reduc.es the total volume and the volume flow of the blood, increases its concentration, and produces edema. The evidence does not support the idea that local loss of blood and/or fluid at the site of injury is an adequate explanation for shock. Rut such a loss of fluid is a factor. It contributes to thr circulatory drfic+ncy in proportion to the volume of blood and fluid lost.
W. : Effect of Insulin and Hypoglycemia Schizophrenic Patients Treated With Insulin).
Hadorn,
on the Heart Ztsehr.
klin.
(as Shown in Med.
130:
643,
1936. This study is based on 43 schizophrenics doses of insulin. During hypoglycemia, rise, arrhythmias, and electrocardiographic consisted of S-T depression, flattening or and of the QRS complex. These heart believes that there is no permanent heart
without heart disease, who received large there occurred tachycardia, blood pressure changes. The electrocardiographic changes inversion of T, and prolongation of QRST changes are reversible; hence the author damage from the insulin treatment. KATZ.
Enger, R., and Arnold, H.: The 1: 2-Nitrosonaphthol Patients and Persons With Normal Blood Pressure: f. klin.
Med.
130:
Reaction in Hypertensive I. Blood Studies. Ztschr.
725, 1936.
A negative nitrosonaphthol reaction was obtained in specially normals, in essential hypertension, in amyloid nephrosis with sufficiency, and in acute nephritis. A positive reaction was found tensive nephritis and in malignant nephrosclerosis.
treated blood in marked renal inin chronic hyperKATZ.
Rich, Arnold R., and Duff, G. Lyman: The Production sclerosis and Arteriolonecrosis by Means of Proteolytic Hopkins
Hosp.
61:
of Hyaline ArterioloEnzymes. Bull. Johns
63, 1937.
Arteriolar lesions having the rharacteristirs of hyaline arteriolosclerosis occur at the site of injection of tryptic enzymes of animal or plant origin into the subcutaneous tissues of normal dogs. Previous medial hypertrophy or intimal proliferation is essential for the production of these changes. Whether the enzymes act directly upon the vessel wall or whether the lesion results from the action of products of protein decomposition is at present undetermined.
HINES.
SELECTED ABSTRACTS
(2) and the ratio of systole to the interval of the pulse as well as the frequency of the pulse increases. From these two conclusions he draws the inference that a high degree of arterial sympathetic tone is associated or bound up with a high degree of vagal or parasympathetic tone. STEELE.
Moon, Virgil
H. : Shock, Its Mechanism
and Pathology.
Arch.
Path.
24:
794, 1937.
Shock is a circulatory deficiency, not cardiac and not vasomotor in origin, characterized by decreased total blood volume, decreased volume flow and by hemoconeentration. An imposing array of evidence from diverse sources supports the interpretation that substances absorbed from injured tissue produce progressive circulatory tleficienry by their efiects on the minute vessels in systemic areas. Under the influence of these substances, and of other agents, the capillaries and venules become ntonic and dilated, and their walls become abnormally permeable to the fluids of the blood. This results in stasis and leakage of fluid from the vessels. It also increases the volume capacity of the vascular system, reduc.es the total volume and the volume flow of the blood, increases its concentration, and produces edema. The evidence does not support the idea that local loss of blood and/or fluid at the site of injury is an adequate explanation for shock. Rut such a loss of fluid is a factor. It contributes to thr circulatory drfic+ncy in proportion to the volume of blood and fluid lost.
W. : Effect of Insulin and Hypoglycemia Schizophrenic Patients Treated With Insulin).
Hadorn,
on the Heart Ztsehr.
klin.
(as Shown in Med.
130:
643,
1936. This study is based on 43 schizophrenics doses of insulin. During hypoglycemia, rise, arrhythmias, and electrocardiographic consisted of S-T depression, flattening or and of the QRS complex. These heart believes that there is no permanent heart
without heart disease, who received large there occurred tachycardia, blood pressure changes. The electrocardiographic changes inversion of T, and prolongation of QRST changes are reversible; hence the author damage from the insulin treatment. KATZ.
Enger, R., and Arnold, H.: The 1: 2-Nitrosonaphthol Patients and Persons With Normal Blood Pressure: f. klin.
Med.
130:
Reaction in Hypertensive I. Blood Studies. Ztschr.
725, 1936.
A negative nitrosonaphthol reaction was obtained in specially normals, in essential hypertension, in amyloid nephrosis with sufficiency, and in acute nephritis. A positive reaction was found tensive nephritis and in malignant nephrosclerosis.
treated blood in marked renal inin chronic hyperKATZ.
Rich, Arnold R., and Duff, G. Lyman: The Production sclerosis and Arteriolonecrosis by Means of Proteolytic Hopkins
Hosp.
61:
of Hyaline ArterioloEnzymes. Bull. Johns
63, 1937.
Arteriolar lesions having the rharacteristirs of hyaline arteriolosclerosis occur at the site of injection of tryptic enzymes of animal or plant origin into the subcutaneous tissues of normal dogs. Previous medial hypertrophy or intimal proliferation is essential for the production of these changes. Whether the enzymes act directly upon the vessel wall or whether the lesion results from the action of products of protein decomposition is at present undetermined.
HINES.