On summarizing the observations above described, we see that in cases of benign and malignant hypertensions and acute diffuse glomerulonephritis, the minute volume is considerably increased, as compared with the normal standards, and that it diminishes nearly proportionally to the decrease of blood pressure, whilst in cases of the end stage of chronic diffuseglomerulonephritis, i. e. secondary contracted kidney, it remains approximately normal or rather tends to diminish. According to Weizsacker, 9) Liljestrand and Stenström, 10) and Dautrebande, 11) anaemia can sometimes give rise to an increase of the minute volume of the heart. The reason why the secondary contracted kidney, which in the majority of cases is accompanied by anaemia, is not increased in the minute volume, is to be sought in the slightness of the anaemia and also in the enfeebled heart function due to emaciation through the prolonged course of the renal insufficiency. Thus it may follow that all the diseases which are accompanied by increased arterial blood pressure do not always produce an increase in the minute volume, as Liljestrand and Stenström11) have advanced, and also that the minute volume of hypertension seems to bear no direct relation to the insufficiency of the renal function. It is perceptible that the minute volume of malignant hypertension is usually quantitatively greater than that of benign hypertension, but since the blood pressure of malignant hypertension is generally higher than that of benign hypertension, the difference of the increased minute volume between both the hypertensions will probably depend upon the degree of the increased arterial blood pressure, and the cause of the hypertension in both diseases, having no qualitative difference, will presumably be the same, inasmuch as there are between them occasionally states of transition impossible to discriminate clinically. In the case of nephrosclerosis and acute diffuse glomerulonephritis the minute volume seems to be intimately associated with blood pressure since I have observed that in the fluctuating blood pressure the minute volume runs parallel to the variation of blood pressure, so that we may infer also from this that the hypertension in this disease has a different cause from other renal diseases with raised blood pressure. There are not a few authors who are ready to attribute a factor of non-nephritic hypertension to the increased output of the heart or an increased cardiac efficiency, thus, in patients of cardiac neurosis Hochhaus12) has postulated from the heart systole occurring swiftly and plentifully, that the hypertension in them is due to the increased heart function, and Gross13) has advanced that the hypertension in exophthalmic goiter is provoked by an increased heart function; in several cases of young men with high blood pressure of unknown origin, Külbs14) has preliminarily attributed its cause to an excessive heart action. One of the factors in which the increased minute volume results may be augmented gas metabolism of the tissue cells, the action of the circulatory system being increased secondarily in order to respond to an excessive demand for oxygen in the tissue. According to my determinations of gaseous exchange in different kinds of hypertensions, as will be reported later in another paper, of nephrosclerosis, malignant hypertension in which the renal function is profoundly disturbed, brings on an increased oxygen consumption, while benign hypertension gives a nearly normal rate of basal metabolism. Thus in malignant hypertension the increased minute volume is supposed to have responded to the change of gaseous metabolism, but in benign hypertension it is based on exaggerated cardiac function of another cause.
1. In the dogs, whose dorsal roots corresponding to the operation field were previously scctioned, the epinephrine liberation from the suprarenal body and the blood sugar content of the ear vein blood were simultaneously determined after an intravenous introduction of peptone in a dose of 0.1 to 0.3 grm. per kilo of body weight. Neither fastening nor anaesthesia was resorted to. The epinephrine liberation began to accelerate with a short latency, say half a minute or less, reached its acme in some minutes or a little later, and recovered in a half to two hours or later. The acceleration of such a magnitude as five to thirty times of the preformative rate of liberation was observed in the dogs poisoned moderately or intensively. When too large a quantity of peptone was introduced, collapse developed consequently very early and rapidly and death ensued within a short time, the acceleration was very slight. The duration of acceleration also corresponded quite closely with that of poisoning symptoms; when the animal was still depressant the output was invariably greater than the preformative rate, that is, the rate of liberation under the quite physiological state, while the rate regained the initial value, when the animal behaved wholly normally. In short, fluctuation of rate of epinephrine discharge from the suprarenal capsule ran strikingly parallel with the symptoms of shock by peptone. The blood sugar content fluctuated also after peptone. At first occurred, as a rule, hyperglycaemia of not very large magnitude. The acme was found one quarter to one hour after peptone, namely about at the midst of the depressant stage, and the level decreased then gradually, so that eventually hypoglycaemia of such a degree as 0.08-0.05% resulted. The lowest value was found usually two to three hours after injection, and in a further one to two hours the hypoglycaemia disappeared entirely. The moment at which the blood sugar level reached its smallest value was found therefore somewhat later than the recovery of the clinical symptoms as well as of the epinephrine discharge to their normal states. In regard to the blood sugar fluctuation after peptone, the de-afferented dogs by no means differed from quite normal, viz. non-de-afferented ones. 2. Contrary to the results summarized in the above paragraph, no definite acceleration in the epinephrine liberation on administration of peptone was established by the cava pocket experiments under anaesthesia.
1. Durch Injektion von Organemulsion des Meerschweinchens, Rindes, Pferdes und Hundes kann man in 1/3 Fällen Autohämolysin erzeugen. 2. Das Autohämolysin ist komplexer Natur. 3. Dieses Autohämolysin ist wenig widerstandfäfig. Es wird durch halbstündiges Erhitzen auf 50°C oder Lagern in Zimmertemperatur wirkungslos. 4. Das Autohämolysin bindet an die roten Blutkörperehen nur in der Temperatur unter 7°C. 5. Das Autohämolysin wird durch Kaolin nicht absorbiert. 6. Das experimentelle Autohämolysin ist im Blutplasma präexistiert und kaun durch Kälte in vivo auf eigene Erythrozyten hämolytisch einwirken. 7. Es gibt 2 Sorten von Erythrozyten; die eine ist mit Rezeptor für das Autohämolysin versehen, die audere nieht. 8. Das Autohämolysin ist mit Forssmannsehem Autikörper nicht identisch. 9. Das Auftreten von Autohämolysin ist von Wassermannscher Reaktion begleitet; Wassermannscher Antikörper und Autohämolysin sind aber niclit identisch. 10. Sobald die Eigenhemmung stärker wird, wird das Autohämolysin negativ. 11. Das experimentelle Autohämolysin steht mit Syphilis in keiner direkten Beziehung.