File:American journal of physiology (1898) (14782775742).jpg

Identifier: americanjourna33ameruoft (find matches)
Title: American journal of physiology
Year: 1898 (1890s)
Authors: American Physiological Society (1887- ) American Physiological Society (1887- ). Abstracts of papers presented at the fall meeting American Physiological Society (1887- ). Proceedings
Subjects: Physiology Physiology
Publisher: (Bethesda, Md., etc.) American Physiological Society (etc.)
Contributing Library: Gerstein - University of Toronto
Digitizing Sponsor: University of Toronto

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h amylnitrite the normal blood pressure, which was high,dropped sharply and fell below the critical region. Gruber: this Journal, 1913,xxxii, p. 221. There resulted an increase in muscular contraction due to thebetterment in circulation caused by the dilation of the vessels before the criticalregion was reached. During the time that the pressure was below the criticalregion the muscle contraction fell. As the blood pressure again rose to normalthe muscle contraction increased similarly. 2 Cannon and Nice: Loc. cit., p. 55; Gruber: Loc. cit., p. 226. 350 Charles M. Gruber alin caused a betterment in the height of contraction, while amyl-nitrite caused no appreciable change. Still other results were obtained in which adrenalin caused nochange in mean blood pressure but an increase in pulse pressure,with a resultant increase in the contraction. I found, as did Cannonand Nice, that the first increase in the arterial pressure duringsplanchnic stimulation is caused by the contraction of the
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Figure 7. — Top record, contractions of tibialis anticus muscle 64 per minute against aspring having an initial tension of 120 gm. Bottom record, the time in half minutes.At the points indicated by arrows 0.5 cc. of adrenalin (1:1,000,000) was injectedinto the tube leading from the pressure bottle. The irrigation pressure was 95mm. of mercury. arteries in the splanchnic area.^ This brings about a bettermentin the height of muscular contraction, the period of which isvery short. It was found possible to prevent an increase of blood pressureduring splanchnic stimulation by pulling on a fine cord loopedabout the aorta whenever the blood pressure showed a tendency torise. Maintaining an even blood pressure did not, however, pre-vent a second prolonged rise, which followed immediately upon thefirst in every case. The second rise must be due to the secretionof adrenalin during splanchnic stimulation. Fig. 7 is offered as further evidence that adrenalin does not actby bettering the circula

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