| Abstrakt: |
It has been assumed by certain observers1that the sudden pronounced fall in arterial blood pressure, the characteristic feature of acute anaphylactic shock in dogs, is due to a reduction in the available systemic blood volume as a result of splanchnic engorgement. This engorgement they believe is a passie congestion due to hepatic obstruction. We have endeavored to test this theory by studying the effects on carotid blood pressure of a mechanical obstruction to hepatic outflow sufficient to produce a combined hepatic and intestinal passive congestion equal to the passive congestion observed during anaphylactic shock. We have taken the increase in portal blood pressure as the measure of this passive congestion.The normal portal blood pressure averages about 9 mm. Hg. in our series of dogs. This pressure is increased to about 18 mm. Hg. during anaphylactic shock, the maximum being reached by the end of one minute. The portal blood pressure then gradually falls, and is restored to normal in from 8 minutes to 15 minutes.To prepare animals for the mechanical test, the inferior vena cava was ligated immediately below the liver in a series of dogs. Examination of these dogs six weeks later, at the time of the tests showed an hypertrophied collateral circulation fully compensating for the vena caval ligation.To make the tests, an unclosed ligature was placed about the vena cava immediately below the diaphragm. By partially closing this ligature, any desired degree of hepatic-intestinal passive congestion could be produced without interfering with the return circulation from the hind quarters. It was found that carefully controlled increased resistance to hepatic outflow, sufficient to raise the portal blood pressure to 20 mm. Hg., which is greater than the maximum portal pressure during anaphylactic shock, was without marked effect on the carotid blood pressure. |
