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The indirect measurement of mean venous oxygen tension during anoxia
684
AMERICAN
HEART
JOURNAL
kidney should prevent a rise in blood pressure, or remedy it if permanently established, provdied there are no causes for hypertension remaining kidney or elsewhere in the body,
it
has become either in the AUTHOR.
Thomas, C. B.: Relationship
Chronic
Experimental of the
Acute
Hypertension.
Hypertension
Pressor Response Bull. Johns Hopkins
Prom Section of Moderator to the Hosp.
Nerves:
Development and 74: 335, 1944.
Course
of
The acute and chronic pressor responses are of similar magnitude and general character in a given animal. A depressor influence usually appears within a few minutes of the maximal acute pressor response following moderator nerve section, which brings the pressure down to normal for a day or two and which may be present in some degree for several weeks. Chronic hypertension usually appears within forty-eight hours after complete moderator nerve section, and disappears only if nerve regeneration occurs.
Morton, the
B. M., Thrombosis
Shearburn, of Veins
E. W., and Burger, Pollowing Injury.
R. E.: Surgery
Synthetic 14: 915,
Vitamin 1943.
K
and
A group of experiments performed to study the possible influence of vitamin K on thrombus formation in dogs has been described. The radial and saphenous veins of the legs of fift,y-two dogs were traumatized mechanically by sacrifying the The veins were removed at forty-eightand ninetyintima with a hooked needle. Twenty-seven of the animals received a surplus of six-hour intervals afterwards. synthetic vitamin K along with the regular diet for a week prior to the injury, and Prot,hrombin times, hematocrit the remaining twenty-five were utilized as controls. determinations, and clotting times were made in each animal at intervals, without any demonstrable effect of synthetic vitamin K administration. The incidence of thrombosis after injury to the intima of t.hc veins was not significantly increased coincident with the administration of synthetic vitamin K: The being 33 per cent in the control group and 38 per cent in the vit,amin K group. The prothrombin values, which are imsmall difference does not seem important. portant in the coagulation process, did not significantly change after the administration of synthetic vitamin K. There was no significant difference in the results obThose dogs with a tained by the Squibb and Abbott synthetic preparations. hematocrit reading below 40 per cent, however, revealed a slightly higher incidence of thrombosis in both the control and vitamin K fed group.
Clinically, Virginia at the except
the incidence of thrombophlebitis has been Hospital in the smaller group of women given time of delivery than in the larger group receiving in the normal diet.
less in the University vitamin K just before uo exogenous vitamin
of o1 pi
AUTHORS. Davis, B. D.: The Anoxia. J. Clin.
Indirect
Measurement
Investigation
23:
666,
of Mean 1944.
Venous
Oxygen
Tension
During
A method is presented for determining the mean venous oxygen tension (MVpO,) indirectly by means of equilibrating gas mixture of low p0, with pulmonary arterial blood. Reproducible results were produced under standard but nonbasal conditions, rangitig, in fifteen individuals, from 26 to 32 mm. Hg at atmospheric pressure. Observations at simulated altitudes of 8,000 to 20,000 feet indicated that the cardiac output rose progressively with altitude, reaching 189 per cent of normal at 20,000 feet,. This circulatory compensation decreased the tissue anoxia at the
vaihs altitudes t”nan the value constant.
of
by 40 per cent, the MVpQ, at ?O,GOO 13.5, mm. which would have obtained
feet being N.8 if the cardiac
mm. jarlie: output were A7TT,‘TBO3”.
Bollman, Y. E., and Tourniquet Shock.
Flock, E. V.: Am. J. Physiol.
Changes 142: 290,
tn Phosphate 1941.
of
?Yfuscle
During
The changes which occur in the phosphates of muscle; the blood suppiy 3f wL?!::h has been completely occluded, are those of autolyzing muscle. Adenosine triphos phste almost disappears after three hours and phosphocreatine is almost completely QYirolyzed in one hour. The inorganic phosphates of the muscle rapidly increase The total of the acid-soluble phosphates is to a maximum in about four hours. not changed. If the flow of blood is restored to the muscle within three hours there is resynthesis of adenoeine triphosphate and phosphocreatine with a COPresponding decrease of the inorganic phosphate. Fatal shock does not develop even though large amounts of muscle have been occluded. When the oeelusion is released after more than three hours there is no regeneration of adenosine triphoaphate or phosphocreatine but considerable inorganic phosphate is washed from the injured muscle into the blood, Fatal shock develops in rats so treated if the muscles of more than one leg and thigh have been occluded for three and a half hours or if the occlusion of only one thigh and leg persisted for six hours before release. This type of SllOCB is definitely not due to adenosine tripliosphate washed out of the muscle because adenosine triphosphate is destroyed during the otclusiou and its decomposition products appear to be relatively nontoxic. In rats surviving release after occlusion of one leg for four hours there is almost. complete necrosis of’ the injured muscle but sufficient cells remain alive to restore themselves. after four to six weeks there is restoration of function of the leg1 although the original size ~of the muscle bundles is not completely restored.
Sherman, G. P., and 439, 1944.
Ducey,
E. F.:
Cardiac
R&%mnration.
-iin.
d. Roentgenoi.
51:
1 direct comparison was made between the tran~erse cardiac diameter 3i 4wo hundred adult males, obtained within ninety days of death, and the weight of th& hearts at autopsy. In this study, the results by the Cngerleider method are much more closely ctirrelated with the actual cardiac weight than a.re those of the other two roentgen methods studied. There is constant correlation between the percentage deviation of the transverse diameter, as obtained by the Ungerleider method, and the percentage deviation in heart weight as calculated from Zeek’s table. This correlation expressed numerically has a value of 1 to 3.3. Marked deviation from normal body weight and pericardial effusion greater than ZOO c.c. impair the accuracy of the method to sech an extent as to preclude it.s use without qualification. .?mrmxe. Max, Area
MI., and Wilcox, B. of the Orthodiagram.
B.:
A
Am.
Simple Graphic SXetkod Par J. Roentcgnol. 51: 4&J-, 1944.
h simple graphic method for the determination of the area k described. It requires no equipment not readily available Its application to one hundred cases checked by the planimeter a suffieientl.~ high degree of accuracy for elinieal purposes.
Xessuring;
the
of the orthodiagrzLm to any physician. shows it to have Q3THORS,
AMERICAN
HEART
JOURNAL
kidney should prevent a rise in blood pressure, or remedy it if permanently established, provdied there are no causes for hypertension remaining kidney or elsewhere in the body,
it
has become either in the AUTHOR.
Thomas, C. B.: Relationship
Chronic
Experimental of the
Acute
Hypertension.
Hypertension
Pressor Response Bull. Johns Hopkins
Prom Section of Moderator to the Hosp.
Nerves:
Development and 74: 335, 1944.
Course
of
The acute and chronic pressor responses are of similar magnitude and general character in a given animal. A depressor influence usually appears within a few minutes of the maximal acute pressor response following moderator nerve section, which brings the pressure down to normal for a day or two and which may be present in some degree for several weeks. Chronic hypertension usually appears within forty-eight hours after complete moderator nerve section, and disappears only if nerve regeneration occurs.
Morton, the
B. M., Thrombosis
Shearburn, of Veins
E. W., and Burger, Pollowing Injury.
R. E.: Surgery
Synthetic 14: 915,
Vitamin 1943.
K
and
A group of experiments performed to study the possible influence of vitamin K on thrombus formation in dogs has been described. The radial and saphenous veins of the legs of fift,y-two dogs were traumatized mechanically by sacrifying the The veins were removed at forty-eightand ninetyintima with a hooked needle. Twenty-seven of the animals received a surplus of six-hour intervals afterwards. synthetic vitamin K along with the regular diet for a week prior to the injury, and Prot,hrombin times, hematocrit the remaining twenty-five were utilized as controls. determinations, and clotting times were made in each animal at intervals, without any demonstrable effect of synthetic vitamin K administration. The incidence of thrombosis after injury to the intima of t.hc veins was not significantly increased coincident with the administration of synthetic vitamin K: The being 33 per cent in the control group and 38 per cent in the vit,amin K group. The prothrombin values, which are imsmall difference does not seem important. portant in the coagulation process, did not significantly change after the administration of synthetic vitamin K. There was no significant difference in the results obThose dogs with a tained by the Squibb and Abbott synthetic preparations. hematocrit reading below 40 per cent, however, revealed a slightly higher incidence of thrombosis in both the control and vitamin K fed group.
Clinically, Virginia at the except
the incidence of thrombophlebitis has been Hospital in the smaller group of women given time of delivery than in the larger group receiving in the normal diet.
less in the University vitamin K just before uo exogenous vitamin
of o1 pi
AUTHORS. Davis, B. D.: The Anoxia. J. Clin.
Indirect
Measurement
Investigation
23:
666,
of Mean 1944.
Venous
Oxygen
Tension
During
A method is presented for determining the mean venous oxygen tension (MVpO,) indirectly by means of equilibrating gas mixture of low p0, with pulmonary arterial blood. Reproducible results were produced under standard but nonbasal conditions, rangitig, in fifteen individuals, from 26 to 32 mm. Hg at atmospheric pressure. Observations at simulated altitudes of 8,000 to 20,000 feet indicated that the cardiac output rose progressively with altitude, reaching 189 per cent of normal at 20,000 feet,. This circulatory compensation decreased the tissue anoxia at the
vaihs altitudes t”nan the value constant.
of
by 40 per cent, the MVpQ, at ?O,GOO 13.5, mm. which would have obtained
feet being N.8 if the cardiac
mm. jarlie: output were A7TT,‘TBO3”.
Bollman, Y. E., and Tourniquet Shock.
Flock, E. V.: Am. J. Physiol.
Changes 142: 290,
tn Phosphate 1941.
of
?Yfuscle
During
The changes which occur in the phosphates of muscle; the blood suppiy 3f wL?!::h has been completely occluded, are those of autolyzing muscle. Adenosine triphos phste almost disappears after three hours and phosphocreatine is almost completely QYirolyzed in one hour. The inorganic phosphates of the muscle rapidly increase The total of the acid-soluble phosphates is to a maximum in about four hours. not changed. If the flow of blood is restored to the muscle within three hours there is resynthesis of adenoeine triphosphate and phosphocreatine with a COPresponding decrease of the inorganic phosphate. Fatal shock does not develop even though large amounts of muscle have been occluded. When the oeelusion is released after more than three hours there is no regeneration of adenosine triphoaphate or phosphocreatine but considerable inorganic phosphate is washed from the injured muscle into the blood, Fatal shock develops in rats so treated if the muscles of more than one leg and thigh have been occluded for three and a half hours or if the occlusion of only one thigh and leg persisted for six hours before release. This type of SllOCB is definitely not due to adenosine tripliosphate washed out of the muscle because adenosine triphosphate is destroyed during the otclusiou and its decomposition products appear to be relatively nontoxic. In rats surviving release after occlusion of one leg for four hours there is almost. complete necrosis of’ the injured muscle but sufficient cells remain alive to restore themselves. after four to six weeks there is restoration of function of the leg1 although the original size ~of the muscle bundles is not completely restored.
Sherman, G. P., and 439, 1944.
Ducey,
E. F.:
Cardiac
R&%mnration.
-iin.
d. Roentgenoi.
51:
1 direct comparison was made between the tran~erse cardiac diameter 3i 4wo hundred adult males, obtained within ninety days of death, and the weight of th& hearts at autopsy. In this study, the results by the Cngerleider method are much more closely ctirrelated with the actual cardiac weight than a.re those of the other two roentgen methods studied. There is constant correlation between the percentage deviation of the transverse diameter, as obtained by the Ungerleider method, and the percentage deviation in heart weight as calculated from Zeek’s table. This correlation expressed numerically has a value of 1 to 3.3. Marked deviation from normal body weight and pericardial effusion greater than ZOO c.c. impair the accuracy of the method to sech an extent as to preclude it.s use without qualification. .?mrmxe. Max, Area
MI., and Wilcox, B. of the Orthodiagram.
B.:
A
Am.
Simple Graphic SXetkod Par J. Roentcgnol. 51: 4&J-, 1944.
h simple graphic method for the determination of the area k described. It requires no equipment not readily available Its application to one hundred cases checked by the planimeter a suffieientl.~ high degree of accuracy for elinieal purposes.
Xessuring;
the
of the orthodiagrzLm to any physician. shows it to have Q3THORS,