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Absorption of khellin and its estimation in blood and tissues
468
AMERICAN
HEART
JOURNAL
carbon dioxide produced a similar electrocardiographic picture after fifteen minutes, though the abnormality was slightly Iess marked (rate, 130 per minute). The patient could perform violently exerting tasks although he felt precordial pain after about five minutes. He was hospitalized and a duodenal ulcer was found. It healed uneventfully, but without alleviating his pain, which became more frequent and radiated to his neck and his left arm. It was felt that Buerger’s disease, juvenile arteriosclerosis, and myocarditis could be excluded with reasonable certainty. The patient was finally placed in a “sanitarium for neurotics.” The author comments on the infrequency of cardiac pain with postural hypotension, the significance of the positive anoxemia test, and the possibility of true myocardial damage having gradually been produced by recurrent postural hypoxic episodes. SAGEN. Chini,
V.: tim.
Med.
Clinical Aspects 35:443, 1947.
of the
Associated
Coronary
and
Cerebral
Set-
Syndrome.
The author studied the frequency and types of various cerebral disturbances which may follow myocardial infarction. This clinical picture has been called “cerebral type of myocardial infarction”; the author refers to it as “associated coronary and cerebral syndrome.” Myocardial infarction may be followed by restlessness, sciousness, coma, syncope, or epilepsy. The neurological ionally mask the main symptoms of the disease. The
author
reports
thirty
clinical
cases which
mental confusion, stuper, signs may be preponderant,
are divided
into
four
Group 1 includes patients with coronary and cerebral episodes which ent. The only connecting link is the existence of arteriosolerosis in both Group 2 includes patients with a neurological syndrome which masks the ance. Group 3 includes patients with angina pectoris and episodes due to of the cerebral vessels. Group 4 includes patients having a coronary followed after a short period by cerebral disturbances. . The cerebral phenomena hemorrhage, cerebral anoxemia the brain, or anatomical lesions operative in these episodes.
loss of conand occas-
groups: are definitely independthe heart and the brain. main coronary disturbfunctional disturbances occlusion which was
may be due to the following causes: embolism, thrombosis, caused by low blood pressure, shock, vascular reflexes, edema of More than one factor may be existing before the coronary attack.
Whenever a focal syndrome is present, either embolism as the cause. A sudden occurrence is in favor of embolism, common in thrombosis. The absence of thromboendocarditis thrombosis.
or thrombosis should be considered while a gradual occurrence is more at necropsy is in favor of cerebral LUISADA.
Barsoum, G. Estimation
S.,
Kenawy, in Blood
M. and
R. and El-Sheehy, A.: Absorption Tissues. J. Roy. Egyptian M. A. 30:312
of Khellin (June), 1947.
and
its
The authors undertook to investigate the rate of the absorption of khellin after its administration by different channels and to determine the concentration which khellin reaches in the blood and tissues in animals and man. Khellin is extracted from blood or tissue by alcohol and chloroform. The concentration of this drug isdetermined by the modified calorimetric method of I. R. Fahmy or it is dissolved in Tyrode’s solution and assayed by the biological method on the rectal cecum of the fowl (Anrep, Barsoum, Kenawy, and Misrahy 1946; Anrep, Kenawy, Barsoum, With concentrations of khellin in the blood varying between 1.0 and and Riad Fahmy, 1947) 200 micrograms per cubic centimeter, the plasma or serum contains about 10 to 20 per cent more khellin than the red blood cells. The authors found that khellin is readily given off by the corpuscles when they are exposed to serum or to Tyrode’s solution containing no khellin; t.herefore, khellin in the red blood corpuscles is not pharmacologically wasted. The The experiments with intravenous injections of khellin were made on anesthetized dogs. arterial blood pressure was recorded in the carotid artery and the injections were made slowly so as not to cause a fall of the blood pressure. After an intravenous injection the concentration of
SELECTED
ABSTRACTS
‘1 ho
Within a few minutes the khellin conkhellin in the blood reaches a very high level for a short time. centration diminishes, and in about 30 to 40 minutes it reaches a steady level which is maintainect for several hours. The rapid diminution of the khellin concentration in the circulating blood is (lute to its gradual and more or less uniform distribution among all the tissues of the body. After intramuscular injection, khellin is extremely rapidly absorbed into the general circlliation, and its concentration soon reaches a steady level, at which it is maintained for a long ti:lle. Maximal concentration reached after intravenous injection is much higher than afterintramusc~iiar injection of the same dose. Diminution of khellin in the circulating blood is not due to its c~limination by the kidneys in an unchanged form. Since khellin remains in the circulation for a consillcsrable time, administration of repeated doses should lead to an accumulation of the drug in the c,il-t IIlating blood. Animals receiving large doses of khellin show-ed, after repeated injections, ‘1 prq~~~~-tionately greater accumulation of khellin in their blood. Human subjects were divided into two groups, the first comprising those who receivctl their injection for the first time and the second, those who received daily injection for some days herore The concentration of khellin in the blood was apprecial)l! the collection of the blood samples. higher in those subjects who already had repeated injections of the drug. Khellin is absorbed from the stomach, from the small intestine, and from the large intest!ne. The absorption from the stomach was studied in anesthetized dogs after complete separation 01 I he pylorus from the duodenum. Absorption from the large intestine was studied only in man. ‘l‘hc absorption of khellin from the stomach and especially from the intestine is very rapid. .\bsol-ption from the alimentary tract is, therefore, suitable for the maintenance of a high conrent rat ion of khellin in the blood, while intramuscular absorption is more suitable when it is desired to T:I~s~. the concentration of khellin in a short time. The disappearance of khellin from the tissues is extremely slow and is not related to ;!ny particular organ. Its concentration in the blood does not diminish more rapidly than in +hc tissues. 13H,1
Kikhmeister, Forsch.
H., 1:278
and (Sept.
Taube, I.: 25), 1947.
Capillary
Permeability
in
Malnutrition.
!:T.
Krr zl.
Protein content, number of erythrocytes, and volume of packed red cells in venous blrlotl before and after application of an arm cuff at 40 mm. Hg for one-half hour were determineti in eleven edematous patients (nine with hunger edema, and two with nephritis) and in fourteen normal subjects (method of Landis and associates: J. Clin. Investigation 2:717, 1932). Frl)nl values so obtained, the loss of fluid and of protein in the venous blood after venostasis was calculated. Further, the colloid osmotic pressure of serum was determined in both sample* of blood (method of Keys and Taylor: J. Biol. Chem. 109:47, 1935). Patients with most marked edema showed the highest losses of fluid and protein (as much as 20.8 per cent and 1.53 per cent). There was, however, no relation between the total protein ctrntent in blood and the loss of both fluid and protein after stasis. The colloid osmotic pressure leas not always dependent on the total protein content and sank more strongly than did the protc.ln ; in 55 per cent of the patients it decreased after stasis, as a result of the escape of proteins (especially of albumin). However, the values of protein content and of the colloid osmotic pressure fount1 in the venous blood after stasis in edematous patients are either within or near normal limits. It must be assumed, therefore, that hunger edema is not only due to hypoproteinemia and to the consecutive fall in osmotic pressure, but also to changes in the capillary walls and in their function,
Hirsch, S. : The Autonomy (Nov. and Dec.), 1947.
of the
Coronary
Circulation.
.4rch.
d. mal.
du coc~,r
40:.1.1.3
The author redescribes the findings of his researches of the past seven years, during nhlch time he has studied histologically the structures contained in the epicardial fat. He found specialized arterioles, the walls of which contained large, clear epitheliod cells and a sphincter-like
AMERICAN
HEART
JOURNAL
carbon dioxide produced a similar electrocardiographic picture after fifteen minutes, though the abnormality was slightly Iess marked (rate, 130 per minute). The patient could perform violently exerting tasks although he felt precordial pain after about five minutes. He was hospitalized and a duodenal ulcer was found. It healed uneventfully, but without alleviating his pain, which became more frequent and radiated to his neck and his left arm. It was felt that Buerger’s disease, juvenile arteriosclerosis, and myocarditis could be excluded with reasonable certainty. The patient was finally placed in a “sanitarium for neurotics.” The author comments on the infrequency of cardiac pain with postural hypotension, the significance of the positive anoxemia test, and the possibility of true myocardial damage having gradually been produced by recurrent postural hypoxic episodes. SAGEN. Chini,
V.: tim.
Med.
Clinical Aspects 35:443, 1947.
of the
Associated
Coronary
and
Cerebral
Set-
Syndrome.
The author studied the frequency and types of various cerebral disturbances which may follow myocardial infarction. This clinical picture has been called “cerebral type of myocardial infarction”; the author refers to it as “associated coronary and cerebral syndrome.” Myocardial infarction may be followed by restlessness, sciousness, coma, syncope, or epilepsy. The neurological ionally mask the main symptoms of the disease. The
author
reports
thirty
clinical
cases which
mental confusion, stuper, signs may be preponderant,
are divided
into
four
Group 1 includes patients with coronary and cerebral episodes which ent. The only connecting link is the existence of arteriosolerosis in both Group 2 includes patients with a neurological syndrome which masks the ance. Group 3 includes patients with angina pectoris and episodes due to of the cerebral vessels. Group 4 includes patients having a coronary followed after a short period by cerebral disturbances. . The cerebral phenomena hemorrhage, cerebral anoxemia the brain, or anatomical lesions operative in these episodes.
loss of conand occas-
groups: are definitely independthe heart and the brain. main coronary disturbfunctional disturbances occlusion which was
may be due to the following causes: embolism, thrombosis, caused by low blood pressure, shock, vascular reflexes, edema of More than one factor may be existing before the coronary attack.
Whenever a focal syndrome is present, either embolism as the cause. A sudden occurrence is in favor of embolism, common in thrombosis. The absence of thromboendocarditis thrombosis.
or thrombosis should be considered while a gradual occurrence is more at necropsy is in favor of cerebral LUISADA.
Barsoum, G. Estimation
S.,
Kenawy, in Blood
M. and
R. and El-Sheehy, A.: Absorption Tissues. J. Roy. Egyptian M. A. 30:312
of Khellin (June), 1947.
and
its
The authors undertook to investigate the rate of the absorption of khellin after its administration by different channels and to determine the concentration which khellin reaches in the blood and tissues in animals and man. Khellin is extracted from blood or tissue by alcohol and chloroform. The concentration of this drug isdetermined by the modified calorimetric method of I. R. Fahmy or it is dissolved in Tyrode’s solution and assayed by the biological method on the rectal cecum of the fowl (Anrep, Barsoum, Kenawy, and Misrahy 1946; Anrep, Kenawy, Barsoum, With concentrations of khellin in the blood varying between 1.0 and and Riad Fahmy, 1947) 200 micrograms per cubic centimeter, the plasma or serum contains about 10 to 20 per cent more khellin than the red blood cells. The authors found that khellin is readily given off by the corpuscles when they are exposed to serum or to Tyrode’s solution containing no khellin; t.herefore, khellin in the red blood corpuscles is not pharmacologically wasted. The The experiments with intravenous injections of khellin were made on anesthetized dogs. arterial blood pressure was recorded in the carotid artery and the injections were made slowly so as not to cause a fall of the blood pressure. After an intravenous injection the concentration of
SELECTED
ABSTRACTS
‘1 ho
Within a few minutes the khellin conkhellin in the blood reaches a very high level for a short time. centration diminishes, and in about 30 to 40 minutes it reaches a steady level which is maintainect for several hours. The rapid diminution of the khellin concentration in the circulating blood is (lute to its gradual and more or less uniform distribution among all the tissues of the body. After intramuscular injection, khellin is extremely rapidly absorbed into the general circlliation, and its concentration soon reaches a steady level, at which it is maintained for a long ti:lle. Maximal concentration reached after intravenous injection is much higher than afterintramusc~iiar injection of the same dose. Diminution of khellin in the circulating blood is not due to its c~limination by the kidneys in an unchanged form. Since khellin remains in the circulation for a consillcsrable time, administration of repeated doses should lead to an accumulation of the drug in the c,il-t IIlating blood. Animals receiving large doses of khellin show-ed, after repeated injections, ‘1 prq~~~~-tionately greater accumulation of khellin in their blood. Human subjects were divided into two groups, the first comprising those who receivctl their injection for the first time and the second, those who received daily injection for some days herore The concentration of khellin in the blood was apprecial)l! the collection of the blood samples. higher in those subjects who already had repeated injections of the drug. Khellin is absorbed from the stomach, from the small intestine, and from the large intest!ne. The absorption from the stomach was studied in anesthetized dogs after complete separation 01 I he pylorus from the duodenum. Absorption from the large intestine was studied only in man. ‘l‘hc absorption of khellin from the stomach and especially from the intestine is very rapid. .\bsol-ption from the alimentary tract is, therefore, suitable for the maintenance of a high conrent rat ion of khellin in the blood, while intramuscular absorption is more suitable when it is desired to T:I~s~. the concentration of khellin in a short time. The disappearance of khellin from the tissues is extremely slow and is not related to ;!ny particular organ. Its concentration in the blood does not diminish more rapidly than in +hc tissues. 13H,1
Kikhmeister, Forsch.
H., 1:278
and (Sept.
Taube, I.: 25), 1947.
Capillary
Permeability
in
Malnutrition.
!:T.
Krr zl.
Protein content, number of erythrocytes, and volume of packed red cells in venous blrlotl before and after application of an arm cuff at 40 mm. Hg for one-half hour were determineti in eleven edematous patients (nine with hunger edema, and two with nephritis) and in fourteen normal subjects (method of Landis and associates: J. Clin. Investigation 2:717, 1932). Frl)nl values so obtained, the loss of fluid and of protein in the venous blood after venostasis was calculated. Further, the colloid osmotic pressure of serum was determined in both sample* of blood (method of Keys and Taylor: J. Biol. Chem. 109:47, 1935). Patients with most marked edema showed the highest losses of fluid and protein (as much as 20.8 per cent and 1.53 per cent). There was, however, no relation between the total protein ctrntent in blood and the loss of both fluid and protein after stasis. The colloid osmotic pressure leas not always dependent on the total protein content and sank more strongly than did the protc.ln ; in 55 per cent of the patients it decreased after stasis, as a result of the escape of proteins (especially of albumin). However, the values of protein content and of the colloid osmotic pressure fount1 in the venous blood after stasis in edematous patients are either within or near normal limits. It must be assumed, therefore, that hunger edema is not only due to hypoproteinemia and to the consecutive fall in osmotic pressure, but also to changes in the capillary walls and in their function,
Hirsch, S. : The Autonomy (Nov. and Dec.), 1947.
of the
Coronary
Circulation.
.4rch.
d. mal.
du coc~,r
40:.1.1.3
The author redescribes the findings of his researches of the past seven years, during nhlch time he has studied histologically the structures contained in the epicardial fat. He found specialized arterioles, the walls of which contained large, clear epitheliod cells and a sphincter-like