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The magnitude and time of development of the collateral circulation in occluded femoral, carotid, and coronary arteries
6%
SELECTED ABSTRACTS
The criteria usually given for selection of patients were arterial hypertension. ignored. From a consideration of what is known about the pathologic physiology of arterial hypertension and the effects of denervation it would seem that not much could be expected from any such denervating operations. In general the results were poor. In only one patient was there a brilliant result, although in five others there was some degree of success in reducing blood pressure. Six more patients felt better, but their arterial pressures were not, lowered. Eleven died within a year and a In nine patients there was no change. half, with their condition unchanged (transient relief of symptoms occurring in five of these). Eight died within two weeks after the operation. Such criteria as age, duration of hypertension, vascular complications in the brain and the heart, heart failure, and liability of arterial pressure were not prognostically significant. The main role in deciding the outcome seemed to be played by the presence or absence of malignant hypertension os evidenced by renal and retinal lesions. ACTHORS.
Stead, Eugene A., Jr., and Ebert, Richard V.: of the Sympathetic Nervous System. Arch.
Postural Int.
Med.
Hypotension: 67:
546,
A Disease
1941.
Patients with postural hypotension do not pool more blood in the lower part of the body on standing than do normal subjects under similar conditions. The pooling of the normal amount of blood causes an abnormal fall in blood pressure. The reflex vasoconstriction, which maintains the arterial pressure in normal subjects under similar conditions, does not occur in patients with postural hypotension and distinguishes it from other types of poor postural adaptation. Postural hypotension is a disease of the sympathetic nervous system. It cannot be definitely stated whether the involvement of the sympathetic system is peripheral or central. The observations reported in this study point to the interpretation that the lack of vasoconstriction in response to a fall in arterial pressure is produced by a lesion or lesions in the sympathetic centers or their efferent tracts in the central nervous system rather than by lesions in the more peripheral portions of the postural blood pressure reflex arc. In certain patients only the postural vasoconstrictor If the lesions are more extensive, other signs of loss of sympathetic reflex is affected. function may be present, such as disturbances in sweating, absence of vasoconstriction and vasodilatation, in the extremities when the temperature of the body is changed, and absence of an increase in heart rate when the blood pressure is lowered. AUTRORS.
Eckstein, Richard W., Gregg, Donald E., and Pritchard, Walter H.: The Magnitude and Time of Development of the Collateral Circulation in Occluded Femoral, Carotid, and Coronary Arteries. Am. J. Physiol. 132: 351, 1941. The time rate of collateral development has been studied in the femoral, carotid, coronary arteries by means of the retrograde pressure and flow. In the femoral artery immediately after occlusion the retrograde pressure and flow approximate 20 mm. Hg and 10 to 15 C.C. per minute, respectively. Immediately a small pulse appears, and these values rise rapidly for a few hours and then more slowly for days and weeks until pulse and flow may approach those existing in the other intact femoral artery. In the carotid artery the initial retrograde pressure and flow are somewhat greater than in the femoral artery; a pulse is always present, and these approach more quickly the normal for the other carotid. and
Following
tllcb I ~~tr~~gra~l~~ tlow is n~rly constant al V:L~IJCS , :ir111 1I~:III :tf’tw S~,II~(L Ilours ii, together will1 11~ l~eripheral diastolic pressure, increases \-er~ slowly to ol)t:tin sizable values in :I week or SO. As in coronary arteries o~ludrrl for many weeks, t,he major source of such retrograde flow may be the other coronary arterie>. Evidence is given to indicate that initial retrograde flow is due to increased differential pressure opening preexisting collatc~rxls. Tlw mechanism for further collateral extension is not known. In addition to the flow, the i,isc of the peripheral tliastolic luessure in all tile arteries and the peripheral pulse in frmor:tl and carol ill nsry serve as an index 01 collateral extension. The peripheral pulse and retrograde flow are elevated fllllowing irrcrrasc~~l venou* return and augmented hlontl pressure. lmi may be either incr~easeI1 or ~lr~~reasrtl by neosynephrine. between
coronary
0.5
to
5.S f'.v.
occlusion
per
rnirr~tf~
ilUTHORS.
Sigler, Louis H.: Hyperactive Cardioinhibitory Carotid Sinus Reflex. A Possible Aid in the Diagnosis of Coronary Disease, Srch. ht. &fed. 67: 177. 19-11. The normal carotid sinus mechanism is a protec,tive adaptation to help maintain normal circulation. The adequate stimuli are changes in the intracarotid blood pressure. When the response to carotid sinus stimulation is unusually great, it is called a hyperactive carotill sinus reflex. Hyperactivity may exhibit itself in extreme cardioinhibit,ion, vasodeprrssion, and cerebral manifestations. This paper deals with an investigation of the hyperactive cardioinhibitory reflex in It was found :I series of 1,886 patients, including I.151 males and 745 females. that the reflex occurs with greater frequency and in higher degrees of response in males than in females. Tts frequenry and degrees of response also increase as age advances. Coronary disease is the most common condition in which the reflex occurs with the greatest frequency and the highest response. The more severe the coronary disease, the more apt the reflex is to occur and the greater its degree. Persons with other diseases and even some normal persons may present a hpprractive reflex, although not so often and to a much lesser degree. It appears that the hyperactive rartlilA~ibitory carotid sinus reflex is due to lowered resistance at the synapses in the c~ardioinhibitory center and more so in the extracardiac and intracardiac gxnglionic cells as well as in the myoneural junctions, allowing the transmission of afferent and effrrent impulses in a large am1 at times an overwhelming volume. Corouar,v disease with its associated ischemia is a possible local cause for such lowering of resistance. An ahnormal constitutioual state and some defect in the nervous system may be ot,her causes. 111 view of the great frequency of a hyperactive reflex in ,.oronary disease. it in recommended as a possible aid in the tliagnosis of such tlirease in persons of the arteriosclerotic aye who show .suspicious signs or sympton1.s. It is also suggeste(l that this reflex receive more study, since additional knowledge may help to explain tile various cardiac arrhythmias and sudden, hitherto unexplained death. -4UTHOK.
and in Paterson, J. C.: Some Factors in the Causation of Intimal Haemorrhages (‘anall. M. A. .T. 44: 114, 1941. the Precipitation of Coronary Thrombi. that The evidence supporting the hypothesis thrombosis is an intimal hemorrhage is reviewed. to result from the rupture of capillaries which are
the common cause of coronary Intimal hemorrhages are shown derivetl from the coronary lumen.
SELECTED ABSTRACTS
The criteria usually given for selection of patients were arterial hypertension. ignored. From a consideration of what is known about the pathologic physiology of arterial hypertension and the effects of denervation it would seem that not much could be expected from any such denervating operations. In general the results were poor. In only one patient was there a brilliant result, although in five others there was some degree of success in reducing blood pressure. Six more patients felt better, but their arterial pressures were not, lowered. Eleven died within a year and a In nine patients there was no change. half, with their condition unchanged (transient relief of symptoms occurring in five of these). Eight died within two weeks after the operation. Such criteria as age, duration of hypertension, vascular complications in the brain and the heart, heart failure, and liability of arterial pressure were not prognostically significant. The main role in deciding the outcome seemed to be played by the presence or absence of malignant hypertension os evidenced by renal and retinal lesions. ACTHORS.
Stead, Eugene A., Jr., and Ebert, Richard V.: of the Sympathetic Nervous System. Arch.
Postural Int.
Med.
Hypotension: 67:
546,
A Disease
1941.
Patients with postural hypotension do not pool more blood in the lower part of the body on standing than do normal subjects under similar conditions. The pooling of the normal amount of blood causes an abnormal fall in blood pressure. The reflex vasoconstriction, which maintains the arterial pressure in normal subjects under similar conditions, does not occur in patients with postural hypotension and distinguishes it from other types of poor postural adaptation. Postural hypotension is a disease of the sympathetic nervous system. It cannot be definitely stated whether the involvement of the sympathetic system is peripheral or central. The observations reported in this study point to the interpretation that the lack of vasoconstriction in response to a fall in arterial pressure is produced by a lesion or lesions in the sympathetic centers or their efferent tracts in the central nervous system rather than by lesions in the more peripheral portions of the postural blood pressure reflex arc. In certain patients only the postural vasoconstrictor If the lesions are more extensive, other signs of loss of sympathetic reflex is affected. function may be present, such as disturbances in sweating, absence of vasoconstriction and vasodilatation, in the extremities when the temperature of the body is changed, and absence of an increase in heart rate when the blood pressure is lowered. AUTRORS.
Eckstein, Richard W., Gregg, Donald E., and Pritchard, Walter H.: The Magnitude and Time of Development of the Collateral Circulation in Occluded Femoral, Carotid, and Coronary Arteries. Am. J. Physiol. 132: 351, 1941. The time rate of collateral development has been studied in the femoral, carotid, coronary arteries by means of the retrograde pressure and flow. In the femoral artery immediately after occlusion the retrograde pressure and flow approximate 20 mm. Hg and 10 to 15 C.C. per minute, respectively. Immediately a small pulse appears, and these values rise rapidly for a few hours and then more slowly for days and weeks until pulse and flow may approach those existing in the other intact femoral artery. In the carotid artery the initial retrograde pressure and flow are somewhat greater than in the femoral artery; a pulse is always present, and these approach more quickly the normal for the other carotid. and
Following
tllcb I ~~tr~~gra~l~~ tlow is n~rly constant al V:L~IJCS , :ir111 1I~:III :tf’tw S~,II~(L Ilours ii, together will1 11~ l~eripheral diastolic pressure, increases \-er~ slowly to ol)t:tin sizable values in :I week or SO. As in coronary arteries o~ludrrl for many weeks, t,he major source of such retrograde flow may be the other coronary arterie>. Evidence is given to indicate that initial retrograde flow is due to increased differential pressure opening preexisting collatc~rxls. Tlw mechanism for further collateral extension is not known. In addition to the flow, the i,isc of the peripheral tliastolic luessure in all tile arteries and the peripheral pulse in frmor:tl and carol ill nsry serve as an index 01 collateral extension. The peripheral pulse and retrograde flow are elevated fllllowing irrcrrasc~~l venou* return and augmented hlontl pressure. lmi may be either incr~easeI1 or ~lr~~reasrtl by neosynephrine. between
coronary
0.5
to
5.S f'.v.
occlusion
per
rnirr~tf~
ilUTHORS.
Sigler, Louis H.: Hyperactive Cardioinhibitory Carotid Sinus Reflex. A Possible Aid in the Diagnosis of Coronary Disease, Srch. ht. &fed. 67: 177. 19-11. The normal carotid sinus mechanism is a protec,tive adaptation to help maintain normal circulation. The adequate stimuli are changes in the intracarotid blood pressure. When the response to carotid sinus stimulation is unusually great, it is called a hyperactive carotill sinus reflex. Hyperactivity may exhibit itself in extreme cardioinhibit,ion, vasodeprrssion, and cerebral manifestations. This paper deals with an investigation of the hyperactive cardioinhibitory reflex in It was found :I series of 1,886 patients, including I.151 males and 745 females. that the reflex occurs with greater frequency and in higher degrees of response in males than in females. Tts frequenry and degrees of response also increase as age advances. Coronary disease is the most common condition in which the reflex occurs with the greatest frequency and the highest response. The more severe the coronary disease, the more apt the reflex is to occur and the greater its degree. Persons with other diseases and even some normal persons may present a hpprractive reflex, although not so often and to a much lesser degree. It appears that the hyperactive rartlilA~ibitory carotid sinus reflex is due to lowered resistance at the synapses in the c~ardioinhibitory center and more so in the extracardiac and intracardiac gxnglionic cells as well as in the myoneural junctions, allowing the transmission of afferent and effrrent impulses in a large am1 at times an overwhelming volume. Corouar,v disease with its associated ischemia is a possible local cause for such lowering of resistance. An ahnormal constitutioual state and some defect in the nervous system may be ot,her causes. 111 view of the great frequency of a hyperactive reflex in ,.oronary disease. it in recommended as a possible aid in the tliagnosis of such tlirease in persons of the arteriosclerotic aye who show .suspicious signs or sympton1.s. It is also suggeste(l that this reflex receive more study, since additional knowledge may help to explain tile various cardiac arrhythmias and sudden, hitherto unexplained death. -4UTHOK.
and in Paterson, J. C.: Some Factors in the Causation of Intimal Haemorrhages (‘anall. M. A. .T. 44: 114, 1941. the Precipitation of Coronary Thrombi. that The evidence supporting the hypothesis thrombosis is an intimal hemorrhage is reviewed. to result from the rupture of capillaries which are
the common cause of coronary Intimal hemorrhages are shown derivetl from the coronary lumen.