Hypovolemic Shock and Edema Due to Increased Capillary Permeability

Melvin Horwith, MD, Jack W. C.

Hagstrom, MD, Robert

C. K.

Riggins, MD, and E. Hugh Luckey, MD

patient had fatal hypovolemic shock and edema. As in previously reported cases, the mechanism of shock appears to be loss of protein and fluid from the vascular bed. Extensive studies of all patients have revealed no cause for this extraordinary vascular permeability. Analysis of the reported cases suggests that subsequent patients with this syndrome should have analyses per-

formed to determine the presence of vascular reactants such as kinins. A study of these cases suggests a method of treatment of similar episodes of hypovolemic shock. Observations from this case and the one previously reported from this center suggest that vasopressor agents such as catecholamines probably are contraindicated.

plasma, blood, and isotonic saline, the blood and plasma volumes returned to predicted levels and remained stable. Further laboratory studies excluded the presence of occult hemorrhage, Addison's disease, myocardial infarction, dia¬ betes insipidus, salt-losing nephritis, or abnormal renal function as contributory causes of hypovolemic shock. Three months following this episode, he was readmitted to the hospital with "mild" serum hepatitis which resolved without specific therapy. In May 1960, the patient had a third attack of hypotension and shock that was similar to that of July 1958, and it also subsided spontaneously. In November 1961, again after an upper-respiratory tract infection, he noted the recurrence of diaphoresis, nausea, vomiting, faintness, and syncope, and was read¬ mitted to a local hospital. His temperature was normal, but the pulse rate and blood pressure were unobtainable; in addition, physical examination revealed firm, nonpitting


rarity of hypovolemic shock accompanying massive edema is emphasized by the absence of published description of this entity until a report was issued from this center in I960.1 Subsequently, two additional cases have been described,2,3 and another one has been brought to our attention by a personal communication from R. F. Jacox, MD, in February 1963. The purpose of this paper is to re¬ port in detail the clinical and necropsy findings in a fifth case. The patient in this case died during an episode of shock and edema secondary to loss of protein and fluid from the vascular to the extravascular compartments.

generalized edema. Laboratory studies showed the follow¬ ing: hematocrit reading, 65%; white blood cell count, 14,000/cu mm, with a differential count of 64% polymor¬ phonuclear leukocytes, 15% band forms, 20% lymphocytes, and 1% monocytes; urinalysis disclosed 2+ albuminuria. Serum electrolyte values were as follows: sodium, 138 mEq/liter; chloride, 110 mEq/liter; and potassium, 4.4 mEq/liter; carbon dioxide combining power was 23 milli¬ mols/liter, and blood urea nitrogen (BUN) was 13 mg/100 ml. Blood volume determinations confirmed loss of plasma volume. In the first hospital day, 22 units of plasma, 2 units of serum albumin, and large volumes of isotonic sa¬ line were required to maintain the patient's blood pressure. In addition, he received 150 mg prednisolone daily which





The patient, a 52-year-old white man, was well until July 1958, when he experienced the first of five recurrent episodes of increasingly severe hypovolemic shock; the last attack led to his death in March 1962. The first episode was characterized by profuse diaphoresis and faintness. and subsided spontaneously after several hours. Thereafter

he remained well until November 1958, when he noted the sudden recurrence of faintness, profuse diaphoresis, flush¬ ing, severe thirst, nausea, and vomiting, following an upperrespiratory tract infection. On admission to another hospi¬ tal, he was alert, but both the pulse rate and blood pressure were unobtainable. The skin was cold and dry, and no edema was noted. Initial laboratory studies showed a hema¬ tocrit reading of 69%; white blood cell count, 13,350/cu mm differential count of 51% polymorphonuclear leukocytes, 27% band forms, and 22% lymphocytes. Urinalysis findings were normal, and the specific gravity was 1.028. Serum electrolyte values were as follows: sodium, 128 mEq/liter; chloride, 86 mEq/liter; and potassium, 6.4 mEq/liter. The blood volume was initially measured at 4,120 cc (76% of predicted value) ; plasma volume, 1,610 cc (50% of pre¬ dicted value); and red blood cell volume, 2,570 cc (112% of predicted value). Results from the guaiac test were normal for occult blood in the feces. After multiple transfusions of
From the departments of medicine and pathology, the New York Hospital\p=m-\CornellMedical Center, New York. Reprint requests to 1300 York Ave, New York 10021 (Dr. Hor-

days. By the third hospital day, the patient's blood and plasma volumes had become normal but he was markedly edematous. A spontaneous diuresis then supervened, but the recovery was accompanied by congestive heart failure and pulmonary edema, presumably due to mobilization of interstitial fluid. With the exception of transitory azotemia, anemia, and hyperbilirubinemia, an extensive evaluation revealed no other significant findings, and he was dis¬ charged. In January 1962, the patient was referred to the endo¬ crine clinic of the New York Hospital. Results from physi¬



and discontinued


the next


cal examination at that time were unremarkable except for a blood pressure of 150/100 mm Hg. He was instructed to return immediately if he experienced the premonitory signs of a fifth episode. In March 1962, an upper-respiratory tract infection de¬ veloped with fever, cough, malaise, and rhinorrhea which lasted for one week. Five days later, he noted recurrence of thirst, polyuria, weakness, myalgia, flushing, and puffiness of his face. Although he had no diaphoresis or faintness, he feared an impending attack and was admitted to this hos¬ pital. No family history of a similar disorder was obtained. On physical examination his temperature was 102.2 F (39 C), the pulse rate was 80 beats per minute and regu¬ lar, the blood pressure was 132/86 mm Hg, and he ap¬ peared perfectly well. The skin was warm, dry, flushed, and not edematous. There were no other significant find¬ ings. The following data were obtained from initial labora¬ tory studies: hematocrit reading, 44%; hemoglobin level, 14.8 gm/100 ml; white blood cell count 6,000/cu mm, with a differential count of 80% polymorphonuclear leukocytes, 3% band forms, 16% lymphocytes, and 1% eosinophils; find-

Downloaded from www.jama.com by guest on November 18, 2009

ml during replacement therapy. Microscopically. A few atherosclerotic plaques were present on the luminal surface of the wall of the aorta. and 83 kg (183 lb).2 gm/100 ml. Necropsy Findings.4 cc/kg. well-nour¬ ished. and saline solutions. The radioactive iodinated serum albumin studies con¬ firmed the clinical observations.2 mg/100 ml. after this. In these areas there was myocytolysis. rose from 5. on the basis of a normal value of 77 ± 10 cc/kg). He was apprehensive. There were scattered. the electrophoretic pattern reflected the exoge- During the course of this episode. 173 cm (5 ft 8 inches) tall. and the electrocardiogram was normal.jama. 2.5 cc/kg body weight). he received a total of 8. slightly viscous fluid.100 cc of dextrose. For the first 12 hours the patient's hematocrit reading and blood pressure remained stable. very little evidence of radioactive material was found in the contents of the gas¬ trointestinal tract collected at necropsy. Special Laboratory Studies— Blood volume studies in November 1958 revealed a blood volume of 4.120 cc (76% of predicted value). in areas asso¬ ciated with the grossly described petechiae and elsewhere. The initial serum laboratory values were as follows: sodium. The abdominal panniculus was 3 cm thick at the umbilicus.030. subendocardial petechiae at the base of the left inter¬ ventricular septum. water. and 2. epidardium. 7. diaphoretic. and phlebotomy when pulmo¬ nary edema supervened. 5. There was slight.4 gm/100 ml (albumin.729 cc (61. were discrete areas of myocardial necrosis. results from guaiac tests on the stools were normal.5 utilizing iodinated I 131 serum albumin. pleural effusions. BUN level. and signs of congestive heart failure signaled the return of edema fluid to the vascular compartment.570 cc (112% of predicted value). and had cool skin throughout his course. The total urinary output was negligible. occasional erythrocytes. a rapid and massive shift of protein from the vascular compartment to the extravascular space. 8 units/ml/hr. nonpitting edema.444 cc (34. and the pericardial cavity contained about 190 cc of similar fluid. transfusions were begun immediately. and myocardium were all grossly normal. and he complained of thirst. The peritoneal cavity contained a physiologic amount of serous fluid and a few fibrous adhe¬ sions. a plasma volume of 1. with a normal pattern on paper electrophoresis. 0. The mucosal surfaces of the major bronchi were slightly hyperemic. found the half-life to be between 14 and 23 days.2 to 1. fell to 89 mg/100 ml.5 and 17 days. Large amounts of levarterenol bitartrate and later. the serum electrolyte values remained normal. 144 mEq/liter and chloride. oxygen. his pulse pressure decreased slightly.3 gm/100 ml. carbon dioxide com¬ bining power was 28 millimols/liter. respectively. these abnormalities did not recur. The skin overlying both thighs was extremely edematous and tense. blood volume studies very early in the course of the attack. Routine Laboratory Studies. a falling hematocrit reading with venous hypertension. 24 units/ml/hr. In sections from both lungs. Approximately 8% of the injected iodi¬ nated I 131 serum albumin appeared in the urine during a 59-hour period compared to 3. focal. and interstitial edema.—The patient was stocky. Renal functional studies showed no indication of signifi¬ cant glomerular or tubular disease. sodium salicylate. Routine serum elec¬ trolyte values were abnormal only during the November 1958 episode when there was hyponatremia and hyperkalemia. In spite of supportive measures. The lungs together weighed 800 gm. Immunological protein analysis of pleural fluid showed significant amounts of ct-macroglobulins and /3-lipoproteins. The cardiac valves. and vasopressor agents. Blood volume studies in No¬ vember 1961 again demonstrated loss of plasma volume.4% of the injected iodinated I 131 serum albumin in the first 24 hours in con¬ trol subjects. the paren¬ chyma was pink-red and crépitant.—Findings from urinalysis were normal except for proteinuria on one occasion asso¬ ciated with evidence of maximal concentration of urine. The concentration of total proteins and of the estimated globulins in the pleural fluid exceeded that in the plasma. The half-life for the injected iodinated I 131 serum albumin was 16 hours. a moderate leukocytosis with a moderate shift to the left accompanied the hemoconcentration. including the intravenous administration of hydrocortisone.7 units (Bodansky) .729 cc (61. which required the use of digitalis. a period during which. The left and right pleural cavities contained about 350 and 170 cc of tan. and the sedimentation rate was 13 mm/hr. Findings from studies of adrenal cortex function were normal.4 Sterling. Hemograms were remarkable only in the demonstration of hemoconcentration with the progression of each episode.5 cc/kg (normal). Electrocardiograms were normal. Despite this therapy. oxaloacetic transaminase. The heart weighed 410 gm. On the second hospital day. only partial distribution equilibrium can occur. there was marked edema of the epicardial adipose tissue. not markedly abnormal. Following the inception of shock and the infusion of massive amounts of albumin. homogenous. globulin. When the patient was admitted to the New York Hospital in March 1962. eosinophilic Downloaded from www. serum albumin. especially below the level of the ostia of the renal arteries. in the normal control. at the base were 13 and 3 mm thick. One hour later he became rapidly hypotensive and serial hematocrit readings confirmed progressive hemoconcentration. and a red blood cell volume of 2. the progressively increasing hematocrit value and the demonstrated loss of protein and fluid from the vascular compartment helped indirectly to document the marked hypovolemia. extensive or interconnecting foci of necrosis were not present. 107 mEq/liter. Approximately 90% of the radioactivity found in the ac¬ cumulated fluid in peripheral tissues and in the body cavi¬ ties was protein bound.5 cc/kg body weight. 2009 . Blood samples for estima¬ tion of kinins were not satisfactory inasmuch as the blood was not immediately mixed with ethanol which is necessary to prevent proteolytic enzyme activity. the half-life in normal controls varies be¬ tween 10. 19 mg/100 ml. ie. the bronchioles and alveoli were shown to be filled with deeply staining.2 to 6. focal atheromatous narrowing of the lumina of all of the large coronary arteries.444 cc or 35. his blood pres¬ sure became unobtainable and he died 59 hours following admission. normal = 77 ± 10 cc/kg) . and globulin. infiltrates of neutrophils and mononuclear cells.2 gm/ 100 ml).000 cc of plasma protein fraction (Plasmanate). the specific gravity was 1. BUN. 1. clear. cholesterol. rose to 26 mg/100 ml. fell from 2. Depending upon the type of label employed to tag the albumin. bilirubin. respec¬ tively. but nonpitting. 202 mg/100 ml.1% to 5. and capillaries in the myocardium were engorged with erythrocytes. pyruvic transami¬ nase. The plasma volume at this time was 2. Electrophoresis of serum proteins was normal in all sera examined prior to the onset of the attacks. alkaline phosphatase. Plasma obtained by phlebotomy 55 hours after injection of the iodinated I 131 serum albu¬ min contained less than 1% of original iodinated I 131 serum albumin.610 cc (50% of predicted value). Scattered throughout the sub¬ endocardial myocardium of the left ventricle. During the subse¬ quent 39 hours. In an attempt to maintain the patient's blood volume.ings from urinalysis were normal. total protein. 1. hemoconcentration to a hematocrit reading of 63% followed and he developed generalized firm. cho¬ lesterol. prior to the development of shock. The rapid and continu¬ ing loss of protein from the vascular bed precluded accurate blood volume determinations during the shock phase. cyanotic. The mesothelial surfaces were smooth and glistening. angiotensin amide were given intermittently in vain attempts to maintain adequate blood pressure.com by guest on November 18. revealed a blood volume of 4. Iodinated I 131 serum albumin blood volume was 4. and plasma volume was 2.5 gm/100 nously administered albumin.6 It is also of interest that in spite of the gen¬ eralized nature of this vascular leak.950 cc albumin.5 cc per kg). normal == 35. how¬ ever. the myocardium of the walls of the left and right ventricles. with a mean of 18 days.

cells of the adrenal medulla were positive for the Henle reaction. history of exposure to any toxic material. according to the technique of Gershon and Ross. y-globulin was also found in the extracellular fluid and other globulin moieties were not propor¬ tionately increased in plasma.com by guest on November 18. petechiae in the arachnoid. pancreas. sternocleidomastoid. The pleural fluid con¬ tained significant concentrations of a2-macroglobulins and /?-lipoproteins.370 gm. Sections of the heart. heart. 3 X 3-cm area of hyperemia of the arachnoid over the left parietal lobe. and rectus abdominis showed varying degrees of interstitial edema. and veins were engorged with erythrocytes. kidney. but there were no proliferated hypolemmal nuclei or loss of striation. eg. and kidneys. and was grossly normal except for the presence of a discrete. soft. in this case. The gallbladder contained about 30 cc of viscous. Convoluted and col¬ lecting tubules were normal. Plasmapheresis and marked hemoconcentration were the most notable laboratory findings in these patients. and spinal cord were normal. and she thus differs from the other patients. Studies with Evans blue or iodinated I 131 serum albumin all demonstrated prompt leakage of plasma proteins from the vascular compartment. Each kidney weighed 1 £0 gm and was grossly normal. The lymph nodes. The final pathologic diagnoses were as follows: diffuse interstitial edema secondary to (clinical) hypovolemic shock. hyperplasia of „he adrenal cortices (minimal) : nodular hyperplasia of the prostate. plump nuclei. but occasional hepatic cord cells contained fat vacuoles. characteristics. there was focal thickening of the basement membranes of several glomeruli as well as occasional focal hyaline thickening of the walls of arterioles. Marked thrist was noted early in the attack in four patients. each lasting an average of 5 to 14 days. Sections of the duo¬ denum stained for enterochromaffin granules. et al1 and Weinbren3 do not resemble angioneurotic edema. testes. microscopically. The case described by Luke2 died in shock.9 were thought by some to have a similar type of of other areas of the arachnoid and of the motor cortex. Specially stained sections hemoconcentration.material. the substantia nigra. Sections of skeletal muscle from the psoas. The marked creatinuria and potassium diuresis in Jacox's patient are provocative in the light of the complaints related to muscle weakness. The only com¬ mon preceding signs and symptoms in three pa¬ tients suggested an upper-respiratory tract infec¬ tion. burns. dark-green bile admixed with six. Sections of the kidney observed with the electron microscope showed no specific or signifi¬ cant changes that were not observed in sections of kidneys from individuals of comparable age. heart. and the parenchyma was tan. and psoas. vastus lateralis. The plasma samples from three of these patients. medulla. when subjected to electrophoresis. had an increase in the concentration of y-globulins. most prominent in the sections of the vastus lateralis.jama. Microscopically. or particular age predeliction. there was minimal diffuse hyperplasia of the zona fasciculata. Profound muscle weakness was pres¬ ent in all patients. spleen. thyroid. nausea. especially so during the course of an attack. passive hyperemia of the liver. It must be as¬ sumed that this was an absolute increase and not relative to the hemoconcentration since. not due to hemorrhage. the lentiform nucleus. pectoralis major. The episodes described in the case reported here and those in the cases reported by Clarkson. gastrocnemius. pulmonary edema. In addition to the patient in the case described above. in four. and cholelithiasis.7 showed no diminution in intracellular chromaffin granules. Sections from the lower lobes of both lungs showed minimal secondary atelectasis. the peduncles. The mechanism for this sudden and re¬ peated loss of the capacity of the capillaries to con¬ tain molecules as large as albumin and globulins within the vascular bed is not understood. the lobular architecture was well preserved. and stomach. in our pa¬ tient. hypothalamus. and liver. Focal submucosal petechiae were present in the cardia of the stomach. A review of the prodromata. 2009 . Not included in this group is a case described by Preston.600 gm. ex¬ ceeded the protein concentration in the plasma. is al¬ always due to physical trauma. skeletal muscle. The liver weighed 1. clearly defined syn¬ drome. stained by the fluorescent antibody technique with antihuman y-globulin. This pa¬ tient had a previous history of urticaria and angioneurotic edema which started in childhood. and not understood. there were some internalized. and other evidence suggestive of an allergic reaction. The concentration of total protein. This was probably the result of back diffusion of water which occurred after the initial shock phase and was also due to the exogenous albumin used in therapy. The adrenal glands together weighed 17 gm and contained the expected amount of yel¬ low lipid material in the cortices. parathyroid glands. we are aware of only four other patients1 who had hypo¬ volemic shock and edema in whom no concomitant disease was discovered. but were not studied sufficiently to permit Downloaded from www. Anorexia. rectus abdominis. Ammon's horn. splenomegaly. cerebellum. Comment most Plasma loss from the vascular bed without appar¬ ent cause is rare. bone marrow. and myalgias. but maintained a normal blood pressure and did not show evidence of marked :i Hypovolemic shock. arteries. In addition. following progressive edema which began as edema of the labia on the third postpartum day. At¬ tacks occurred on an average of one every six to ten months over a period of three to four years. including globulins in the pleural fluid. The two cases reported by Thom¬ as. Microscopically. and vomiting were present in all patients. their inclusion in this report. fatty change in the liver (minimal) . He had marked eosinophilia. and responses to therapy fails to permit classification of these patients into a single. capillaries. Considering those three males and two females. there is no com¬ mon ethnic background. failed to show localized deposits of y-globulin or complement fixation at any site. The pros¬ tate was symmetrically enlarged to about one times normal size and microscopic examination of sections showed adenomatous and fibromuscular hyperplasia. hypophysis. and skin were normal grossly and microscopically. Re¬ views10 '* of the ultrastructure of capillaries and of the effects of pharmacologie agents on increasing capillary permeability1213 point out that several naturally occurring substances present in tissues edema. oval calculi that measured about 6 mm in greatest dimension. The wall of the gallbladder was not appreciably thickened.8 The patient. multiple serous effusions. Microscopic sections taken from this area showed the presence of hemorrhage in the arach¬ noid and subarachnoid spaces. focal necrosis of the subendocardial myocardium. dark-green. developed edema. The brain weighed 1.

F. A. Risa-131. 15.. Publisher. M. or albumin. and Small Arteries. is not physiologic and does not aid in restoring blood pressure to normal. Freeman. 1960.: Generalized Edema Occurring Only at the Menstrual Period.W.. Majno. Berson. This same covery phase. Amer J Clin Path 30:425-434 (Nov) 1958. However.S. S. 16.: Refractory Hypotension in Man\p=m-\IsThis Irreversible Shock? Clinical and Biochemical Observations. 1959. Mayo Clin Proc 39:715-737 (Sept) 1964. B. dextran 75.I. Palade.: Histamine in Human Disease. It is apparent that the augmented decrease in the vol¬ ume of the vascular bed. p 119. S. 14.S." in Reymonds.. (eds. 8. MC.G. J.: A Man With Cyclical Oedema. JAMA 101:1126-1127 (Oct 7) 1933.: Studies in Clinical Shock and Hypotension.. We did not employ plasma expanders such as dextran 40 or dextran 75. Lesions similar to those pres¬ ent in this patient have been described in the myo¬ levarterenol Downloaded from www. J. tone. Luke. G. G.. 13. Guy's Hosp Rep 111:69-79 (No. G.: Metabolism of 1-131 Labeled Human Albumin. 7. Lt James F. These cases certainly support the current consensus that administration of levarterenol is contraindicated in the therapy of hypovolemic shock. which was caused by sympathomimetic agents.15 Smith and Moore16 reviewed the data which clearly indicated that vasopressors cause a marked reduction in average plasma volume. large infusions of noncolloidal substances... Meticortelone.. Bay¬ Furth.: Peripheral Blood Flow and Capillary Filtration Rates. Cortril. saline. Fawcett D. Thomas. Iodinated I 131 serum albumin—Albumotope 1-131. 3. J Exp Med 115:367-382 (Feb) 1962. inas¬ much as plasma proteins with much greater molec¬ ular weights disappeared rapidly into the extracellu¬ lar fluid. Cortifan. B. Amer J Med 29:193-216 (Aug) 1960.W. I. Szakacs. Kitchen. The resulting accumulation of to human disease reveals no mention of any disease state in which increased histamine release is asso¬ ing edema could be relieved by peritoneal dialysis dur¬ an acute episode and especially during the re¬ ciated with a similar picture of hypovolemic shock.ui in a report on the use of dextran in the therapy of shock.D. 10.M. et al: Cyclical Edema and Shock Due to Increased Capillary Permeability.D. C. and Zweifach. Dextran—Expandex. Amer J Cardiol 5:619-627 (May) 1960. Smith.): The Microcirculation. 2. and Ross..E. W. M. Ill: University of Illinois Press. The Site of Action of Histamine and Serotonin Along the Vascular Tree: A Topographic Study. References 1. Direct toxic effects of the on the myocardium constitute an addi¬ tional contraindication to its use in the quantities frequently employed in the treatment of refractory shock. Hydrocortisone—Cortef. S.N.. and Rubenstein. and Mitchell.. and Palade. 5. Preston. Weinbren. New Eng J Med 267:733-742 (Oct) 1962. and Spathis. A.com by guest on November 18.M. that are capable of exerting a significant oncotic pressure to reverse the hypovolemic shock. Meti-Derm. phenomenon is important in the prophylactic ex¬ pansion of plasma volume given prior to surgery for cardium of individuals who received levarterenol.: Studies on the Relationship of 5-Hydroxytryptamine and the Enterochromaffin Cell to Anaphylactic Shock in Mice. may be used to coun¬ teract the shock.E. B. Urbana.E. Arterioles. ard Clarkson. However. Fur¬ ther evidence for the vasopressor-induced hypovolemia is shown by the hypotension that frequent¬ ly ensues after discontinuation of the intravenous administration of vasopressor agents. and Eugene D. Hurn. A. 4. T.jama.: Spontaneous Periodic Edema. Gershon. Cohn and Luria. MD assisted in the Generic and Trade Names of Sterane.: Studies on Inflammation: II. Drugs Prednisolone—Delta-Cortef.A. They showed an increase in cardiac output and a decrease in peripheral resistance that was signifi¬ cantly greater with administration of dextran than with the administration of sympathomimetic agents.. J Clin Invest 30:1228-1237 (Nov) 1951. Kisch. Hydeltra. and McFarlane. Sterling. 6. 2009 .: Studies on Inflammation: I.H.: Pathologic Changes Induced by 1-Norepinephrine: Quantitative Aspects. Arch Intern Med 116:562-566 (Oct) 1965. K.17 IS The clinical and laboratory experience gained from the study of these cases strongly suggests that therapy should be directed toward replacement of intravascular fluid volume by saline suspensions of macromolecular substances. Ill: Charles C Thomas.L. Jacox. Bradykinin is one of these as is histamine. Code. and Moore. Ralph F.R. B. sug¬ gest that there are significant advantages to its use. I. Clin Sci 20:161-170 (April) 1961. pheochromocytoma. USN.E.A. All three patients to whom levarterenol was given appear to have exhibited a greater resistance to therapy and died during the course of an attack. 12.L.. J. M. and Luria..: "The Fine Structure of Capillaries.W. F. 18. In the event that macromolecular dextrans are not available. and Cannon. G. G. McCreedy.. 17. There is some ques¬ tion as to whether or not these substances would be retained within the vascular compartment.. G.: The Turnover Rate of Serum Albumin in Man as Measured by 1-131 Tagged Albumin. Levarterenol bitartrate—Levophed Bitartrate.capable of affecting vascular permeability. Brit Med Bull 19:155-160 (May) 1963. 1) 1962.. unless there is adequate fluid volume within the vascular compartment. an attempt was made to keep up with the disappearance rate by massive replacement of plasma and albumin.H. et al: Tracer Experiments With 1-131 Labeled Human Serum Albumin: Distribution and Degradation Studies. an extensive review of the relationship of histamine are eg. MD. and Mehlman.: Electron Microscopy of the Cardiovascular System Springfield. preparation of this report.: Fatal Post-Partum Shock Due to Massive Angioneurotic Edema. HydrocorDextran 40—Rheomacrodex. L.14 Although plasma proteins leak from the vascular bed in this type of hypovolemic shock. Plasma protein fraction—Plasmanate. Szakacs. The changes in the myocardium of this pa¬ tient are not specific. J Clin Invest 32:746-768 (Aug) 1953. Clarkson. plasma. and Schoefl. L. eg. J Cell Biology 11:571-605 (Dec) 1961. Rees. Sterolone. Lancet 2:544\x=req-\ 546 (Sept 14) 1963.R. Amer J Obstet Gynec 83: 322-327 (Feb) 1962. MD. Paracortol. That this regimen was unsuccessful is apparent from the refractoriness exhibited by this group of patients. 9. R. Majno. 11. E. G.. Hycortole. The Effect of Histamine and Serotonin on Vascular Permeability: An Electron Microscopic Study.: 1-Norepinephrine Myocarditis. Plavolex. J. Biophys Biochem Cytol 11:617-626 (Dec) 1961. Cohen. Angiotensin amide—Hypertensin. 19: Cohn.