Venous serum

E618 Greenland, P., Bowley, N.J., Meiklejohn, B., Doane, K.L. and Sparks, C.E. (1990). Blood cholesterol concentration Fingerstick plasma vs venous serum sampling. Clin. Chem. 56, 628-630. 

TABLE 2-4 Difference in Composition of Capiliai y and Venous Serum" ... 

Blood obtained by skin puncture is contaminated to some extent with interstitial and intracellular fluids. The major differences between venous serum and capillary serum are illustrated in Table 2-4. 

Ischemic exercise is usually used for the diagnosis of McArdle s disease and the lack of venous lactate increase is believed to be the sine qua non for the diagnosis. In a patient described by Sahn and Magee5 venous serum lactate increased in the arm after isometric and isotonic ischemic exercise, although the increase was significantly less than in a normal control. Histochemical reactions and biochemical assays confirmed the absence of phosphorylase. Although the symptoms were... 

Fasting serum (portal venous) As for peripheral venous serum 9-50 p.mol/liter Collected at surgery A3... 

The most common laboratory tests performed to determine acid-base status include an arterial blood-gas determination—pH, Pco, and HCO3 levels, as well as Po because hypoxia can result in lactic acidosis, venous serum CO, electrolytes because electrolyte levels are affected by acid or base states, and urine tests, including urinalysis, urine pH, and litmus dipstick tests. 

Preferred product for peripheral venous administration 0 Measure serum calcium every 6 h during acute therapy... 

Even between episodes, most patients have increased serum creatine kinase (CK) forearm ischemic exercise causes no rise of venous lactate concentration. This is a... 

Serum CK is consistently increased in all forms of AMD. Forearm ischemic exercise causes a normal rise of venous lactate concentration in patients with childhood or adult AMD. The electrocardiogram (ECG) is altered in Pompe s disease, with a short P-R interval, giant QRS complexes and left ventricular or biventricular hypertrophy, but is usually normal in the later-onset forms. The EMG shows myopathic features and fibrillation potentials, bizarre high-frequency discharges and myotonic discharges. 

There is no glycemic response to glucagon or epinephrine (Fig. 42-1), whereas a galactose load causes a normal glycemic response. Forearm ischemic exercise produces a blunted venous lactate rise or no response. Serum CK activity is variably, often markedly, increased. The ECG shows left ventricular or biventricular hypertrophy in most patients, and the EMG may show myopathic features alone or associated with fibrillations, positive sharp waves and myotonic discharges. This mixed EMG pattern in patients with weakness and distal wasting often reinforces... 

Hypercoagulable states include malignancy activated protein C resistance deficiency of protein C, protein S, or antithrombin factor VIII or XI excess antiphospholipid antibodies and other situations. Estrogens and selective estrogen receptor modulators have been linked to venous thrombosis, perhaps due in part to increased serum clotting factor concentrations. Although a thrombus can form in any part of the venous circulation, the majority of thrombi begin in the lower extremities. Once formed, a venous... 

Serum alkaline phosphatase elevations have been reported following administration of salt-poor albumin (B5). Placenta is very rich in a heat-stable alkaline phosphatase, and albumin prepared from placental blood has a high activity of this enzyme. In one cirrhotic patient who received 1-6 units per day of albumin obtained from pooled human blood and/or human placenta, the alkaline phosphatase before infusion was 5 Bodansky units and by the thirteenth day of administration had reached a value of 160 units. The physician administering the albumin at first thought the patient was having a severe toxic liver reaction and stopped the therapy. The alkaline phosphatase then started to go down and within 10 days returned to normal levels. Analysis of the albumin indicated that it contained 470 units of alkaline phosphatase activity and was probably responsible for the observed elevations in the serum enzyme activity. Albumin prepared from venous blood did not cause an alkaline phosphatase elevation, but placenta-albumin caused elevations with a half-life of about 8 days (Ml). 

The joining chain (J in Figs. 1 and 2) is attached to IgA in the submucosa, forming the 10 S dimer which, by the process of pinocytosis, enters the mucosa and there becomes attached to the secretory component (SC), giving rise to the 11 S dimer. Secretory component prevents hydrolysis of S IgA in the lumen of the gut. The 7 S IgA monomer does not become attached to the J chain but enters the circulation via the venous-lymphatic circulation. This physicochemical property of IgA probably accounts for its relatively increased values in the serum of some children with kwashiorkor. 

Fig. 1. Model of subarachnoidal space, CSF flow, and molecular flux (N1). After CSF production in choroid plexus of the ventricles (1,2,3), CSF passes the aperture (4,5), reaches the cistemae (6-9), and divides into a cortical and a lumbar branch of the subarachnoidal space. Finally, CSF drains through the arachnoid villi into venous blood. The illustration represents an idealized cross section through the subarachnoid space. Molecules diffuse from serum with a concentration C(ser) flu ough tissue along the diffusion path x into the subarachnoid space with a concentration C(csF)- Th molecular flux J depends on the local gradient Ac/Ax or dddx and the diffusion constant D. The CSF concentration increases with decreasing volume exchange, i.e., decreasing CSF volume bulk flow (F= 500 ml/day). The flow rate of a molecule in CSF is r= FIA, where A is the varying cross section of the subarachnoid space.

On the day of admission, the patient had developed a deep venous thrombosis in his right calf, a site not involved in the injury. In investigating the underlying cause of the deep venous thrombosis, serum homocysteine was measured and found to be 17.4 pmol/L (normal is < 14 pmol/I.).To distinguish between folic acid and vitamin B12 deficiencies, a serum methylmalonic acid (MMA) assay was performed it yielded a result of 0.59 pmol/I. MMA (normal is < 0.30 pmol/L). This confirmed the presence of vitamin B12 deficiency, despite a serum B12 concentration that was within the normal range. 

Harbauer (1984) first described a venous model of thrombosis induced by mechanical injury and stenosis of the jugular vein. In a modification, both arterial and venous thrombosis is produced in rabbits by stenosis of the carotid artery and the jugular vein with simultaneous mechanical damage of the endothelium. This activates platelets and the coagulation system and leads to changes in the bloodstream pattern. As a consequence, occluding thrombi are formed as detected by blood flow measurement. The dominant role of platelets in this model is shown by the inhibitory effect of an antiplatelet serum in both types of vessels (Just 1986). The test is used to evaluate the antithrombotic capacity of compounds in an in vivo model of arterial and venous thrombosis where thrombus formation is highly dependent on platelet activation. 

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