Efferent therapy

Nikolaev VG, Sarnatskaya VV, Bardakhivskaya K1 et al (2003) New approaches to adsorptive therapy of liver failure. Efferent Therapy 1 26-39... 

Kuznetsov SY, Yankovsky OK, Burkov NV et al. (1997) Production of active forms of oxygen leucocytes as an integrated indicator of biocompatibility of haemosorbents. Efferent Therapy 2 46-50... 

Kardanov VZ, Petrosian EA, Pasechnikov VD et al. (2005) The estimation of efficiency of use of the haemosorbents modified with glutathion in treatment of an ischaemic syndrome -reperfusion extremities in experiment. Efferent Therapy 2 23-26... 

Kartel NT (1995) Possibihties of therapentic action of medical sorbents on the basis of the activated coals. Efferent Therapy 4 11-18... 

Petrosian EA, Sergienko VI, Snkhinin AA (2001) Estimation of detoxification properties of the haemosorbents modified with sodinm hypochlorite. Efferent Therapy 2 34-38... 

Petrosian EA, Zelenov VI, Snkhinin AA (2003) Comparative estimation of detoxication properties of haemosorbents after their modification with various agents. Efferent Therapy 4 27-30... 

Kartel NT (1998) Biocompatibility of carbon sorbents. Efferent Therapy 4 3-9... 

Batalov MI, Levin GY (2000) Oxidizing modification of fibrous carbon haemosorbents. Efferent Therapy 1 45 8... 

Kruchinskiy NG, Savelyev VA, Tephakov Al et al (2002) Change of haemostasis eqnitibrinm in a hemosorption session. Efferent Therapy 1 36-40... 

Kruchinskiy NG, Novikov DV, Akuhch NV et al (2005) Apphcation of a low-molecular heparin at carrying out of a hemosorption at patients of a therapeutic profile. Efferent Therapy 1 40-44... 

Keywords silicon dioxide, medicinal chemistry, surface chemistry, sorbent, efferent therapy, enteosorption, medicinal preparation, infectious diseases, detoxication, bioactive silica, purulent wound, pyoinflammatory diseases, diarrhea... 

The GFR decreases in patients receiving ACE inhibitors because of inhibition of angiotensin II vasoconstriction on efferent arterioles. Serum creatinine concentrations often increase, but modest elevations (e.g., absolute increases of less than 1 mg/dL) do not warrant changes. Therapy should be stopped or the dose reduced if larger increases occur. 

Kolesnik M (1995) Efferent methods in combined therapy of patients with glomemlonephritis. Thesis for degree of Dr Med Sci, Kyiv (In Ukrainian)... 

Laser therapy in combination with efferent methods of detoxification effectively eliminates AChR antibodies from blood and restores an optimal ratio between discocytes and pathological forms of erythrocytes. On the basis of our data, plasmapheresis can be recommended for use together with the endovascular laser blood irradiation, ELBl in treatment of myasthenia. The duration of ELBl should not exceed 30 min. 

BCG is a viable strain of Mycobacterium bovis that has been used for immunization against tuberculosis. It has also been employed as a nonspecific adjuvant or immunostimulant in cancer therapy but has been successful only in intravesical therapy for superficial bladder cancer. BCG appears to act at least in part via activation of macrophages to make them more effective killer cells in concert with lymphoid cells in the cellular efferent limb of the immune response. Lipid extracts of BCG as well as nonviable preparations of Corynebacterium parvum may have similar nonspecific immunostimulant properties. A chemically defined derivative of the BCG cell wall, [Lys18]-muramyl dipeptide, has been licensed in Japan to enhance bone marrow recovery after cancer chemotherapy. 

Another example includes the specific effects of ACE inhibition on the prevention of renal insufficiency. In comparison with triple therapy, the reduction of intraglomerular pressure induced by ACE inhibitors (277) as well as by angiotensin II antagonists (278), is much more marked, and it protects the kidney from glomerular, vascular, and tubu-lointersitial lesions observed in various experimental models, especially renal ablation and diabetes (279). Besides the fall in efferent arteriole resistance, the interruption of the RAS inhibits tubulointerstitial inflammation and the production of cytokines, which are observed in these various experimental models (280, 281). 

Direct contact of the bladder epithelium with the catabolites acrolein and 4-hydroxy-cyclophosphamide is responsible for the hemorrhagic cystitis that can be a consequence of therapy with cyclophosphamide [78]. Aggressive hydration provides prophylaxis against this toxicity to the efferent urinary tract [79]. The sulfhydryl compound mesna has also demonstrated uroprotec-tive ability during therapy with cyclophosphamide [80]. Although hemorrhagic cystitis is a dose-related toxicity, chronic low doses of orally administered cyclophosphamide are also associated with development of this adverse event [81]. 

Functional renal insufficiency is manifested as increases in serum creatinine and blood urea nitrogen. As cardiac output and renal blood flow decline, renal perfusion is maintained by the vasoconstrictor effect of angiotensin II on the efferent arteriole. Patients most dependent on this system for maintenance of renal perfusion (and therefore most likely to develop functional renal insufficiency with ACE inhibitors) are those with severe heart failure, hypotension, hyponatremia, volume depletion, and concomitant use of NSAIDs. - Sodium depletion (usually secondary to diuretic therapy) is the most important factor in the development of functional renal insufficiency with ACE inhibitor therapy. Renal insufficiency therefore can be minimized in many cases by reduction in diuretic dosage or liberalization of sodium intake. In some patients, the serum creatinine concentration will return to baseline levels without a reduction in ACE inhibitor dose. Since renal dysfunction with ACE inhibitors is secondary to alterations in renal hemodynamics, it is almost always reversible on discontinuation of the drug. ... 

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