KEY ROLE OF THE ALTERNATE COMPLEMENT PATHWAY IN HYPERACUTE REJECTION OF RAT HEARTS TRANSPLANTED INTO FETAL SHEEP1

1996 ◽  
Vol 62 (3) ◽  
pp. 407-411 ◽  
Author(s):  
Hiranya A. Rajasinghe ◽  
V. Mohan Reddy ◽  
Wayne W. Hancock ◽  
Mohamed H. Sayegh ◽  
Frank L. Hanley
Keyword(s):  
Hyperacute Rejection ◽  
Complement Pathway ◽  
Rat Hearts ◽  
Alternate Complement Pathway

Opsonic Activity in the Newborn: Role of Properdin

PEDIATRICS ◽  
1973 ◽  
Vol 52 (1) ◽  
pp. 134-137
Author(s):  
Thomas P. Stossel ◽  
Chester A. Alper ◽  
Fred S. Rosen
Keyword(s):  
Complement Pathway ◽  
Opsonic Activity ◽  
Cord Serum ◽  
Alternate Complement Pathway

Relative to pooled adult serum, most cord sera have normal or slightly diminished opsonic activity. Fifteen percent of the cord sera had markedly impaired opsonic power. This activity did not correlate with immunoglobulin or C3 levels but was associated with significantly subnormal concentrations of GBG, a component of the properdin system. The deficient opsonic activity of some cord serum is thus due to hypofunction of the alternate complement pathway.

scholarly journals Nonspecific complement activation by streptococcal structures. II. Properdin-independent initiation of the alternate pathway.

1976 ◽  
Vol 143 (6) ◽  
pp. 1352-1366 ◽  
Author(s):  
J W Tauber ◽  
M J Polley ◽  
J B Zabriskie
Keyword(s):  
Complement Activation ◽  
Group A Streptococci ◽  
Complement Pathway ◽  
Defense System ◽  
Plant Polysaccharides ◽  
Microbial Structures ◽  
Alternate Pathway ◽  
Alternate Complement Pathway ◽  
Group A

Complement consumption by isolated membranes and walls from Group A streptococci and various other gram-positive microbes has been tested. These microbial structures were found to activate the alternate complement pathway. However, unlike endotoxin, inulin, or other plant polysaccharides, activation of complement by our material was found to bypass properdin. The activating factor(s) also differs from cobra venom in its/their requirement for factor D. Preliminary experiments suggest this factor isolated from membranes to be a protein and to have a mol wt greater than 40-60,000 daltons. Our studies have led us to speculate that the phylogenetic role of the alternate complement pathway may be the primordial nonspecific defense system which has retained certain fundamental aspects up to the present time.

Role of phospholipases A2 and C in myocardial ischemic reperfusion injury

1991 ◽  
Vol 260 (3) ◽  
pp. H877-H883 ◽  
Author(s):  
M. R. Prasad ◽  
L. M. Popescu ◽  
I. I. Moraru ◽  
X. K. Liu ◽  
S. Maity ◽  
...  
Keyword(s):  
Immunoglobulin G ◽  
Ischemic Myocardium ◽  
Lower Amount ◽  
Cellular Injury ◽  
Membrane Phospholipids ◽  
Nonesterified Fatty Acids ◽  
Subcellular Organelles ◽  
Phospholipases A2 ◽  
Rat Hearts

We investigated the role of phospholipase A2 (PLA2) and phospholipase C (PLC) in myocardial phosholipid degradation and cellular injury during reperfusion of ischemic myocardium. For this purpose, isolated rat hearts were perfused with isotopic arachidonic acid to label its membrane phospholipids. Hearts preperfused with antiphospholipase A2 (anti-PLA2) retained a significantly higher amount of radiolabel in phosphatidylcholine and phosphatidylinositol and a corresponding lower amount of radiolabel in lysophosphatidylcholine and nonesterified fatty acids (P less than 0.05) after 30 min of reperfusion following 30 min of normothermic global ischemia compared with hearts preperfused with nonimmune immunoglobulin G. In similar experiments, antiphospholipase C (anti-PLC)-treated hearts were associated with significantly (P less than 0.05) higher radiolabel in all phospholipids and lower radiolabel in diacyglycerol compared with nonimmune immunoglobulin G-treated hearts. Measurement of phospholipase activity in subcellular organelles of these hearts showed decreased PLA2 activity in cytosol, mitochondria, and microsomes of anti-PLA2-treated hearts and decreased PLC activity of microsomes in anti-PLC-treated hearts. Furthermore, both the antiphospholipases attenuated the release of creatine kinase and lactate dehydrogenase into perfusate and increased contractility as well as coronary flow in the reperfused hearts. Results of this study suggest that both PLA2 and PLC are involved in the degradation of phospholipids and cellular injury that occur during reperfusion of ischemic myocardium.

Correlation between myocardial contractile force and cytosolic inorganic phosphate during early ischemia

1997 ◽  
Vol 272 (3) ◽  
pp. H1333-H1341 ◽  
Author(s):  
M. X. He ◽  
S. Wang ◽  
H. F. Downey
Keyword(s):  
Inorganic Phosphate ◽  
Contractile Force ◽  
Left Ventricular ◽  
Resonance Spectroscopy ◽  
Rat Hearts ◽  
Initial Control ◽  
Myocardial Contractile Force ◽  
Myocardial Contractile ◽  
Developed Pressure

To test the role of inorganic phosphate (Pi) in downregulation of myocardial contractile force at the onset of ischemia, Pi of rat hearts was determined with 31P nuclear magnetic resonance spectroscopy. Forty cycles of brief hypoperfusion (30% of baseline flow for 33 s) were used to achieve a time resolution of 0.512 s for comparing dynamic changes in Pi and contractile force. Initial control values of left ventricular developed pressure (LVP), heart rate, and oxygen consumption were 136 +/- 11 mmHg, 236 +/- 4 beats/min, and 95 +/- 3 microl O2 x min(-1) x g(-1); these values were unchanged at the end of the experiment. During the first 10 s of hypoperfusion, Pi increased at a rate (percentage of the total observed change) faster than the decrease in LVP; Pi and LVP then changed at the same rate during the remainder of the hypoperfusion. ADP did not change in advance of LVP. Intracellular pH did not change. The results indicate that Pi plays an important role in initiating the downregulation of myocardial contractile force at the onset of ischemia. Perfusion pressure also declined faster than LVP at the onset of ischemia, indicating potential importance of vascular collapse in contractile downregulation during early ischemia.

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