7i4  Theories  of  Blood-Coagulation  {^(R^wn?™' 
inducing  the  coagulation  of  peptone  plasma  and  hirudin  plasma 
which,  as  is  well  known,  remain  fluid  because  they  contain  an  anti- 
coagulating  substance,  called  antithrombin.    In  opposition  to  our  as- 
sumption, Howell  thinks  that  the  lipoid  is  not  a  constituent  of  throm- 
bin, but  acts  by  neutralizing  the  antithrombin,  which  hindered  the 
spontaneous  conversion  of  prothrombin  into  thrombin.    The  real 
existence  of  antithrombin  is  of  course  unquestionable  and  it  has 
been  proved  beyond  doubt  that  antithrombin  may  be  neutralized  by 
thrombin,  the  two  substances  being,  in  all  probability,  capable  of  form- 
ing a  compound.    Now  the  question  arises  whether,  when  lipoid 
is  added  to  peptone  or  hirudin  plasma,  the  removal  of  the  antithrom- 
bin function  is  due,  as  Howell  claims,  to  the  direct  neutralization 
of  antithrombin  by  this  lipoid,  or  to  a  neutralization  of  antithrom- 
bin by  thrombin  generated  under  the  influence  of  the  same  lipoid, 
the  latter  reacting  with  the  serozyme  or  proserozyme  also  contained 
in  the  aforesaid  plasma.    In  other  words,  according  to  this  second 
interpretation,  the  neutralization  of  antithrombin  by  the  lipoid  would 
be  merely  apparent  or  at  least  indirect,  the  direct  agent  of  this 
neutralization  being  the  thrombin  which  the  lipoid  has  caused  to 
appear.    I  believe  that  such  a  conclusion  is  forced  upon  us  by  some 
recent  and  careful  experiments  by  Gratia.    Without  entering  into 
the  somewhat  complicated  details,  they  have  shown  that  the  lipoid 
does  not  at  all  neutralize  the  antithrombin  when  the  serozyme  or 
proserozyme  has  been  previously  removed,  that  is,  when  the  pro- 
duction of  thrombin  has  been  made  impossible.    Even  when  the 
lipoid  is  added  in  large  excess,  the  abolition  of  the  antithrombin 
function  occurs  only  in  proportion  to  the  amount  of  serozyme  pres- 
ent, that  is,  in  proportion  merely  to  the  quantity  of  thrombin  that 
can  be  generated.  Consequently,  a  direct  influence  of  the  lipoid  on 
the  antithrombin  cannot  be  admitted. 
Furthermore,  Howell's  view  could  hardly  be  brought  into  har- 
mony with,  a  very  essential  fact,  which  has  been  mentioned  above. 
Were  his  assumption  correct,  it  should  be  admitted  that  serum 
yielded  by  the  coagulation  of  recalcified  oxalated  plasma  deprived  of 
its  platelets  contains  a  large  amount  of  antithrombin,  since  the 
addition  of  lipoid  to  such  a  serum,  itself  poor  in  thrombin,  produces 
in  this  fluid  plenty  of  the  latter  principle ;  upon  the  whole,  the  serum 
should  in  this  respect  resemble  very  closely  the  plasma  from  which 
it  is  derived.    But,  such  being  the  case,  it  would  be  very  difficult  to 
