PMID- 22683731
OWN - NLM
STAT- MEDLINE
DCOM- 20121018
LR  - 20131121
IS  - 1540-0514 (Electronic)
IS  - 1073-2322 (Linking)
VI  - 38
IP  - 2
DP  - 2012 Aug
TI  - Mesenteric lymph return is an important contributor to vascular hyporeactivity 
      and calcium desensitization after hemorrhagic shock.
PG  - 186-95
LID - 10.1097/SHK.0b013e31825f1c9b [doi]
AB  - Vascular hyporeactivity is an important factor in irreversible shock, whereas 
      calcium desensitization is one of the mechanisms of vascular hyporeactivity, and 
      the intestinal lymphatic pathway plays an important role in multiple organ injury 
      after severe hemorrhagic shock (HS). In this study, our aims were to determine 
      the effects of mesenteric lymph on vascular reactivity during HS and the 
      mechanisms involved. First, the in vivo pressor response was observed by 
      intravenous injection of norepinephrine (3 mug/kg) at different time points after 
      HS. We found that mesenteric lymph duct ligation (MLDL) and mesenteric lymph 
      drainage (MLD) enhanced the pressor response at multiple time points after shock. 
      Next, vascular reactivity and calcium sensitivity in superior mesenteric artery 
      (SMA) vascular rings were examined using an isolated organ perfusion system. 
      Vascular reactivity and calcium sensitivity were higher for SMA rings from rats 
      that had undergone HS plus MLDL or MLD that those from rats that had undergone 
      only HS. The effects of MLDL and MLD on vascular reactivity and calcium 
      sensitivity were significantly increased following incubation with the calcium 
      sensitizer angiotensin II and were reduced after incubation with the calcium 
      sensitivity inhibitor insulin. When SMA rings from normal rats were incubated 
      with mesenteric lymph from rats subjected to HS, lymph obtained 0 to 0.5 h after 
      shock enhanced vascular reactivity and calcium sensitivity, whereas lymph 
      obtained 1 to 3 h after shock blunted these effects. We finally examined vascular 
      reactivity and calcium sensitivity in HS rats subjected to MLD at 0 to 3 h or 1 
      to 3 h after shock. We found that contractile activity of SMAs in response to 
      norepinephrine or Ca was higher in HS rats subjected to MLD at 1 to 3 h after 
      shock compared with rats subjected to MLD at 0 to 3 h after shock. These results 
      indicate that mesenteric lymph return plays an important role in biphasic changes 
      in vascular reactivity during HS. Even more importantly, mesenteric lymph 1 h 
      after shock was an important contributor to vascular hyporeactivity, and its 
      mechanism of action was related to calcium desensitization. Targeting lymph may 
      therefore have therapeutic potential in the treatment of severe shock-induced 
      hypotension.
FAU - Zhao, Zi-Gang
AU  - Zhao ZG
AD  - Institute of Microcirculation, Hebei North University, Hebei, People's Republic 
      of China.
FAU - Niu, Chun-Yu
AU  - Niu CY
FAU - Wei, Yan-Ling
AU  - Wei YL
FAU - Zhang, Yu-Ping
AU  - Zhang YP
FAU - Si, Yong-Hua
AU  - Si YH
FAU - Zhang, Jing
AU  - Zhang J
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Shock
JT  - Shock (Augusta, Ga.)
JID - 9421564
RN  - 0 (Vasoconstrictor Agents)
RN  - 11128-99-7 (Angiotensin II)
RN  - SY7Q814VUP (Calcium)
RN  - X4W3ENH1CV (Norepinephrine)
SB  - IM
MH  - Angiotensin II/pharmacology
MH  - Animals
MH  - Calcium/administration & dosage/*pharmacology
MH  - Dose-Response Relationship, Drug
MH  - Ligation
MH  - Lymph/physiology
MH  - Lymphatic Vessels/*physiology
MH  - Male
MH  - Mesenteric Artery, Superior/drug effects/*physiology
MH  - Mesentery
MH  - Muscle Contraction/drug effects
MH  - Muscle, Smooth, Vascular/drug effects
MH  - Norepinephrine/administration & dosage/pharmacology
MH  - Random Allocation
MH  - Rats
MH  - Rats, Wistar
MH  - Shock, Hemorrhagic/*physiopathology
MH  - Vasoconstriction/drug effects/*physiology
MH  - Vasoconstrictor Agents/pharmacology
EDAT- 2012/06/12 06:00
MHDA- 2012/10/19 06:00
CRDT- 2012/06/12 06:00
PHST- 2012/06/12 06:00 [entrez]
PHST- 2012/06/12 06:00 [pubmed]
PHST- 2012/10/19 06:00 [medline]
AID - 10.1097/SHK.0b013e31825f1c9b [doi]
PST - ppublish
SO  - Shock. 2012 Aug;38(2):186-95. doi: 10.1097/SHK.0b013e31825f1c9b.