You will be presented with the full text of a biomedical research paper. Please write an abstract for this paper. Your response should include the abstract and no additional text.

Paper text:
hypovolemic shock , a condition in which tissue perfusion is disturbed to sustain aerobic metabolism , occurs due to improper low intravascular volume leading to decrease preload , stroke volume , and cardiac output [ 2 , 3 ] .
hemorrhagic shock ( hs ) usually happens when trauma is accompanied with intense blood loss , and in such condition the management of the patients is complex and difficult [ 47 ] .
hs causes poor tissue oxygenation and accumulation of oxygen debt that can lead to multiorgan failure [ 8 , 9 ] and increases the morbidity rate . on the other hand
the kidney function directly depends on renal perfusion pressure ( rpp ) and this organ is particularly sensitive to hs .
hs exacerbates renal damage via decreasing oxygen delivery to the kidney induced hypoxia [ 1214 ] which induces acute kidney injury ( aki ) .
renin angiotensin system ( ras ) has a pivotal role in kidney function , and it adjusts the body fluid and blood pressure [ 18 , 19 ] .
this system shows both roles of vasoconstriction and vasodilation in kidney and systematic vascular bed , which depend on angiotensin converting enzymes 1 and 2 ( ace1 and ace2 ) levels [ 20 , 21 ] .
angiotensin ( ang ) i is hydrolyzed to ang ii via ace , while hydrolysis of ang ii by ace2 generates ang1 - 7 that subsequently acts upon the mas receptor [ 22 , 23 ] .
ang1 - 7 stimulates nitric oxide ( no ) production that may or may not depend on the release of bradykinin [ 24 , 25 ] .
it may also act directly via increasing of prostaglandins to exert the vasodilatory and natriuretic actions .
acute infusion of ang1 - 7 increases the glomerular filtration rate ( gfr ) and renal blood flow ( rbf ) , and it is reported that , in preconstricted afferent arterioles of the rabbit kidney , ang1 - 7 induces vasodilation depending on no .
due to limited use of hypertonic solution in hs , we hypothesized that ang1 - 7 administration may promote renal hemodynamic parameters after hs . to test this hypothesis , the rbf responses to ang1 - 7 , sodium chloride hypertonic solution , or combination of both ang1 - 7 plus hypertonic solution compared with vehicle infusion
this study was approved in advance by the ethics committee of the isfahan university of medical sciences .
27 male wistar rats weighting 230 to 270  g from water and electrolyte research center animal house were used .
the animals were housed at a room temperature of 24  1c with a 12-hour light / dark cycle and fed with rat chow and water ad libitum and allowed 1 week to acclimatize to these conditions .
animals were placed in lateral position on a surgical table with heating lamp to control body temperature between 36.5 and 37.5c .
the left jugular vein was exposed , ligated distally , and cannulated with polyethylene tube to infuse the solutions .
the left femoral artery was catheterized and the catheter was driven forward into the abdominal aorta below the renal arteries to measure direct blood pressure .
the femoral catheter was attached to a pressure transducer and a bridge amplifier ( scientific concepts , vic . ,
melbourne , australia ) to measure mean arterial pressure ( map ) ( in fact , we considered renal perfusion pressure as map ) . in order to induce hs ,
the left kidney was exposed and placed in a cup secured to the operating table .
the left renal artery was surrounded by a transit - time ultrasound flow probe ( type 2sb ; transonic systems , ithaca , ny , usa ) interfaced with a compatible flowmeter ( t108 ; transonic systems ) to measure direct rbf . throughout the experiment map and rbf
were measured continuously and data were recorded as two - second averages via a data acquisition system .
after 30-minute stabilization period , rats underwent controlled hs at map 45  mmhg for a period of 45 minutes .
blood withdrawal was carried out in two phases : blood was withdrawn first in 10  min to stabilize map at 45  mmhg and second when map > 45 .
the total blood volume withdrawn was measured , and the animals were randomly assigned into the following treatment groups .
group 1 ( n = 7 ) as control was subjected to treatment with vehicle ( saline ) .
groups 2 ( n = 6 ) , 3 ( n = 9 ) , and 4 ( n = 5 ) as treated groups received ang1 - 7 ( 300  ngkg in saline ) , ang1 - 7 in hypertonic sodium chloride 7.5% ( 5  ml / kg ) , and hypertonic solution alone .
the dose of ang1 - 7 ( 300  ng / kg ) was selected based on previous studies to have at least 10 percent change in renal blood flow [ 28 , 29 ] .
the prepared volume of the each infused fluid was equal to the volume of blood withdrawal during hs .
animals were monitored for another 15  min after infusion , and map and rbf were measured continuously as described above .
the data for map , rvr , and rbf were corrected for kidney weight before induction of the hs as basal measurement is tabulated in table 1 .
the animal weights were recorded as 223.0  8.4 , 243.2  11.9 , 232.5  3.6 , and 228.4  8.2  g , and the volumes of blood withdrawal to induce hs were 3.0  0.25 , 3.3  0.20 , 3.5  0.19 , and 3.4  0.26  ml in groups 1 to 4 , respectively . there is no statistical difference between the groups in weight ( p = 0.36 ) and blood volume withdrawal ( p = 0.37 ) .
as blood volume was withdrawn , map reduced to about 45  mmhg to induce hs .
this pressure was controlled at constant level during 45  min of shock by blood withdrawal .
map and rbf responses to vehicle , ang1 - 7 , ang1 - 7 plus hypertonic solution , and hypertonic solution alone infusion are shown in figure 1 .
map and rbf were increased by all the treatment solutions significantly ( ptime < 0.0001 ) .
rbf response to ang1 - 7 , ang1 - 7 plus hypertonic solution , and hypertonic solution alone were statistically different from that in vehicle treated group ( p = 0.05 ) .
for example at 5  min after infusion , the rbf response to ang1 - 7 , ang1 - 7 plus hypertonic solution , and hypertonic solution alone were 1.36  0.25 , 1.37  0.23 , and 1.37  0.14  ml / min / g tissue while this response to vehicle administration was 0.56  0.12  ml / min / g tissue ( p < 0.05 ) .
rvr response during 30  min of shock could not be determined due to the lowest rbf .
however , postinfusion records indicated that rvr response in vehicle treated group was greater than other groups insignificantly ( p = 0.27 ) . during post shock , from starting of infusion until end of experiment
the result indicated that the urine responses to ang1 - 7 infusion were statistically greater than saline group ( p < 0.05 ) ( figure 2 ) . to consider nitrite level , no significant differences were observed between the groups neither before nor after the treatments .
low cardiac output and map are considered as predictors of poor outcome in patients which reduces rbf and disturbs kidney functions [ 30 , 31 ] .
restoration of the hemodynamic status is pivotal for rbf recovery after hs . in this study ,
rbf responses to ang1 - 7 , ang1 - 7 plus hypertonic solution and hypertonic solution alone were statistically different from that in vehicle treated group while there was a tendency for increasing map in response to hypertonic solution groups more than ang1 - 7 and vehicle treated groups . in addition , coadministration of ang1 - 7 and hypertonic solution did not result in a synergistic effect on rbf compared to administration of ang1 - 7 or hypertonic saline alone .
it is expected that both saline and hypertonic solutions produce plasma expansion , blood pressure , and gfr elevation .
the suitable map level is pivotal to preserve renal function , and at a specific level of map , rbf decreases and causes aki .
however , the exact minimum level of map to prevent the kidney disturbance still remains unknown .
it is reported that map above 65  mmhg might be necessary to prevent aki .
patients with low map who also received the highest doses of vasopressors are significantly linked to aki occurrence .
the vasodepressor effect of ang1 - 7 mediated by prostaglandins and no [ 3638 ] , and ang1 - 7 and its signaling pathways may antagonize the actions of angii type 1 receptor [ 39 , 40 ] .
one point is important here ; the lower concentrations of ang1 - 7 are required to stimulate no compared to that for ang ii acting via the ang ii type 2 vasodilatory receptor [ 4143 ] .
acute administration of ang1 - 7 enhances gfr and rbf that reflects the vasorelaxant properties .
ang1 - 7 also shows the ability to stimulate the formation of no [ 44 , 45 ] , and it stimulates the phosphorylation of enos and the associated kinase akt in endothelial cells .
in addition and similar to bradykinin , ang1 - 7 shows a pathway that releases no , and the vasorelaxant actions of ang1 - 7 may be reflected by the release of vasoactive prostaglandins , prostacyclin , and pge2 .
it was also reported that the systemically hypotensive effectiveness of ang1 - 7 administration was greater in spontaneously hypertensive and renovascular hypertensive than normotensive animal models [ 37 , 48 , 49 ] .
it is reported that ang1 - 7 receptor antagonist ( a779 ) decreased no concentration to restore the risen vasopressin levels during hemorrhagic shock , and it also interacts with the vasopressin v2 receptor . in addition ang-(1 - 7 ) as a potent antidiuretic peptide [ 52 , 53 ] also influences water excretion   possibly by effect on vasopressin system .
our data from serum nitrite level did not support no formation by ang1 - 7 administration ; however it still seems that ang1 - 7 increased rbf via formation of no [ 44 , 45 ] possibly within the kidney .
our result also did not show the synergistic effect from ang1 - 7 plus hypertonic solution because hypertonic solution is liable for large transcapillary absorptive forces which exert maximum intravascular volume expansion immediately at the end of infusion   to increase map , organ flow , and urine output .
map elevation by hypertonic solution may increase vascular resistance as nakamoto et al . reported that hypertension is accompanied with increase of vascular resistance by no - dependent mechanism created through vascular endothelium , and this phenomenon may limit the production of no by ang1 - 7 .
ang1 - 7 potentially could increase rbf and urine output due to rvr decreasing after hs .
however increased map by isotonic normal saline containing ang1 - 7 after hs is not similar to sodium chloride hypertonic solution .
background . 
 angiotensin 1 - 7 ( ang1 - 7 ) plays an important role in renal circulation . hemorrhagic shock ( hs ) 
 may cause kidney circulation disturbance , and this study was designed to investigate the renal blood flow ( rbf ) response to ang1 - 7 after hs . methods . 
 27 male wistar rats were subjected to blood withdrawal to reduce mean arterial pressure ( map ) to 45  mmhg for 45  min . 
 the animals were treated with saline ( group 1 ) , ang1 - 7 ( 300  ngkg1  min1 ) , ang1 - 7 in hypertonic sodium chloride 7.5% ( group 3 ) , and hypertonic solution alone ( group 4 ) . 
 results . 
 map was increased in a time - related fashion ( ptime < 0.0001 ) in all groups ; however , there was a tendency for the increase in map in response to hypertonic solution ( p = 0.09 ) . 
 ang1 - 7 , hypertonic solution , or combination of both increased rbf in groups 2 - 4 , and these were significantly different from saline group ( p = 0.05 ) ; that is , ang1 - 7 leads to a significant increase in rbf to 1.35  0.25  ml / min compared with 0.55  0.12  ml / min in saline group ( p < 0.05 ) . conclusion . 
 although ang1 - 7 administration unlike hypertonic solution could not elevate map after hs , it potentially could increase rbf similar to hypertonic solution . 
 this suggested that ang1 - 7 recovers rbf after hs when therapeutic opportunities of hypertonic solution are limited .