[Effects of tannic acid pretreatment on cardiovascular function during hemorrhagic shock in rats].

OBJECTIVE: To investigate the effects of tannic acid pretreatment on cardiovascular function during hemorrhagic shock in rats. METHODS: Sprague-Dawley (SD) rats were randomly divided into two groups of shock and tannic acid pretreatment+shock. (1) In vivo experiment: the model of hemorrhagic shock in rats was reproduced by bleeding to 40 mm Hg (1 mm Hg = 0.133 kPa) being maintained for 120 minutes. Tannic acid in the dosage of 5 mg/kg was injected intravenously 10 minutes before hemorrhagic shock in tannic acid pretreatment+shock group. The mean arterial pressure (MAP), myocardial contractility and vascular reactivity were measured before hemorrhagic shock and at 180 minutes after hemorrhagic shock. In another experiment, the rats subjected to hemorrhagic shock and blood reinfusion were injected with norepinephrine (NE) intravenously at 60,120 and 180 minutes, and the vascular reactivity was observed. (2) In vitro experiment: the heart was harvested after shock and fixed on a Langendorff system. The perfusion pressure was maintained at 100 mm Hg. The effects of tannic acid pretreatment on myocardial contractility was observed. RESULTS: (1)In vivo experiment showed that tannic acid pretreatment significantly increased MAP at 60 minutes and 150 minutes, and left ventricular systolic pressure (LVSP) at 60 minutes, and the heart rate was obviously slowed at 120 minutes, and left ventricular end diastolic pressure (LVEDP) was lowered (all P < 0.05). The vascular reactivity was significantly improved at 120 minutes in tannic acid pretreatment+shock group compared with shock group (P < 0.05). (2) In vitro experiment proved that tannic acid pretreatment significantly slowed heart rate at 90 minutes as well as increased +dp/dtmax at 10 minutes and 20 minutes and -dp/dtmax at 10 minutes (all P < 0.05). CONCLUSION: Pretreatment with tannic acid improves cardiovascular function following hemorrhagic shock to some extent in rats.

[Effect of poly-adenosine diphosphate ribosyl-polymerase on vascular hyporeactivity in rats with hemorrhagic shock].

OBJECTIVE: To study the effects of poly-adenosine diphosphate ribosyl-polymerase (PARP) on vascular hyporeactivity during hemorrhagic shock in rats. METHODS: Sprague-Dawley (SD) rats were randomly divided into three groups: shock, 3-aminobenzamide (3-AB) pretreatment+shock, and sham operation. Bleeding from the femoral artery to induce hemorrhagic shock model. The blood pressure changes following 3 microg/kg norepinephrine (NE) injection were observed in vivo. The response of vascular rings of superior mesenteric artery (SMA) to NE was determined ex vivo. The nitrogen monoxide (NO) contents of plasma and tissue homogenate of SMA were measured using the assay kit based on the nitrate reductase reaction. RESULTS: The maximum increase of mean arterial pressure in response to NE immediately following shock in the shock group was significantly lower than in the sham operation group (P<0.01) and the value at 1 hour after blood reinfusion in the shock group was obviously lower than in the 3-AB pretreatment+shock group (P<0.05) and in the sham operation group (P<0.01). The maximum concentration force in the sham operation group [(0.367 1+/-0.221 3)g/mm] was significantly increased than in the 3-AB pretreatment+shock group [(0.286 4+/-0.153 2) g/mm, P<0.05] and in the shock group [(0.185 6+/-0.111 3)g/mm, P<0.01]. The cumulative dose-response curves of SMA to NE shifted to the left, and the contraction force was markedly increased as NE concentration reaching 10(-6), 10(2+) and 10(-5) mol/L in the 3-AB pretreatment+shock group compared to the shock group (all P<0.05). There were no significant difference on plasma NO content among the three groups. However, the NO contents of plasma and tissue homogenate of SMA in the 3-AB pretreatment+ shock group were slightly lower than in the shock group (P>0.05). CONCLUSION: PARP is involved in the vascular hyporeactivity in hemorrhagic-shocked rats.

[The optimal resuscitation pressure of several resuscitation fluids in controlling hemorrhagic shock in rats].

OBJECTIVE: To investigate the optimal mean blood pressure of different resuscitation fluids in resuscitating hemorrhagic shock in rats. METHODS: One hundred and eighty Sprague-Dawley (SD) rats were used to reproduce hemorrhagic shock model by 35% and 45% depletion of blood volume, and they were randomly divided into Lactated Ringer solution (LR), 7.5% NaCl/6% Dextran 40 (HSD), and LR+hydroxyethyl starch (HES) groups. Mean arterial pressure (MAP) was maintained at 60, 80 and 100 mm Hg (1 mm Hg=0.133 kPa) respectively with these fluids. Left intraventricular systolic pressure (LVSP), the maximal change rate of left intraventricular pressure (+/-dp/dt max), blood gases and 12-hour survival rate were observed. RESULTS: In 35% hemorrhagic shock rats, LR and LR+HES could better maintain the MAP at the set level, but HSD could not maintain MAP at 100 mm Hg, reaching only 85 mm Hg. In 45% hemorrhagic shock rats, LR and HSD, also could not elevate MAP to 100 mm Hg, and LR infusion could restore MAP to about 85 mm Hg, HSD to 80 mm Hg and LR+HES to 60 mm Hg. Overall 12-hour survival rate was highest in group with LR+HES to maintain MAP at 60 mm Hg with satisfactory hemodynamic parameters and blood gases. HSD group ended up with a lowest survival rate. CONCLUSION: Different fluids to resuscitate hemorrhagic shock showed a different optimal MAP. LR between 85-100 mm Hg, HSD at 80 mm Hg and LR+HES at 60 mm Hg, may throw better effect on resuscitating moderate and severe hemorrhagic shock.

[Changes in systemic and local vascular reactivity in hemorrhagic shock and the therapeutic effect of delta opioid receptor antagonist ICI174,864].

OBJECTIVE: To investigate the changes in systemic and local vascular reactivity following hemorrhagic shock of different severity and the therapeutic effect of alpha opioid receptor antagonist ICI174,864. METHODS: Fifty-six Wistar rats were used in two experiments. In experiment I, 32 rats were equally divided into sham operation group, 1 hour, 2 hours and 3 hours hypotension groups. In the latter groups, rats were bled to a mean arterial blood pressure (MAP) of 40 mm Hg (1 mm Hg=0.133 kPa) and maintained at this level for 1, 2, 3 hours, respectively. The pressor response of blood pressure and the contractile response of superior mesenteric artery (SMA) to norepinephrine(NE, 3 ug/kg) were observed after shed blood was reinfused. In experiment II, 24 rats were divided into shock control, ICI174,864 0.5 mg/kg and 1.0 mg/kg groups. The response of blood pressure and SMA contractility to NE (3 microg/kg) were observed at 1, 2, and 4 hours after ICI174,864 administration. RESULTS: Following hemorrhagic shock, the systemic and local (SMA) vascular responsiveness was significantly decreased significantly and it was time dependent. Shed blood reinfusion alone did not restore the decreased vascular reactivity. ICI174,864 improved the decreased vascular reactivity in dose-dependent manner. CONCLUSION: Hemorrhagic shock can induce systemic and local vascular hyporeactivity. The decreased vascular reactivity is closely associated with the severity and duration of shock. Loss of systemic vascular reactivity parallels to that of the regional vessel. delta opioid receptor antagonist ICI174,864 has some beneficial effect in improving vascular hyporeactivity.