[Show abstract][Hide abstract]ABSTRACT: To study ultrastructure of gastrointestinal tissue and enzymology in pigs after cardiopulmonary resuscitation (CPR) in conditions of hypertensive perfusion.
Sixteen experimental pigs were induced ventricular fibrillation (VF) by direct current shock. CPR was conducted 4 minutes after VF, and 10 pigs were successfully resuscitated. These 10 pigs were divided into control group (n=5) and hypertensive perfusion group (n=5) through random number table method. Norepinephrine was administered to maintain the mean arterial pressure (MAP) at 130% of the baseline in the hypertensive perfusion group. Serum diamine oxidase (DAO) and gastrointestinal ATPase level were determined, and gastrointestinal mucosa damages were examined with light microscope, and mitochondria injury was observed by electric microscope 24 hours after recovery of spontaneous circulation (ROSC).
The serum DAO level showed a significant increase at 2 hours and 4 hours after ROSC in hypertensive perfusion group and control group compared with baseline (hypertensive perfusion group: 15.66±2.24 U, 15.76±0.95 U vs. 8.38±0.70 U, control group: 14.87±1.34 U, 13.85±0.52 U vs. 9.92±0.78 U, all P<0.05), but when the individual value was compared between two groups, no significant difference was found. The Na(+)-K(+)-ATPase and Ca(2+)-ATPase of gastric tissue showed significant increase in the hypertensive perfusion group compared with the control group at 24 hours after ROSC (Na(+)-K(+)-ATPase: 6.07±1.49 μmol×mg(-1)×h(-1) vs. 2.89±1.48 μmol×mg(-1)×h(-1), Ca(2+)-ATPase: 7.67±1.86 μmol×mg(-1)×h(-1) vs. 3.07±1.50 μmol×mg(-1)×h(-1), both P<0.05). There was no significant difference in ATPase activity of intestinal tissue between the two groups. Gastrointestinal mucosa damages and mitochondrial injury in the hypertensive perfusion group were less obviously than in the control group.
Gastrointestinal function injury, abnormal energy metabolism, increased serum DAO levels, destruction of intestinal microvilli were found after CPR. Hypertensive perfusion could improve cell energy metabolism, reduce the mucosal injury, and protect the digestive tract from injury due to CPR.
No preview · Article · Feb 2013 · Zhonghua wei zhong bing ji jiu yi xue
[Show abstract][Hide abstract]ABSTRACT: During cardiac arrest, the gastrointestinal tract is sensitive to ischemia. Protection of the gastrointestinal tract is a critical factor in determining prognosis following cardiopulmonary resuscitation (CPR). This study seeks to determine the extent of gastrointestinal tract injury and the potential protective effect of inducing hypothermia following a porcine cardiac arrest model and CPR.
Ventricular fibrillation was induced by programmed electrical stimulation in 16 male domestic pigs (n = 8 per group). Four minutes after ventricular fibrillation, CPR was performed. Pigs that successfully restored spontaneous circulation then received intravenous infusions of saline at either 4°C or room temperature to produce hypothermic and control conditions respectively. Serum diamine oxidase and gastrointestinal adenosine triphosphate enzyme activity were determined and histopathology of the gastrointestinal tract was performed by light microscopy and electron microscopy.
Significant injury of the gastrointestinal tract after CPR was found. Na(+)-K(+) and Ca(2+) adenosine triphosphate enzyme activity in the gastric tissue were significantly high in animals receiving hypothermia treatment compared to controls. Hypothermia also significantly reduced serum diamine oxidase after CPR compared to the control group. Moreover, severe injury sustained by the gastrointestinal tissue was significantly ameliorated under hypothermic conditions compared to controls.
Gastrointestinal injury and abnormal energy metabolism are strikingly evident following CPR. Hypothermia, which is induced by an infusion of 4°C saline, can rapidly reduce internal body temperature, improve energy metabolism, and ameliorate injury to the gastrointestinal mucosa after CPR.
No preview · Article · Dec 2012 · Chinese medical journal
[Show abstract][Hide abstract]ABSTRACT: Background:
This study aimed to determine the potential protective effect of inducing hypertransfusion to the gastrointestinal tract following a porcine model of cardiac arrest and cardiopulmonary resuscitation (CPR) by evaluating the influence of gastrointestinal ultrastructure, ATPase and serum diamine oxidase.
Ventricular fibrillation was induced by programmed electrical stimulation in 16 male domestic pigs (n=8/group). Four minutes after ventricular fibrillation, CPR was performed. The pigs that successfully restored spontaneous circulation received intravenous infusion of either norepinephrine to maintain the mean arterial pressure at 130% of the baseline before ventricular fibrillation or normal saline. Serum diamine oxidase and gastrointestinal ATPase activity were determined, and histopathological examination of the gastrointestinal tract was performed by light and electron microscopy.
CPR caused significant injury to the gastrointestinal tract, elevating serum diamine oxidase and causing destruction of intestinal microvillus in control animals. Na(+)-K(+) ATPase and Ca(2+) ATPase activity in gastric tissue were significantly elevated in animals receiving hypertransfusion treatment compared with the control animals. Hypertransfusion also significantly reduced serum diamine oxidase to below control levels after CPR. Moreover, severe injury sustained by the gastrointestinal tissue was markedly ameliorated under hypertransfusion conditions compared with the control animals.
Gastrointestinal injury and abnormal energy metabolism were strikingly evident following CPR. Hypertransfusion inducing hypertension can improve energy metabolism and ameliorate gastrointestinal mucosal injury, indicating that hypothermia significantly ameliorates gastrointestinal injury sustained following cardiac arrest.
[Show abstract][Hide abstract]ABSTRACT: The aim of this study was to study the effects of norepinephrine (NE)-induced hypertension (HT) on renal biochemistry, enzymology, and morphology after restoration of spontaneous circulation (ROSC) by cardiopulmonary resuscitation (CPR) in swine.
After 4 minutes of ventricular fibrillation, standard CPR was carried out. The survivors were then divided into 2 groups. The HT group (n = 5) received 0.4 to 1.0 μg kg⁻¹ min⁻¹ of NE continuously to maintain the mean arterial pressure (MAP) at 130% of the baseline (ie, MAP before ventricular fibrillation). The normal pressure (NP) group (n = 5) received 0.2 to 0.5 μg kg⁻¹ min⁻¹ NE continuously to maintain MAP at the baseline level. Hemodynamic status and oxygen metabolism were monitored, and blood urea nitrogen and creatinine were measured in blood samples obtained at baseline and at 10 minutes, 2 and 4 hours after ROSC. At 24 hours after ROSC, the animals were killed and the kidney was removed to determine Na⁺-K⁺-ATPase and Ca²⁺-ATPase activities and histologic changes under a light and electron microscopy.
mean arterial pressure, cardiac output, and coronary perfusion pressure were significantly higher (P < .01), whereas the oxygen extraction ratio was lower in the HT group than in the NP group (P < .05). Blood urea nitrogen and creatinine increased in the NP group but did not change in the HT group. Renal ATP enzyme activity was significantly higher in the HT group than the NP group (Na⁺-K⁺-ATP enzyme: 4.024 ± 0.740 U versus 3.190 ± 0.789 U, Ca²⁺-ATP enzyme: 3.615 ± 0.668 versus 2.630 ± 0.816; both P < .05). The HT group showed less cellular edema, necrosis, and fewer damaged mitochondria compared with the NP group.
These data suggest that inducing HT by NE helps to maintain stable hemodynamic status and oxygen metabolism and may protect the kidney in terms of biochemistry, enzymology, and histology after CPR.
No preview · Article · Sep 2011 · The American journal of emergency medicine