[The evaluation of cerebral function by diffusion weighted imaging after norepinephrine-induced hypertensive perfusion therapy in pig model of cardiac arrest].

OBJECTIVE: To evaluate the changes in cerebral function of pigs with cardiac arrest (CA) after recovery of spontaneous circulation (ROSC) after hypertension perfusion therapy induced by norepinephrine (NE). METHODS: Ventricular fibrillation (VF) was induced by electrical stimulation, and standard cardiopulmonary resuscitation (CPR) was performed after VF for 4 minutes. The pigs with successful ROSC were randomly divided into two group, each n=5. The pigs in the hypertensive reperfusion group were given with NE immediately to maintain the mean arterial pressure (MAP) at 130% before VF for 4 hours; MAP of the pigs in normal reperfusion group was maintained for 4 hours as baseline. The changes in hemodynamics were observed for 4 hours in both groups. Cerebral cortex was scanned with diffusion weighted imaging (DWI) before VF and 1 hour and 3 hours after ROSC, and the dynamic changes in brain functional imaging were observed. Twenty-four hours after ROSC, brain biopsy were collected and examined after hematoxylin and eosin staining (HE). RESULTS: Compared with the normal reperfusion group, heart rate (HR), MAP, cardiac output (CO) and coronary perfusion pressure (CPP) in the hypertensive reperfusion group showed a tendency to increase (ROSC 30 minutes HR: 167±8 bpm vs. 140±15 bpm, ROSC 1 hour MAP: 131±9 mm Hg vs. 108±10 mm Hg, ROSC 1 hour CO: 4.9±0.1 L/min vs. 3.4±0.5 L/min, ROSC 2 hours CPP: 118±12 mm Hg vs. 88±1 mm Hg, P<0.05 or P<0.01). There was no obvious abnormality as shown by DWI before and after resuscitation, and the apparent diffusion coefficient (ADC) showed a tendency to decrease after resuscitation in both groups. The ADC in the normal reperfusion group was decreased more than that in the hypertensive reperfusion. Pathological study showed that the protective effect of the hypertensive reperfusion on brain tissue was better than that of the normal reperfusion group. CONCLUSION: Hypertensive reperfusion can produce hemodynamic changes, and an increase in cerebral blood flow, thus it produces a protective effect on brain to promote the recovery of neurological function in pigs with CA after resuscitation.

Effects of hypothermia on brain injury assessed by magnetic resonance imaging after cardiopulmonary resuscitation in a porcine model of cardiac arrest.

OBJECTIVE: To evaluate the effects of hypothermia on cerebral edema and metabolism, a porcine model of cardiac arrest was assessed by magnetic resonance imaging during the first 72 hours after restoration of spontaneous circulation (ROSC). METHODS: Ventricular fibrillation was induced in 33 pigs. After 8 minutes of untreated ventricular fibrillation, 30:2 cardiopulmonary resuscitation was performed. After ROSC, 30 survival animals were randomly divided into normothermia group (n = 15) and hypothermia group (n = 15). The hypothermia group immediately received endovascular cooling to regulate temperature to 33°C, which was maintained for 12 hours, followed by passive rewarming at 0.5°C/h to 37°C. Diffusion-weighted imaging and (1)hydrogen proton magnetic resonance spectroscopy were acquired for each group at 6, 12, 24, and 72 hours after ROSC. RESULTS: Compared with the normothermia group, the hypothermia group exhibited a higher 72-hour survival (73.3% vs. 33.3%, P = .028) and a superior neurological deficit score (P = .031). Cerebral injury was found in both groups, but a lesser decrease in the apparent diffusion coefficient and N-acetyl aspartate/creatinine (P < .05) and a greater increase in choline/creatinine (P < .05) were found in the hypothermia group. CONCLUSIONS: Magnetic resonance imaging could effectively detect the dynamic trend of cerebral injury in a porcine model of cardiac arrest within the first 72 hours after ROSC. Hypothermia produced a protective effect on neurological function by reducing brain edema and formation of adverse metabolites.

Evaluation of respiratory dysfunction in a pig model of severe acute dichlorvos poisoning.

BACKGROUND: Respiratory failure is the main cause of death in acute organophosphorus pesticide poisoning. In this study, a pulse-induced contour cardiac output monitor was used to evaluate the respiratory status in a pig model of acute dichlorvos poisoning. METHODS: Twenty female pigs were randomly allocated to dichlorvos (n = 7), atropine (n = 7), and control (n = 6) groups. In the dichlorvos group, pigs were administered 80% emulsifiable dichlorvos (100 mg/kg) via a gastric tube. In the atropine group, pigs were similarly administered dichlorvos, and 0.5 hours later, atropine was injected to attain and maintain atropinization. The control group was administered saline solution. Arterial blood gas was measured at 0, 0.5, 1, 2, 4, and 6 hours post-injection. The extravascular lung water index and pulmonary vascular permeability index were recorded by the pulse-induced contour cardiac output monitor. At termination of the study, the animals were euthanized, the lung wet-to-dry weight ratio was determined, and histopathology was observed. RESULTS: In the dichlorvos group, the extravascular lung water index and pulmonary vascular permeability index were substantially increased from 0.5 hours and were particularly high within 1 hour. In the atropine group, these indices increased initially, but decreased from the 1-hour mark. The control group exhibited no obvious changes. In both the dichlorvos and atropine groups, the extravascular lung water index was negatively correlated with partial pressure of oxygen/fraction of inspiration oxygen (PO2/FiO2) and positively correlated with the pulmonary vascular permeability index. Compared with the control group, the lung wet-to-dry weight ratio markedly increased and the histopathological findings obviously changed in the dichlorvos group, but only mildly increased and changed, respectively, in the atropine group. CONCLUSION: The extravascular lung water index is an appropriate and valuable parameter for assessment of respiratory function in acute dichlorvos poisoning.

Effects of norepinephrine on kidney in a swine model of cardiopulmonary resuscitation.

BACKGROUND: 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. METHODS: 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 Ca²âº-ATPase activities and histologic changes under a light and electron microscopy. RESULTS: 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, Ca²âº-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. CONCLUSION: 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.

[The influence of hypothermia therapy on enzymology and pathology of lung after cardiac arrest].

OBJECTIVE: To study the effect of hypothermia on pro-inflammatory mediators in serum, the enzymology and pathology of lung tissue. METHODS: Ventricular fibrillation for 4 minutes was induced in 10 domestic pigs. Standard cardiopulmonary resuscitation was given to them. They were then divided into two groups according to the random table after restoration of spontaneous circulation (ROSC): low temperature group (n=5): pigs were given an infusion 30 ml/kg of 4 centigrade normal saline (NS) at an infusion rate of 1.33 ml * kg(-1) * min(-1), started after ROSC for 22 minutes, then 10 ml * kg(-1) * h(-1) for 4 hours; ambient temperature group (n=5) received the same infusion of NS in room temperature. Hemodynamic parameters were observed, blood samples were collected to measure tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) in serum before ventricular fibrillation and 10 minutes, 2 hours, 4 hours after ROSC. Na(+)-K(+)-ATPase of lung tissue was determined 24 hours after ROSC, and the pathology and ultrastructure of the lung were studied. RESULTS: There was no significant difference in the hemodynamic parameters, except the temperature, between low temperature and ambient temperature groups. TNF-alpha contents at 10 minutes, 2 hours, 4 hours after ROSC in low temperature group were (15.55+/-1.65), (17.06+/-0.86), (12.52+/-1.82) ng/L, and the IL-6 contents were (173.80+/-15.01), (184.09+/-13.44), (73.17+/-6.95) ng/L, while the TNF-alpha contents at 10 minutes, 2 hours, 4 hours after ROSC in ambient temperature group were (20.09+/-1.32), (26.18+/-1.16), (29.18+/-1.20) ng/L, and the IL-6 contents were (176.92+/-16.68), (239.17+/-13.18), (405.48+/-55.49) ng/L. The pro-inflammatory mediators in low temperature group were reduced significantly (P<0.05 or P<0.01). Low temperature could significantly reduce the activity of Na(+)-K(+)-ATPase [(3.78+/-1.14) U/L vs. (6.22+/-1.23) U/L, P<0.01]. The pathology of lung was milder in low temperature group compared with that of ambient temperature group. CONCLUSION: Hypothermia therapy with infusion of 4 centigrade NS can reduce the release of pro-inflammatory mediators, inhibit the ATPase activity of alveolar membrane, and shows a protective effect on lung tissue against low perfusion.