A typically progressive dissection of the internal carotid artery with recurrent hiccups: A case report with continuous 2-year data recording.

Patients with internal carotid artery dissection (ICAD) usually report headache, neck pain, Horner's syndrome, and ischemic stroke. Because the posterior cranial nerve is involved, some patients may show different forms of posterior cranial nerve paralysis. There have been no reports of patients with ICAD showing repeated hiccups. Here, to help clinicians identify ICAD early and gain a better understanding of the atypical manifestations of the disease, we report an atypical case of recurrent hiccup symptoms caused by ICAD.

[Protection of anisodamine on the mitochondrial injury induced by oxidative stress in swine with cardiac arrest].

OBJECTIVE: To investigate the protection of anisodamine on cardiac ischemia/reperfusion (I/R) injury by oxidative stress by observing the changes in oxidation and antioxidant markers in plasma and myocardium, and the damage of cardiac mitochondria structure in pigs with cardiac arrest (CA). METHODS: Twenty-three healthy male swine were divided into three groups using random digits table: sham group (n=5), epinephrine group (n=9), and anisodamine group (n=9). The CA model was reproduced by alternating current. Blood samples were collected before CA, 8 minutes after CA, and 0 minute, 30 minutes, 24 hours after recovery of spontaneous circulation (ROSC), and hearts were harvested at 24 hours after ROSC. The content of malondialdehyde (MDA) and the enzyme activity of superoxide dismutase (SOD) were analyzed by spectrophotography, the cardiac ATP content was assayed by high performance liquid chromatography, the generation of reactive oxygen species (ROS) was detected by laser confocal microscope, and the myocardial ultrastructures were observed with transmission electron microscope to assess mitochondrial damage score. RESULTS: At 30 minutes and 24 hours after ROSC, plasma MDA level of anisodamine group was lower than that of epinephrine group (30 minutes: 43.38±8.12 µmol/L vs. 55.47±10.97 µmol/L, 24 hours: 29.96±6.04 µmol/L vs. 37.87±7.85 µmol/L, both P<0.05). Compared with epinephrine group, the cardiac SOD activity and ATP content of anisodamine group were elevated (SOD: 1.35±0.50 U/mg vs. 0.54±0.19 U/mg, ATP: 4.17±1.06 µmol/g vs. 2.95±0.94 µmol/g, P<0.01 and P<0.05), and the mitochondrial ROS level (RFU) was lowered (88.00±17.67 vs. 107.00±21.35, P<0.05). Although the cardiac MDA content was also reduced, but the difference between two resuscitation groups showed no statistical significance (16.66±2.89 µmol/mg vs. 19.28±3.90 µmol/mg, P>0.05). Using electron microscope, in epinephrine group disordered arrangement of cardiac myocyte arrangement was observed, and the mitochondrial alignment and morphology were significantly different from the sham group (mitochondrial damage score: 0.41±0.08 vs. 0.12±0.01, P<0.01). The level of mitochondrial injury in anisodamine group was milder than that of epinephrine group (mitochondrial damage score: 0.21±0.05 vs. 0.41±0.08, P<0.05). CONCLUSION: Through regulating oxygen radical metabolism, anisodamine alleviates the injury to myocardial mitochondria structure and function injury as induced by oxidative stress.

[Protective effect of anisodamine against myocardial cell apoptosis through mitochondria impairment in cardiac arrest in pigs].

OBJECTIVE: To investigate the protective effect of anisodamine on myocardial mitochondrial damage in cardiac arrest (CA) in pigs. METHODS: Twenty-three male pigs were randomly divided into three groups, epinephrine group (n=9), anisodamine group (n=9) and control group (n=5). CA following ventricular fibrillation (VF) was induced by alternating current. The blood samples were collected before CA, 8 minutes after CA and instantly after recovery of spontaneous circulation (ROSC), and 30 minutes and 24 hours later. Hearts were obtained at 24 hours after ROSC. The changes in Cytochrome C (Cyt C) and caspase-3 in plasma and myocardium were analyzed by enzyme-linked immunosorbent assay (ELISA). The myocardial specimens were observed by transmission electron microscopy for ultrastructural changes, and apoptosis was assessed with Hoechst 33258 staining. RESULTS: The ROSC rate of the anisodamine group was elevated by 22.22% compared with the epinephrine group (77.78% vs. 55.56%, P>0.05). All animals with resumption of ROSC survived up to 24 hours. The plasma contents of Cyt C and caspase-3 in the epinephrine group and the anisodamine group gradually increased after ROSC, and were significantly higher than those in the control group. But the plasma Cyt C level in the anisodamine group was lower than that in the epinephrine group at 30 minutes and 24 hours after ROSC (48.68±19.50 nmol/L vs. 77.51±29.87 nmol/L, 48.98±20.26 nmol/L vs. 82.11±25.09 nmol/L, both P<0.05). There was no significant difference in protein contents of both Cyt C and caspase-3 in plasma and myocardium between two resuscitate groups. Both epinephrine and anisodamine could mitigate cardiac mitochondrial damage after CA, but the anisodamine showed better effect. The myocardium apoptosis ratio in the anisodamine group was lower than that of the epinephrine group [(0.15±0.04)% vs. (0.37±0.04)%, P<0.01]. CONCLUSION: By decreasing the protein content of Cyt C, and reducing the extent of damage to myocardial mitochondria, anisodamine can protect the myocardial ultrastructure, and restrain the mitochondria-induced cell apoptosis after resuscitation.

Effects of subdiaphragmatic cardiac compression on cardiac arrest during liver transplantation.

Cardiac arrest during upper abdominal surgery such as liver transplantation is a rare but very severe complication. Traditional external cardiac compression has been the mainstay of basic life support in general circumstances. Subdiaphragmatic cardiac compression (SDCC), with no incision in the diaphragm, may be a more effective measure. This maneuver can provide more effective and timely cardiac compression via the already open abdomen in surgery and not add extra trauma. This method can provide a quicker and more effective means of circulation support for intraoperative cardiac arrest patients without adding new injuries. Five cases are reported and all the patients had return of spontaneous circulation (ROSC). This is the first report of the SDCC method.

[Effects of rhizoma paridis total saponins on levels of cytokines in blood serum of two-hit rat model induced by multiple fractures and lipopolysaccharide].

OBJECTIVE: To investigate the effect of rhizoma paridis total saponins(RPTS)on the levels of tumor necrosis factor alpha (TNF-alpha), interleukin-1 beta (IL-1 beta) and interleukin-6 (IL-6) in blood serum of two-hit rat model induced by multiple fractures and lipopolysaccharide. METHODS: Sixty-eight Wistar rats were randomly divided into five groups. The models were made in four groups (expect the blank control group) in accordance with the standard of two-hit animal model induced by multiple fractures and lipopolysaccharide. At 1 hour after models made,the rats in RPTS groups were given rhizoma paridis total saponins with different concentrations by intragastric administration. Six hours later, the concentrations of TNF-alpha, IL-1 beta and IL-6 in the blood serum of all rats were detected by ELISA (enzyme linked immunosorbent assay). RESULTS: The concentrations of TNF-alpha, IL-1 beta and IL-6 in blood serum of rats in the model group were remarkably higher than those in the blank control group (P<0.001), and these in the RPTS groups were remarkably lower than those in the model group (P<0001). CONCLUSION: RPTS can decrease the levels of TNF-alpha and IL-6 and IL-1 beta in the blood serum of rats subjected to two-hit induced by multiple fractures and lipopolysaccharide.

[Protective effects of rhizoma paridis total saponins on septic rats].

OBJECTIVE: To investigate the protective effect of rhizoma paridis total saponins and its mechanism on septic rats. METHODS: Septic model was reproduced by cecal ligation and puncture (CLP) in Wistar rats. Rhizoma paridis total saponins was administered to observe its protective effects on septic rats. Blood was collected to determine serum tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 beta(IL-1 beta)levels at 2, 6, 12, 24 and 48 hours after operation by means of enzyme-linked immunosorbent assay (ELISA). The pathological changes of lung tissue were observed with light microscope at 72 hours after operation. The peritoneal macrophages (PMPhi) in rats were isolated and the release of TNF-alpha and IL-1 beta in PMPhi after exposure to lipopolysaccharide (LPS, 100 microg/L) were measured by ELISA. RESULTS: Mortality in the rhizoma paridis total saponins group was significantly lower than the CLP group (50.0% vs. 85.0%, P < 0.05). The levels of TNF-alpha and IL-1 beta in serum were significantly lower than those of the CLP group at the same time (P < 0.05 or P < 0.01). The degree of inflammatory injury to the lung was much milder than that in the CLP group. In the in vitro experiment, it was shown that rhizoma paridis total saponins in concentrations of 5, 10, 20 and 40 mg/L could inhibit remarkably the release of TNF-alpha and IL-1 beta from LPS-stimulated PMPhi of rats (all P < 0.01). The differences in TNF-alpha levels among the groups showed no statistically significant difference(all P > 0.05). The level of IL-1 beta in 5 mg/L group was significantly higher than that of the 10 mg/L group (P < 0.05), but showed no difference with those of 20 mg/L and 40 mg/L groups (both P > 0.05). CONCLUSION: Rhizoma paridis total saponins can protect the CLP rats by inhibiting the activation of rat PMPhi to release cytokines and ameliorating acute lung injury.

[Effect of methylene blue on traumatic shock in rabbits].

OBJECTIVE: To observe the effect of methylene blue (MB) on the changes in plasma nitric oxide (NO), tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6) and visceral pathologic changes in rabbits with traumatic shock. METHODS: Eighteen rabbits were randomly assigned into 3 groups (n=6): sham operation group, traumatic shock with normal saline (NS) resuscitation group (NS group), and traumatic shock with MB resuscitation group (MB group). In NS group and MB group, hemodynamics was monitored, and plasma contents of NO, TNF-alpha and IL-6 were determined before shock, after shock, after resuscitation, and 0.5, 2 and 4 hours after resuscitation. In sham operation control group, hemodynamics monitoring and plasma contents of NO, TNF-alpha and IL-6 were also determined. Tissue samples of the liver and intestine were obtained after experiments for microscopic examination. RESULTS: Compared with NS group, hemodynamics was stable in MB group. The levels of plasma NO in rabbits after traumatic shock were much higher than those of before shock. In NS group, the levels of plasma NO were progressively increased after resuscitation, reaching peak level at 0.5 hour after resuscitation, then decreased thereafter but still remaining higher than those of before shock. But in MB group, the levels of plasma NO after resuscitation were obviously decreased. In sham operation group, the levels of plasma NO showed no significant changes during the whole course. The levels of plasma TNF-alpha and IL-6 in rabbits after traumatic shock were much higher than those of before shock. But after intravenous administration of MB, the levels of plasma TNF-alpha and IL-6 after resuscitation showed no significant difference compared with the baseline levels. In sham operation group, the levels of plasma TNF-alpha and IL-6 showed no significant changes during the entire course. In NS group, the organs showed prominent pathologic changes. But in MB group, less pathologic changes in the organs were milder, and in sham operation group, there was no obvious pathologic changes in the organs. CONCLUSION: NO, TNF-alpha and IL-6 play important roles in the pathologic process of traumatic shock and the administration of MB after resuscitation can decrease the levels of plasma NO, TNF-alpha and IL-6, improve hemodynamics in traumatic shock, and protect the important organs.