Biomedical subjects
Publications and source records attributed to B C Lin.
Iliac vein rupture is rare and primarily results from major trauma or occurs during pelvic surgery. Spontaneous nontraumatic rupture is even more unusual, with only 14 cases reported in the literature. We report an additional case, summarize all of the cases, and discuss the possible causes and treatment of iliac vein rupture and the role of anticoagulants in postoperative management.
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Pneumatic tourniquet and hone cement are often applied in orthopaedic surgery. In lower limb surgery, deep vein thrombosis may occur after release of tourniquet, causing embolism of lungs and vital organs. Paradoxical embolism may develop if the patients present extracardiac or intracardiac right to left shunt, such as atrial septum defect, etc. A 60-year-old female patient suffered from osteoarthritis of both knees was admitted for total knee replacement (TKR). Pneumatic tourniquet was inflated on the operated leg for the orthopaedic surgery which lasted for 2h. Dyspnea, sinus tachycardia and abdominal pain were noted after TKR. Blood gases analysis showed arterial hypoxemia and respiratory alkalosis. Chest X-ray revealed diffused bilateral pulmonary infiltration, pulmonary trunk engorgement, and decreased lung markings. Two days after TKR under the impression of peritonitis, she received exploratory laparotomy in which ischemic bowel and gall bladder were found. Pulmonary and paradoxical embolism were diagnosed, both of which were the well-known complications of TKR with tourniquet and bone cement application. The patient finally succumbed because of multiple organ failures.
The purpose of this analysis was to understand better the problems faced in the management of blunt juxtahepatic venous injuries and to try and simplify the controversies regarding the optimal surgical approach to these injuries. Charts of 92 blunt liver trauma patients treated between July 1, 1991 to June 30, 1993 were reviewed. Nineteen patients with blunt juxtahepatic venous injuries were identified. The isolated left hepatic vein injury group (five patients) were all treated using a nonshunting approach with no mortalities. Half of the isolated right hepatic vein injury group (ten patients) received an atriocaval shunt, and the other half did not. These two different approaches each produced one survivor, with a combined mortality rate of 80% (eight of ten patients). One of the combined injuries group (four patients) received a total hepatectomy followed by liver transplantation. Another received a shunt. The other two were treated without shunting, but all of them expired. The overall mortality rate was 63.2% (12 of 19 patients), with nine patients dying intraoperatively or immediately postoperatively from exsanguination. The other three died 10, 25, and 30 days postoperatively because of sepsis. Juxtahepatic venous injury should be suspected after failure of the Pringle maneuver to stop bleeding and the different venous injuries differentiated by palpation of the adjacent hepatic parenchymal injuries. If an isolated left hepatic vein injury is found and the liver parenchymal injury is limited to segments II, III, or IV, then a nonshunting approach will achieve the optimal outcome.
Hepatic arteritis is a rare complication in systemic lupus erythematosus (SLE). Information about its clinical manifestations is still very limited. Elevated serum r-glutamyl transpeptidase and alkaline phosphatase levels, but without elevated bilirubin and transaminase levels, were found in the present report to be the clinical presentation of hepatic arteritis. This clinical picture originally suggested a disease of the biliary tree. Hepatic arteritis must be included in the differential diagnosis of biliary tract disorders in SLE.
The effects of stimulation of supraoptic nucleus (SON) on the changes of oxytocin (OT), arginine vasopressin (AVP), norepinephrine (NE) and serotonin (5-HT) in the perfusate of locus coeruleus (LC) and changes of pain threshild (PT) were studied by methods of microinjection, radioimmunoassay (RIA) and high pressure liquid chromatography (HPLC) technique. The results showed that the OT contents at 30, 60 and 90 min after stimulation, that of AVP at 30 min and 5-HT at 60 min were increased significantly, while the NE contents at 30 and 60 min were decreased markedly. Injection of V1 antagonist into LC did not affect the analgesic effect caused by administration of L-glutamic acid (L-Glu) into SON, which, however, could be partially inhibited by V2 antagonist or even reversed by OT antagonist. The above results suggested that the analgesic effect due to stimulation of SON is caused by increase of 5-HT and decreases of NE in the LC though the action of OT released by SON on OT and V2 receptor in LC.
AIM: To study the relationship between the anti-arrhythmia action of naloxone (Nal) and its effect on baroreflex sensitivity (BRS). METHODS: Acute myocardial infarction was produced by ligating coronary artery in Sprague-Dawley rats. Ventricular extrasystole (VE), tachycardia (VT), and fibrillation (VF) were recorded on ECG. The slopes of linear regression (b) from systolic blood pressure and cardiac cycle after intravenous injection (i.v.) of phenylephrine 2 micrograms was taken as the BRS. The area of infarct was estimated after TTC staining. RESULTS: Nal 0.5 mg i.v., intracisternal injection (i.c.) of Nal 0.1 mg, and i.c. beta-endorphin (beta-End) antiserum 10 microL suppressed the ischemic arrhythmias, arrhythmia score was 1.8 +/- 1.1 (Nal i.v.) vs 3.8 +/- 2.1 (Saline i.v.); 1.7 +/- 1.5 (Nal i.c.) vs 4.0 +/- 2.6 (Artificial CSF i.c.) and 1.7 +/- 1.6 (beta-End antiserum i.c.) vs 4.1 +/- 2.0 (Serum i.c.) (P < 0.05) and potentiated the BRS, BRS was 4.2 +/- 1.8 (Nal i.v.) vs 2.9 +/- 0.8 (saline i.v.); 4.5 +/- 1.7 (Nal i.c.) vs 2.8 +/- 0.7 (Artificial CSF i.c.) and 4.4 +/- 1.1 (beta-End antiserum i.c.) vs 3.0 +/- 0.9 (Serum i.c.) (P < 0.05). BRS showed negative relations to the arrhythmia scores with r of -0.69 for i.v Nal, -0.72 for i.c. Nal, and -0.67 for i.c. beta-End antiserum (P < 0.05). CONCLUSION: Nal suppressed ischemic arrhythmias via antagonization of beta-endorphin and potentiation of BRS.
OBJECTIVE: To analyse causes of death and possible factors that influenced the operative mortality in patients with blunt hepatic injuries. DESIGN: Retrospective case study. SETTING: Medical center, Taiwan. PATIENTS: 109 adult patients with blunt hepatic injuries were treated surgically over the four year period from September 1987 to August 1991. MAIN OUTCOME MEASURE: Mortality. RESULTS: 36 patients (33%) had hepatorrhaphy or no repair, complex repairs were done for 73 patients (67%) and the overall mortality was 22% (24/109). Of those deaths, however, 4 were not liver-related, giving us a liver-related mortality of 19% (20/105). Fourteen of the liver-related deaths occurred within 24 hours of injury of hemorrhagic shock or coagulopathy. Six occurred after 24 hours of sepsis and multiple system organ failure. Multivariate analysis showed that higher initial aspartate aminotransferase (AST) and Injury Severity Score as well as increasing operative blood loss resulted in a worsening prognosis. CONCLUSION: The initial AST activity and Injury Severity Score as well as the total operative blood loss were the significant factors that influenced the operative mortality after blunt hepatic injuries in our study. Prompt, expeditious, and appropriate surgical management to control operative loss is the only way for the surgeon to reduce the mortality of blunt hepatic injuries.
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The effects of intracerebroventricular injection of Anti-opioid peptide sera on oxytocin-induced enhancement of electroacupuncture (EA) analgesia were observed in this study. It was found that injection of anti-beta-endorphin serum (AEPS) alone could attenuate EA analgesia in rats. Injection of AEPS prior to intraventricular injection of oxytocin could not block the enhancement of EA analgesia by oxytocin. The antidynorphin A1-13 serum (ADYNS) alone could also reduce the EA analgesia, whereas injection of ADYNS prior to injection of oxytocin could potentiate the enhancement of EA analgesia by oxytocin. However, neither the anti-methionine enkephalin serum nor the anti-leucine enkephalin exerted any effect on the enhancement of EA analgesia by oxytocin. The above results showed that the dynorphin attenuate oxytocin-induced enhancement of EA analgesia, but Beta-endorphin and enkephalin do not affect this role of oxytocin. These data suggest the enhancement of EA analgesia by oxytocin is not dependent upon the endogenous pioid peptides in brain.
Although cold syrup containing dextromethorpan bromide is widely administered, the bromism due to cold syrup has not been reported. We report a patient who had negative anion gap with hyperchloremia and conscious loss because of daily intake of cold complex syrup (containing dextromethorphan bromide 0.4 mg/ml, acetaminophen 8.33 mg/ml) for headache for 4-5 years. The bromide content in cold complex syrup resulted in serum levels of bromide that interfered with the automated analyzers for chloride content. When conscious change is due to bromism, hemodialysis instead of forced hydration and diuresis should be performed immediately. Therefore, patients with a markedly negative anion gap with hyperchloremia should be considered as having halide intoxication.
The role of hypothalamic paraventricular nucleus (PVH) in acupuncture analgesia was investigated by local brain stimulation and cauterization. The results showed that electrical or L-glutamate sodium stimulation of PVH could enhance the effect of analgesia of Zusanli acupuncture, both in a dose dependent manner. Electrical cauterization of PVH decreased the effect of acupuncture analgesia, while removal of pituitary had no effect on the enhancing effect by L-glutamate sodium injection.
STUDY OBJECTIVE: Two selective V1 and V2 receptor antagonists of arginine vasopressin, d(CH2)5Tyr(Me)AVP and d(CH2)5[D-Ile2, Ile4, Ala9-NH2]AVP, were given intravenously in burn shocked rats to investigate the respective effects of V1 and V2 receptor blockade on the haemodynamic variables in burn shock. DESIGN: Computer assisted on line real time measurements of mean arterial blood pressure, diastolic blood pressure, left ventricular systolic pressure, dP/dtmax, and heart rate were used to study the effects of the receptor antagonists during burn shock. In addition, the radioactive microsphere method was used to measure the changes of cardiac output and regional blood flows to heart, kidney, and liver in response to the antagonists during burn shock. Third degree burns extending over 30% of body surface area were made by dipping the rat's shaved back into water at 100 degrees C for 20 s. EXPERIMENTAL MATERIAL: Male Sprague-Dawley rats (250-300 g) were used in groups of 6-9 per experiment. MEASUREMENTS AND MAIN RESULTS: Mean and diastolic arterial blood pressures, left ventricular systolic pressure, dP/dtmax and heart rate were measured for 8 h after burns. Cardiac output and regional blood flow were measured at 3 h and 8 h postburn. Results showed that blockade of V1 receptor lowered mean and diastolic arterial blood pressures throughout the 8 h period, and raised left ventricular systolic pressure and dP/dtmax only during the early phase of shock. Cardiac output and blood flows to heart, kidney, and liver were increased by the V1 antagonist at 3 h but not at 8 h postburn. The V2 receptor antagonist increased mean and diastolic arterial blood pressures, left ventricular systolic pressure, and dP/dtmax both during the early and during the late phases of burn shock. It also improved cardiac output and blood flows to the heart, kidney, and liver during the early and late phases of burn shock. However, heart rate was not affected by V1 and V2 receptor antagonists. CONCLUSIONS: The V2 like receptor may be the dominating receptor mediating vasopressin's inhibitory effect on the heart. V1 receptor mediated coronary vasoconstriction contributes to the myocardial depression possibly only at the compensatory phase of shock. In addition V1 receptor mediated vasoconstriction is important in maintaining blood pressure during burn shock.
The purpose of this experiment is to study the role of arginine vasopressin (AVP) in acute cerebral ischemic edema in Mongolian gerbils. The results show that intracerebroventricular injection (ICV) of AVP exacerbates acute ischemic brain edema, while ICV of AVP antiserum significantly decreases the ischemic brain edema. Nimodipine (calcium antagonist) cannot block this role of AVP in brain edema. In addition, the cortical Na(+)-K+ ATPase activity is significantly decreased, while the cAMP content of ischemic cortex and hypothalamus and the cGMP content of the hypothalamus are markedly increased after AVP ICV. These suggest that AVP may play an important role in the pathophysiologic process of ischemic brain edema by inhibiting the Na(+)-K+ ATPase activity of the cerebral cell membrane and the AVP receptors mediated by cAMP and cGMP.
Intraventricular injections of anti-beta-endorphin serum (8 microliters) at 0, 1, 2, 3 h after burn shock (20% body surface area, 100 degrees C, 20 s) in different group rats prolonged the survival time, delayed the decrease of mean arterial pressure (MAP) and heart rate, and postponed the abnormal changes of ECG. The effect was most prominent at 1 h and little at 3 h after burn.
To investigate the effect of arginine vasopressin (AVP) in the peripheral circulation on burn shock in the rat, AVP and its nonselective V1/V2 receptor antagonist d(CH2)5Tyr (Et)VAVP were administered intravenously in burn shocked rats. Cardiovascular parameters were recorded including left ventricular systolic pressure (LVSP), +/- dP/dt max, total area of the cardiac force loop (Lo), mean arterial blood pressure (MAP), heart rate (HR) and electrocardiogram (ECG). Our results showed that AVP failed to increase MAP in burned rats whereas it elicited a greater fall in LVSP, +/- dP/dt max and Lo and MAP than seen in control burned rats and hastened the onset of the decompensatory phase of burn shock resulting in the early death of burn shocked animals. The receptor antagonist d(CH2)5Tyr(Et)VAVP elevated LVSP, +/- dp/dt max and Lo for the eight hour observation period, and allowed MAP to recover from the initial profound fall following burn injury. Furthermore, it prolonged the survival time of the burned rats. AVP treated rats also displayed earlier abnormal changes such as elevation of S-T segment, inversion of T wave and ventricular fibrillation in ECG. The onset of these changes was much delayed in antagonist treated rats.
The difficulty of measuring physiological concentrations of glucose in blood by conventional infrared absorption spectroscopy is due to the intrinsic high background absorption of water. This limitation can be largely overcome by the use of a CO2 laser as an infrared source in combination with a multiple attenuated total reflection (ATR) technique. To demonstrate the applicability of this technique, we compared in vitro measurements of glucose in blood obtained from an experimental infrared laser spectrometer with independent measurements made by a standard YSI 23A laboratory glucose analyzer. The capability of continuous measurement of blood glucose concentration is of primary importance in the future development of a glucose sensor for diabetic patients.