Acute and Critical Care

Original Articles

The Effects of Chemotherapeutic Agents on Renal Function during Continuous Hyperthermic Peritoneal Perfusion: Jong Ho Choi, Eun Sung Kim; Korean J Crit Care Med. 2002;17(1):19-24.

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Abstract PDF: BACKGROUND
Continuous hyperthermic peritoneal perfusion (CHPP) has been introduced to improve the survival of the advanced cancer patients. It is a technique that allows uniform delivery of cytotoxic agents and heat to the peritoneal surface. However CHPP - induced acute changes of body temperature and intraabdominal pressure could produce various abnormal physiologic responses, especially hypoperfusion and hypoxia. These factors may further contribute to the renal dysfunction. Moreover, transperitoneal absorption of drugs resulting in systemic toxicity and certain anticancer drugs have an inherent nephrotoxicity. The aim of the present study was to investigate the effect of anticancer drugs on the kidney in the ovarian cancer patients after CHPP.
METHODS
CHPP with anticancer agents in warm saline was performed in 54 patients with cancer of the ovary at temperature 47 degrees C for 90 minutes under general anesthesia. Forty nine patients were given carboplatin and 5 patients were received cisplatin intraperitoneally at an equi-toxic dose. To clarify the effect of cisplatin and carboplatin on the kidney, serum creatinine and blood urea nitrogen (BUN) were measured before anesthesia, 1, 3 and 7th day after surgery in both agents.
RESULTS
There were no significant changes of creatinine level on 1, 3 and 7 days postoperatively compared to preoperative creatinine in carboplatin patients. In carboplatin patients, postoperative BUN levels were decreased significantly on 1 and 3 days, but they were within normal range. BUN level of postoperative 7 day showed no significant change. In cisplatin patient, there was insignificant increase of BUN and creatinine levels on 1, 3 and 7 days postoperatively.
CONCLUSIONS
These results suggest that carboplatin did not suppress renal function until 7 days after CHPP. Cisplatin markedly increased the creatinine and BUN until 7 days postoperatively, but there was no statistical significance.

The Effects of Moderate Hypothermia on the Formation of Apoptosis in Transient F degrees Cal Cerebral Ischemia Model in Rats: Tae Jung Woo, Seong Wan Baik, Kyoo Sub Chung, Inn Se Kim, Hae Kyu Kim, Jae Young Kwon; Korean J Crit Care Med. 2002;17(1):12-18.

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Abstract PDF: BACKGROUND
Delayed neuronal injury after cerebral ischemia came major neurologic complication after stroke or cardiac arrest. Apoptosis formation after ischemia may be one of a mechanism of delayed neuronal injury. This study was conducted to evaluate the effect of moderate hypothermia on apoptosis formation after one hour of middle cerebral artery degrees Cclusion in rats.
METHODS
Ten Sprague-Dawley rats (300 g) were freely fed till just before operation. Anesthesia was induced with 4 vol% isoflurane in oxygen and then maintained with 2 vol% isoflurane in oxygen. Middle cerebral artery degrees Cclusion (MCAO) was induced by intraluminal monofilament nylon with blunted tip. All rats were divided randomly into two groups. In group 1 (n=5), rectal temperature was maintained at 38 degrees C. In group 2 (n=5), rectal temperature was maintained at 32 degrees C. Rectal temperature was monitored during experiment. After 60 minutes of MCAO, intraluminal monofilament was removed and all rats were returned to cages. Brain were quickly removed and cerebral hemispheres were separated after 23 hours reperfusion. Apoptosis formation were counted with TUNEL stain.
RESULTS
In group 1, after 60 minutes of MCAO and 23 hours reperfusion, 51 3.6% of hipp degrees Campal neurons were TUNEL-positive stained apoptotic cells. In group 2, TUNEL-positve neurons were 26.1 6.5% and significantly less than those of group 1 (p<0.05).
CONCLUSIONS
Sixty minutes of MCAO and 23 hours reperfusion induce hipp degrees Campal neuronal apoptosis. Moderate hypothermia of 32 degrees C reduces apoptosis of hipp degrees Campal neurons after 60 minutes of MCAO and 23 hours reperfusion.

Physiologic Changes Induced with Lipopolysaccharide in Rats: Kyoung Min Lee, Kwang Ho Lee, Kong Been Im, Jong Taek Park, Young Bok Lee; Korean J Crit Care Med. 1999;14(2):137-142.

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Abstract PDF: BACKGOUND: Bacterial endotoxin or lipopolysaccharide (LPS) is believed to mediate the tissue damage and shock observed in Gram-negative sepsis (GNS) by initiating a cascade of events, including activation of the coagulation, fibrinolytic and complement systems, and release of proinflammatory cytokines. However, the clinical pictures that result from GNS and endotoxin are quite different. The physiologic changes induced with LPS were investigated in this study.
METHODS
Fifty two male Sprague-Dawley rats were injected intraperitoneally with Escherichia coli LPS. Blood samples and bronchoalveolar lavage (BAL) fluid were obtained at baseline and at 2, 4, 8, 16, 24, and 48 hours after injection. Nitrate/nitrite levels were measured from plasma and BAL samples. Lipid peroxide (LPO) levels were measured from plasma. We measured also protein concentration and number of polymorphonuclear leukocytes (PMNL) and macrophages from BAL samples.
RESULTS
Administration of LPS caused significant increase in nitrate/nitrite concentrations of plasma and BAL fluid (p<0.01). ED50 of LPS was 1.76 mg/kg in plasma nitrate/nitrite assay. Plasma LPO levels were increased slightly after administration of LPS, but no statistical significance. Protein concentration was increased significantly (p<0.01) 4 hours after the administration of LPS. LPS induced increase of the number of PMNLs and macrophages of BAL samples significantly (p<0.05).
CONCLUSIONS
LPS increased NO production and alveolar permeability in rats. Also, LPS increased the number of inflammatory cells in the lung.

Effects of Mg2+ Intravenous Pretreatment on Brain Energy Metabolism in Acute Ischemic-Reperfusion Model in Cats: 31P and 1H Magnetic Resonance Spectroscopic Study: Eun Ha Suk, Ji Young Kang, Sung Kwan Chun, Pyung Hwan Park, Kun Ho Lim, Jung Hee Lee, Tae Hwan Lim; Korean J Crit Care Med. 1999;14(2):132-136.

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Abstract PDF: BACKGOUND: This study was purposed to evaluate the effects of Mg2+ pretreatment on cerebral ischemic injury in cats.
METHODS
Global cerebral ischemia was induced by ligation of both innominate arteries following ligation of inferior vena cava under lowered mean blood pressure for 20 minutes followed by 3 hrs of reperfusion. Ten cats were divided into 2 groups: Group 1 (n=5) is the control group, for group 2 (n=5) (Mg2+ group), the animals were pretreated with 90 mg/kg of Mg2+ intravenously before subjected to ischemia.
RESULTS
Phosphocreatine/inorganic phosphate (Pcr/Pi) and pH decreased after ischemia and did not recovered during reperfusion. And there were no significant differences between the two groups. The ratios of lactate/N-acetyl aspartate (Lac/NAA) and lactate/creatine (Lac/Cr) increased after ischemia and not recovered during reperfusion. But the ratios were higher for the group 2 than the group 1 during reperfusion (p<0.05). For the Mg2+ group, blood pressure during reperfusion was lower than the control group.
CONCLUSIONS
Mg2+ intravenous pretreatment had no protective effect on this global cerebral ischemia animal model. Even it deteriorated brain energy metabolism by lowering blood pressure.

The Effect of Clonidine Pretreatment on Bupivacaine-induced Cardiac Toxicity in Rabbit: Eun Ju Lee, Jin Young Chon, Yong Woo Choi, Se Ho Moon; Korean J Crit Care Med. 1998;13(2):205-211.

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Abstract PDF: BACKGOUND: Bupivacaine, an amide type local anesthetic, is frequently used for regional anesthesia. Bupivacaine overdose induces cardiac toxicity and directly depresses both cardiac electrophysiology and hemodynamic status. Clonidine, an imidazolin alpha-2-adrenoreceptor agonist, given prophylactically may delay the toxic manifestation of bupivacaine overdose and does not accentuate the subsequent hypotension. We studied the effect of clonidine pretreatment on bupivacaine induced cardiac toxicity.
METHODS
Fourteen rabbits (seven in each group) were anesthetized with ketamine and rompun, and tracheostomy was performed. Spontaneous ventilation with room air was continued throughout the experiment. Electrocardiogram, heart rate, and invasive arterial blood pressure were continuously recorded. Clonidine 5 microgram/kg (clonidine group) or saline (control group) was injected intravenously in randomized fashion. After 15 minutes, an intravenous infusion of bupivacaine was started at 0.3 mg/kg/min. The time of occurrence of the bupivacaine-induced toxic events: first dysrhythmia, 25% and 50% reduction in basal heart rate and mean arterial pressure, and asystole were recorded. At 5, 10, 15, and 20 minutes after bupivacaine infusion, 2 ml of whole blood were withdrawn via femoral arterial catheter for determination of bupivacaine concentration.
RESULTS
The threshold time at the first dysrhythmia was significantly greater in the clonidine group (27.2+/-4.5 min) than control group (19.9+/-1.2 min). The threshold times at the 25 and 50% reduction in basal heart rate were significantly greater in the clonidine group (23.7+/-5.8 min, 33.2+/-5.1 min) than control group (16.6+/-2.9 min, 22.9+/-2.8 min) and in basal mean arterial pressure were significantly greater in the clonidine group (15.6+/-2.6 min, 25.3+/-3.7 min) than control group (9.7+/-2.7 min, 16.3+/-5.8 min). The threshold time at the asystole was significantly greater in the clonidine group (38.2+/-7.7 min) than control group (28.7+/-3.4 min). At 5, 10, 15, and 20 minutes after bupivacaine infusion, there was no significant difference in the plasma bupivacaine concentration between two groups.
CONCLUSION
This study demonstrates that clonidine pretreatment delays the cardiac toxic manifestations of bupivacaine overdose. And plasma bupivacaine concentration was not influenced by clonidine pretreatment.

Case Report

Early Detection of Pulmonary Edema by Pulse Oximeter during Cesarean Section: Case report: Dong Ai An; Korean J Crit Care Med. 1997;12(2):163-168.

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Abstract PDF: This case showed that pulse oximeter was helpful for early detection of pulmonary edema during Cesarean section in a parturient woman with preoperative ritodrine treatment. Though arterial oxygen saturation ( Sp02 ) by pulse oximeter was low before the induction of anesthesia, the woman was anesthetized due to emergency situation. SpO2 was continuously low during the operation, so pulmonary edema was suspected. After the operaton, pulmonary edema was diagnosed on the chest x-ray. On the ECG, anteroseptal wall ischemia was detected. Supplementary O2 and diuretics therapy were performed. On the 3rd postoperative day, arterial blood gas analysis was within normal range. Four days after the operation, ECG was normalized and chest x-ray finding was much improved. 10 days later, chest x-ray finding was normalized.

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