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Yeshayahu Katz

Publications and source records attributed to Yeshayahu Katz.

At least 19 recordsLinked to original sources
PubMed2006

Apoptotic changes in the cortex and hippocampus following minimal brain trauma in mice.

Interpretation of the cellular and molecular pathogenic basis of post-minimal traumatic brain injury is a significant clinical and scientific problem, especially due to the high prevalence of motor vehicle--and other accidents. Pathogenetic brain mechanisms following traumatic impact are usually investigated by using models of severe or moderate trauma. Apoptotic neuronal degeneration after notable brain trauma is a well-known phenomenon, but the source of its activation is not clear, especially after mild, subclinical brain trauma. In the present study, we used a closed head weight-drop model to induce minimal brain injury in mice. Pellets of 5, 10, 15, 20, 25 and 30 g were dropped on the right side of mice's head kept under light ether anesthesia. No abnormal behavioral or neurophysiological changes were seen following the head trauma. Morphological assessment was done 72 h after the traumatic impact using TUNEL assay and silver staining. We found gradual increase of TUNEL-positive and silver-impregnated cells number in different cortical and hippocampal regions of both injured and contralateral hemispheres. The threshold of traumatic impact that caused a significant activation was 10-15 g pellets (evident by silver staining), and 15-20 g for apoptosis. The most sensitive zones for trauma were anterior cingulate cortex and CA3 area of hippocampus. No bilateral hemispheric differences were found. Our results demonstrate that even closed head minimal traumatic brain injury can cause diffused neuronal damage and apoptosis. This results correlate well with cognitive and behavioral deficits described for mice suffering similar mTBI and can also explain the wide variety of mental disturbances described for post-concussion syndrome in patients who suffered mild head injury.

Animals↗
PubMed2006

ACC/AHA guidelines for preoperative cardiovascular evaluation for noncardiac surgery: a critical point of view.

This review examines the issue of preoperative cardiac evaluation from a critical point of view, based on recent medical literature. We reviewed the history of that field and focused on the American College of Cardiology and American Heart Association guidelines, which are a cornerstone in the field of cardiac patients undergoing noncardiac surgery. These guidelines synthesized the data into a comprehensive format and established the concept of integrating the patient's risk with the surgical risk. Nevertheless, there are some weaknesses in the guidelines. We believe that a better understanding of the guideline limitations will allow an improved and more educated practice of its recommendations.

American Heart Association↗
PubMed2006

Prolonged international normalized ratio correlates with a large intravascular fluid balance after major abdominal surgery.

We performed a prospective randomized study of 32 patients who had undergone pancreaticoduodenectomy and did not receive blood during and after surgery. The patients were prospectively assigned to two groups related to fluid balance in the immediate postoperative period. Group 1 (14 patients) were maintained at a positive intravascular fluid balance of 0-1000 mL; Group 2 (18 patients) were maintained at a positive balance of 1000-2000 mL. Complete blood counts and coagulation tests (International Normalized Ratio) and activated partial thromboplastin time (aPTT) were performed at three time points: the day before surgery, on arrival at the postanesthesia care unit, and on leaving the postanesthesia care unit (16 h later). There were significant differences in International Normalized Ratio values between the groups with deterioration during the time they were in the postanesthesia care unit but not in aPTT values. Positive correlation was found between the amount of positive fluid balance and International Normalized Ratio prolongation, but not with aPTT, suggesting that restricted intravascular fluid balance is beneficial for preservation of coagulation after major abdominal surgery.

Aged↗
PubMed2005

Microbubbles: pathophysiology and clinical implications.

Gas embolism is a known complication of various invasive procedures, and its management is well established. The consequence of gas microemboli, microbubbles, is underrecognized and usually overlooked in daily practice. We present the current data regarding the pathophysiology of microemboli and their clinical consequences. Microbubbles originate mainly in extracorporeal lines and devices, such as cardiopulmonary bypass and dialysis machines, but may be endogenous in cases of decompression sickness or mechanical heart valves. Circulating in the blood stream, microbubbles lodge in the capillary bed of various organs, mainly the lungs. The microbubble obstructs blood flow in the capillary, thus causing tissue ischemia, followed by inflammatory response and complement activation. Aggregation of platelets and clot formation occurs as well, leading to further obstruction of microcirculation and tissue damage. In this review, we present evidence of the biological and clinical detrimental effects of microbubbles as demonstrated by studies in animal models and humans, and discuss management of the microbubble problem with regard to detection, prevention, and treatment.

Blood Coagulation↗
PubMed2005

Involvement of nitric oxide in clonidine-induced spinal analgesia.

BACKGROUND: The chronic pain relieving effects following spinal administration of clonidine are probably connected to alpha2-adrenoreceptor-induced augmented synthesis of nitric oxide (NO) in the spinal cord. In contrast, when acute pain is considered, the possible role of NO is still speculative. The aim of the present study was to explore the role of NO in acute pain relief following intraspinal administration of clonidine. METHODS: We used the mouse tail-flick model of acute pain. Spinal injections of the following agents and their combinations were administered: clonidine, L-arginine (NO precursor), the NO production inhibitor nitro-L-arginine-methyl ester (L-NAME), the NO antagonist methylene blue (MB) and nitroglycerine (NO releasing agent). RESULTS: A 95% analgesic response was achieved with 2.0 microg clonidine. L-Arginine produced analgesia, and L-arginine administration followed by clonidine resulted in a pronounced synergistic analgesic effect. This synergistic effect was attenuated by L-NAME. Pre-treatment with MB decreased and nitroglycerine administration did not affect the clonidine-induced analgesia. CONCLUSIONS: NO may be involved in the mediation of the acute pain relieving effects of intraspinally administered clonidine. Further research is warranted to establish the potential benefits and possibility for incorporation of NO promoting agents in therapeutic regional pain regimens.

Acute Disease↗
PubMed2005

Cerebroventricular injection of clonidine causes analgesia mediated by a nitrogen pathway.

Whereas neuroaxially administered clonidine produces analgesia partially mediated by alpha2-adrenoceptor-induced augmented synthesis of nitric oxide (NO), the central mechanisms by which clonidine produces its antinociceptive effects are still speculative. We used the tail-flick model of acute pain in mice to further explore the role of NO in mediating clonidine-induced central analgesia. Cerebroventricular administration of the following agents was studied: clonidine, L-arginine (NO precursor), the NO production inhibitor nitro-L-arginine-methyl ester (L-NAME), the NO antagonist methylene blue (MB), and nitroglycerine (NO-releasing agent). Analgesic response was achieved with clonidine and L-arginine. Simultaneous administration of L-arginine and clonidine produced no additive analgesic effect. Prior administration of L-NAME or MB partially abolished the clonidine-induced analgesic effect, whereas nitroglycerine administration did not affect it. NO may be involved in the mediation of the central antinociceptive effects of clonidine. Further investigation is necessary to determine the possible role of NO-promoting agents in analgesia when co-administered with clonidine.

Acute Disease↗
PubMed2005

Interaction between thiopental and fentanyl in mice is different between hypnotic and lethal doses.

Much is known about the interaction of intravenous anesthetics and opioids at the therapeutic level, but less is known regarding their combined lethal effect, leaving some uncertainty regarding the window of safety for their clinical use. We set out to document the type of interaction between thiopental and fentanyl for both the hypnotic effect (loss of righting reflex) and lethal effect in mice. Hypnotic and lethal dose-response curves were constructed for thiopenthal alone and in combination with fentanyl (0.8 microg/kg, each based on five to seven subgroups of six to ten ICR mice. The dose of fentanyl was that needed to double the lag time to tail flick following a noxious stimulus (the equivalent of human analgesia). While fentanyl did not change the median effective hypnotic dose of thiopental (8.9 mg/kg [95% confidence interval {CI} 8.0-9.9 mg/kg] alone versus 7.8 mg/kg [95% CI 6.7-8.7 mg/kg] in combination), it significantly reduced its median lethal dose from 71.8 mg/kg (95% CI 68.3-74.8 mg/kg) to 64.5 mg/kg (95% CI 63.7-65.2 mg/kg). Most remarkably, it increased the slope of the curve from 0.17 (95% CI 0.10-0.36) to 0.61 (95% CI 0.24-1.10), virtually eliminating the difference between the non-lethal and lethal ranges. We conclude that the type of interaction between thiopental and fentanyl is stronger for the lethal effect than for the hypnotic effect. This may become relevant to clinical situations in humans when higher doses of thiopental are used.

Anesthetics, Intravenous↗
PubMed2005

Single-dose ketamine administration induces apoptosis in neonatal mouse brain.

UNLABELLED: The activity of N-methyl-D-aspartate (NMDA) receptors is critical for neuronal survival in the immature brain. Studies have reported that chronic blockage of these receptors mediates apoptosis in neonatal animals. We investigated the apoptotic effect of a clinically relevant single dose of ketamine, an NMDA receptor antagonist, in the brain of neonatal mice. Seven-day-old ICR mice were injected with ketamine (1.25, 2.5, 5, 10, 20, and 40 mg/kg body weight, subcutaneously in 0.9% NaCl) or with 0.9% NaCl alone as control. Righting reflex testing was performed and mouse brains were examined at 24, 48, and 72 h and 7 days after injection. The number of degenerating neurons was measured using silver staining. Apoptosis was confirmed by DNA fragmentation (terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling). We observed in the sensorimotor cortex and cerebellum of ketamine-treated mice extensive apoptosis, which was clearly dose-dependent and present even after a low dose of ketamine (5 mg/kg). The most prominent apoptotic damage was detected 72 h post-injection (P < 0.001 vs control), at doses ranging from 10 to 40 mg/kg. After 7 d the number of neurodegenerative neurons, at doses ranging from 5 to 40 mg/kg, remained significantly high. The brain weight was comparable to that of untreated control mice and no gross neurobehavioral effects in the righting reflex test or alteration in the pattern of behavior was observed. The results indicate that the administration of ketamine in a clinically relevant single dose triggers long-lasting neuronal apoptosis in certain brain areas of neonatal mice. IMPLICATIONS: The administration of ketamine in a clinically relevant single dose to 7-d-old mice induced apoptosis in the sensorimotor cortex and cerebellum. This effect was dose-dependent and long lasting.

Animals↗
PubMed2004

Thoracic epidural local anesthetics are ineffective in alleviating post-thoracotomy ipsilateral shoulder pain.

OBJECTIVE: This study was conducted to estimate the incidence and clinical predictors of post-thoracotomy shoulder pain and to determine the effectiveness of thoracic epidural block in alleviating this pain. DESIGN: A prospective clinical trial. SETTING: University teaching hospital. PARTICIPANTS AND INTERVENTIONS: Thirty-two adult patients undergoing elective thoracic surgery consented to participate in the study. All operations were open thoracotomies done by the same team of surgeons and anesthesiologists. A thoracic (T6) epidural catheter was placed before induction of general anesthesia. Each patient received 7 mL of lidocaine 2% epidurally and repeated doses of 5 mL of lidocaine 2% every half hour during the operation. Postoperatively, the occurrence of incision or ipsilateral shoulder pain was observed and treated with a maximal dose of 5 mL of lidocaine 2%. If ineffective, indomethacin suppository (nonsteroidal anti-inflammatory drug [NSAID]) was given. Variables such as patient's age, sex, American Society of Anesthesiologists physical status, type, site and duration of surgery, duration of anesthesia, the resection of main bronchus, and the use of thoracostomy tubes were recorded. MEASUREMENTS AND MAIN RESULTS: Postoperatively, 10 patients (31%) had shoulder pain, 4 patients (12.5%) complained of incision pain, and 2 (6.3%) complained of both incision and shoulder pain. A bolus of 5 mL of lidocaine 2% in the epidural catheter relieved incision pain in all the patients, but was ineffective for shoulder pain. Indomethacin suppository was effective in these patients. No correlation was found between any variable and the occurrence of shoulder pain. CONCLUSIONS: It is concluded that post-thoracotomy shoulder pain is a common problem, and the previously mentioned variables did not predict its appearance. Thoracic epidural block is effective in the treatment of incision but not shoulder pain. The NSAID indomethacin suppository was found to be effective for that problem.

Analgesia, Epidural↗
PubMed2004

Retroperitoneal hematoma after spinal anesthesia with the paramedian approach.

UNLABELLED: We present a case of a patient who developed a retroperitoneal bleeding after spinal anesthesia using 22-gauge Quincke needle, with the paramedian approach. Two attempts were needed to accomplish the block. Four hours later the patient complained of back pain radiating to her left calf, with weakness of the quadriceps muscle. Computed tomography revealed a large retroperitoneal hematoma from bleeding lumbar artery. Angiography failed to demonstrate the vessel. The patient was transfused with packed red blood cells and recovered gradually. She had normal coagulation tests throughout the event. IMPLICATIONS: We describe a case of a large retroperitoneal hematoma after the placement of an uneventful spinal block. The patient required four units of packed red blood cells despite having normal coagulation profiles throughout the event. The diagnosis and treatment of retroperitoneal hematoma are discussed.

Amputation, Surgical↗
PubMed2004

Cardiorespiratory parameters during conventional or gasless gynecological laparoscopy under general or regional anesthesia.

BACKGROUND: Conventional laparoscopy is aided by CO2 insufflation, which may impair the cardiorespiratory system and have life-threatening implications. This procedure is conducted under general anesthesia (GA). Gasless laparoscopy supposedly eliminates most of those disadvantages, but is technically more difficult to perform. In the present study, we compared cardiorespiratory parameters of conventional abdominal laparoscopy under GA to gasless laparoscopy under general or epidural anesthesia. MATERIAL/METHODS: This is a prospective study. Twenty four healthy female patients undergoing gynecological laparoscopies lasting <90 min were randomly assigned to one of three groups: group 1, conventional laparoscopy under GA; group 2, gasless laparoscopy under GA; and group 3, gasless laparoscopy under epidural anesthesia. Cardiorespiratory parameters and length of operative, postanesthesia care unit (PACU), and hospitalization periods as well as analgesic requirements in the PACU and complications in the operative and postoperative periods were recorded. RESULTS: No significant differences were detected between groups throughout the operative and postoperative periods, except for a rise in CO2 in group 1 and a lower analgesic requirement in the PACU in group 3. CONCLUSIONS: General and regional anesthesia may be employed in gasless laparoscopy for gynecological surgery.

Adult↗
PubMed2003

Beta-phenylpyruvate and glucose uptake in isolated mouse soleus muscle and cultured C2C12 muscle cells.

Previous investigation demonstrated the potential of beta-phenylpyruvate at high concentration to cause hypoglycemia in mice totally deprived of insulin. For further elucidation of the glucose-lowering mechanism, glucose uptake, and quantity of glucose transporters (GLUT1 and GLUT4) in mouse soleus muscle and C2C12 muscle cell lines were investigated following incubation with beta-phenylpyruvate in various concentrations. A marked enhancement of glucose uptake was demonstrated that peaked at 0.5 and 1.0 mM beta-phenylpyruvate in soleus muscle (P<0.01) and C2C12 cells (P<0.001), respectively. Kinetic analysis in C2C12 cells showed a twofold increase in Vmax compared with controls (P<0.001). In addition, both GLUT1 and GLUT4 levels were increased following exposure to beta-phenylpyruvate. Our findings point to a peripheral hypoglycemic effect of beta-phenylpyruvate.

Animals↗
PubMed2003

beta-Phenylpyruvate induces long-term neurobehavioral damage and brain necrosis in neonatal mice.

Administration of beta-phenylpyruvate at high concentrations reduces blood glucose levels and causes neurophysiological deterioration in insulin-deprived mice. We investigated whether beta-phenylpyruvate administration would cause long-term neurobehavioral and structural central neural damage in mice. Neonatal ICR mice were injected with beta-phenylpyruvate (0.5-2.5mg/g body weight (BW)) or saline (control). Blood glucose was measured. At 43 days of age, the animals were put on a 1-week regimen of restricted water supply, after which the mice were introduced into an eight-arm maze for evaluation of spatial-memory abilities (hippocampal-related behavior). Times for visiting all eight arms and number of entries until completion of the eight-arm visits (maze criteria) were measured. The test was repeated once daily for 5 days. TUNEL assay was used for detection of brain apoptosis. beta-Phenylpyruvate-treated animals (except the 0.5mg/g group) developed hypoglycemia. Treated mice required more time to assimilate the maze structure. Mice treated with 2.5mg/g beta-phenylpyruvate did not meet the maze criteria as compared with control (P<0.001) and suffered from necrotic changes in the hippocampal regions. The above-mentioned neurobehavioral damage was abrogated by coadministration of glucose. We conclude that beta-phenylpyruvate is able to produce necrotic neural damage accompanied by structurally related neurobehavioral dysfunction. Together with its hypoglycemic effect, these findings may explain the neurodegenerative process that occurs in phenylketonuria (PKU), insofar as beta-phenylpyruvate is a metabolite of phenylalanine known to accumulate in vast amounts in this inherited disorder.

Animals↗
PubMed2003

Glucose-lowering effect of beta-phenylpyruvate in neonatal mice: a possible mechanism for phenylketonuria-related neurodegenerative changes.

Following beta-phenylpyruvate injection, mice developed hypoglycemia clinically manifested as tachypnea, tremor, convulsions and death. To further investigate, neonatal mice were injected with beta-phenylpyruvate and their blood glucose determined and brain histology assessed. beta-Phenylpyruvate-injected mice exhibited higher mortality and neurophysiological changes as compared with controls, although without evidence of neural cell death. Accordingly, we hypothesize that the central neural damage in phenylketonuria might be caused by these recurrent beta-phenylpyruvate-induced hypoglycemic events.

Animals↗
PubMed2003

Long-term neurobehavioral and histological damage in brain of mice induced by L-cysteine.

We investigated whether structural central neural damage and long-term neurobehavioral deficits after L-cysteine (L-Cys) administration in mice is caused by hypoglycemia. Neonatal ICR mice were injected subcutaneously with L-Cys (0.5-1.5 mg/g body weight [BW]) or saline (control). Blood glucose was measured. At 50 days of age, mice were introduced individually into an eight-arm maze for evaluation of spatial memory (hippocampal-related behavior). Times for visiting all eight arms and number of entries until completion of the eight-arm visits (maze criteria) were measured. The test was repeated once daily for 5 days. In situ terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) assay was used for detection of brain damage. As early as 20 min and up to 2 h postinjection, animals treated with L-Cys doses higher than 1.2 mg/g BW developed hypoglycemia and looked ill. Several animals convulsed. Long-term survivors required more time, in a dose-dependent manner, to assimilate the structure of the maze, and animals treated with L-Cys (1.5 mg/g BW) exhibited TUNEL-positive changes in the hippocampal regions. All these changes were reversible by coadministration of glucose. We conclude that L-Cys injection can cause pronounced hypoglycemia associated with long-term neurobehavioral changes and central neural damage in mice. Since L-Cys is chemically different from the other excitatory amino acids (glutamate and aspartate), the long-reported L-Cys-mediated neurotoxicity may be connected to its hypoglycemic effect.

Animals↗
PubMed2003

L-cysteine increases glucose uptake in mouse soleus muscle and SH-SY5Y cells.

Previous investigation demonstrated the potential of L-cysteine (L-Cys) at high concentrations to cause hypoglycemia in mice totally deprived of insulin. For further elucidation of the glucose-lowering mechanism, glucose uptake and quantity of glucose transporters (GLUTs 3 and 4) in mouse soleus muscle and C2C12 muscle cells, as well as in human SH-SY5Y neuroblastoma cells, were investigated. A marked enhancement of glucose uptake was demonstrated, peaking at 5.0 mM L-Cys in soleus muscle (P < 0.05) and SH-SY5Y cells (P < 0.001), respectively. In contrast, glucose uptake was not affected in the C2C12 muscle cells. Kinetic analysis of the SH-SY5Y glucose uptake showed a 2.5-fold increase in maximum transport velocity compared with controls (P < 0.001). In addition, both GLUT3 and GLUT4 levels were increased following exposure to L-Cys. Our findings point to a possible hypoglycemic effect of L-Cys.

Animals↗