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Featured researches published by S. Cotev.


Journal of Cerebral Blood Flow and Metabolism | 1987

Head Injury Induces Increased Prostaglandin Synthesis in Rat Brain

Esther Shohami; Y. Shapira; A. Sidi; S. Cotev

Head injury was induced in the left hemisphere of rats, The rats were killed at various time intervals after trauma (immediately, 15 min, 1 and 18 h, and 4 and 10 days), and the rates of synthesis and release of prostaglandin PGE2, 6-keto-PGF1α, and thromboxane TXB2 from cortical slices of both hemispheres were studied. The rate of synthesis of PGE2 after 18 h was six and four times higher than control in the contused and contralateral hemispheres, respectively. By 10 days posttrauma, both hemispheres had normal rate of PGE2 release. TXB2 and 6-keto-PGF1α synthetases were affected already 15 min after the injury, and a similarly elevated rate of synthesis was found in both hemispheres. The maximal effect was detected after 1 or 18 h with return to normal after 4 or 10 days for TXB2, and 6-keto-PGF1α, respectively. Tissue specific gravity was determined for both hemispheres using linear gradient columns. The results of these determinations indicate that development of edema occurs in the contused hemisphere as early as 15 min post trauma; it reaches its maximal level at 18 h and returns to normal at 10 days. Arterial pressure was monitored, and a transient increase was found at 10 min post trauma. We suggest that the production of edema after brain injury may be related to the increased rate of PGE2 and PGI2 synthesis, which occurs at similar time intervals after injury.


Neurological Research | 1989

Accumulation of calcium in the brain following head trauma.

Y. Shapira; G. Yadid; S. Cotev; Esther Shohami

Previous studies have reported accumulation of calcium (Ca) in brain tissue of injured or ischaemic experimental animals. In the present study, head trauma (HT) was induced in the left hemisphere of rats which were subsequently sacrificed 15 min, 1, 2, 4, 24 or 48 h later. Their brains were analysed for oedema formation by the determination of specific gravity (SG), using linear gradient columns, and water content, by dry to wet weight ratio. Total tissue Ca content was measured by atomic absorption spectroscopy. These values, in both the injured and contralateral hemispheres were compared with values obtained from sham-operated rats. Specific gravity of the contused hemisphere was lower than that of the contralateral hemisphere or sham and its water content was higher, at all time points studied. Calcium content was significantly higher in the contused grey matter at 1 h, and in the grey and white matter of both hemispheres at 24 and 48 h after HT. Statistical analysis revealed excellent correlation (cc = 0.65, p less than 0.001) between Ca levels and water content in the grey matter, whenever Ca concentrations were elevated (1, 24 and 48 h). These findings suggest that in the late phase of the post-HT period, Ca accumulation might play a role, along with other mediators, in the development of brain oedema after HT.


Neurosurgery | 1988

Experimental Closed Head Injury in Rats: Prostaglandin Production in a Noninjured Zone

Esther Shohami; Yoram Shapira; S. Cotev

&NA; In a model of closed head injury in rats, a calibrated weight drop device was allowed to fall onto the skulls convexity over the left hemisphere 1 to 2 mm lateral from the midline. Prostaglandin (PG) levels were determined in the frontal cortex region remote from the site of injury where no macroscopic damage could be seen. Differential patterns of temporal changes were evident for PGE2, PGD2, thromboxane (TX) B2, and 6‐keto‐PGF1&agr; in the contused hemisphere, but no changes were found in the contralateral hemisphere. The major changes in PG levels were increased levels of PGD2 and 6‐keto‐PGF1&agr; that persisted from 18 hours until 10 days after injury. The ratio between TXB2 and 6‐keto‐PGF1&agr;, which reflects the vascular tone, increased during the early postinjury period (15 minutes and 1 hour) and decreased later, up to 10 days. Thus, a sustained imbalance in favor of the vasodilator is apparent; this may suggest an improved blood supply to the region. Both PGD2 and PGI2 have protective effects in the brain. We suggest that their endogenous increase may be part of a repair mechanism at the periphery of the injured zone.


Journal of Cerebral Blood Flow and Metabolism | 1988

Dexamethasone and Indomethacin Do Not Affect Brain Edema following Head Injury in Rats

Yoram Shapira; E. Davidson; Y. Weidenfeld; S. Cotev; Esther Shohami

Head trauma was induced in rats by a weight-drop device, falling over the exposed skull over the left hemisphere. The neurological state of the rats was evaluated by a neurological severity score at 1 h and 18 h post head trauma. At 18 h post head trauma, rats were decapitated and tissue from the vicinity of the injury and from a corresponding area in the contralateral hemisphere was taken for specific gravity (SG) determination using linear gradient columns. Slices were taken from the same sites for incubation in Krebs-Ringer solution, and the concentrations of prostaglandin (PG)E2, 6-keto-PGF1α, and thromboxane B2 accumulated in the medium during 1 h were measured by radioimmunoassay. In one experimental group, rats were pretreated with intraperitoneal dexamethasone sodium phosphate (4 mg/kg) 18 and 2 h before head trauma, and a third dose was given 8 h post head trauma. Another group was treated with intraperitoneal indomethacin (10 mg/kg) 1 h before and 7 h after head trauma. Other groups were treated immediately and 8 h after head trauma with 4, 8, 15, or 30 mg/kg of dexamethasone sodium phosphate. Another group of rats was treated with free dexamethasone (10 mg/kg) right after head trauma and 8 h later. Head trauma induced edema, as expressed by decreased SG, in the left hemisphere of all traumatized rats. Neither treatment protocol affected the neurological severity score of the injured rats or the SG of the contused hemisphere. PG synthesis, on the other hand, was significantly reduced following indomethacin or free dexamethasone, both in sham and traumatized rats, but not in dexamethasone sodium phosphate–treated rats. We conclude that pretreatment with indomethacin, dexamethasone sodium phosphate, or dexamathasone, used in the present protocols, does not affect posttraumatic cerebral edema. Thus, the role of PGs as mediators of edema formation remains unclear.


Critical Care Medicine | 1981

Persistent nonketotic hyperglycemia as a grave prognostic sign in head-injured patients.

Merguerian Pa; Azriel Perel; Uri Wald; Moshe Feinsod; S. Cotev

The authors studied 86 consecutive patients admitted to the ICU after severe head trauma. Of these, 19 nondiabetic patients developed persistent nonketotic hyperglycemia (NKH), defined as plasma glucose greater than 270 mg/dl (15 mM/L), 1.7 ± 1.1 (SD) days after injury. When NKH occurred, all patients were in very deep coma (Glasgow Coma Scale score 3), and when intracranial pressure (ICP) was measured (12 patients), its mean value was 59.8 ± 20.4 mm Hg. Although 11 of 19 patients had associated diabetes insipidus (DI), NKH was not related to increased fluid and glucose loading. All patients with NKH died (mean time of survival after NKH was 2.1 ± 1.4 days) in contrast to a 17.1% early mortality rate in patients with severe head injury without NKH. The authors could not show a direct correlation between the height of ICP and the level of blood glucose.


Journal of Cardiothoracic and Vascular Anesthesia | 1993

Perioperative Myocardial Ischemia in Carotid Endarterectomy Under Cervical Plexus Block and Prophylactic Nitroglycerin Infusion

Giora Landesberg; Jacob Erel; Haim Anner; Leonid A. Eidelman; Eran Weinmann; Myron H. Luria; Dan Admon; Jacob Assaf; Dan Sapoznikov; Yacov Berlatzky; S. Cotev

Perioperative myocardial ischemia was evaluated in 36 consecutive carotid endarterectomy procedures carried out on patients with a high (72.2%) prevalence of ischemic heart disease. The procedures were performed under cervical plexus block plus a prophylactic intravenous nitroglycerin infusion. Findings of myocardial ischemia on perioperative (48 hours) continuous electrocardiogram recordings were correlated with preoperative cardiac status, perioperative continuous intra-arterial blood pressure measurements, and postoperative cardiac outcome. In two patients, ST segment analysis was un-interpretable because of bundle-branch blocks. Altogether, 64 episodes of significant ST segment depression were detected in 18 (52.9%) of the remaining procedures. In 8 (23.5%) procedures, ST segment depressions occurred either during carotid artery clamping at the time of the largest rise in blood pressure or within 2 hours of declamping, when blood pressure tended to decline. There were four (11.7%) postoperative cardiac events: three myocardial infarctions (one Q wave and two non-Q wave) and one episode of unstable angina pectoris. All four patients with cardiac events had early signs of myocardial ischemia either at the time of cross-clamping, or soon after declamping of the carotid artery. All myocardial infarctions developed following prolonged (> 10 hours) myocardial ischemia, starting with the first 20 hours after surgery. Thus, ST segment depression occurring during clamping or soon after carotid declamping was associated with cardiac complications (sensitivity 100% and specificity 86.6%) and suggests the possible usefulness of on-line ST segment trend monitoring.


Intensive Care Medicine | 1983

The use of continuous flow of oxygen and PEEP during apnea in the diagnosis of brain death.

Azriel Perel; M. Berger; S. Cotev

The establishment of apnea for the diagnosis of brain death by disconnecting the patient from the ventilator may lead to dangerous hypoxemia at the end of the test period. We established apnea for 4 min in 8 patients with suspected brain death, both by disconnecting them from the ventilator after 10 min ventilation with FIO2=1.0 (method “A”), and by leaving them attached to an IMV ventilator circuit with a continuous flow of 100% O2 and PEEP of 4–8 cm H2O without mechanical ventilation (method “B”). PaO2 decreased during the apneic period by 143 ±65 (SD) mmHg using method “A”, and by 48±28 mmHg using method “B” (p<0.002). The changes in PaCO2 and pH were similar following both apneic methods.We conclude that it is safer to test for apnea by leaving the patients on a continuous flow of 100% oxygen and low PEEP than to disconnect them from the ventilator.


Canadian Journal of Anaesthesia-journal Canadien D Anesthesie | 1997

Continuous spinal anaesthesia using a standard epidural set for extracorporeal shockwave lithotripsy

Ze’ev Shenkman; Leonid A. Eidelman; S. Cotev

PurposeContinuous spinal anaesthesia (CSA) offers considerable advantages over “single shot” spinal or epidural anaesthesia since it allows titration of anaesthesia using small doses of local anaesthetics (LA). We evaluated the feasibility of CSA using a standard epidural set for extracorporeal shockwave lithotnpsy (ESWL).MethodsCharts of 100 consecutive CSAs for ESWL were retrospectively reviewed. Lumbar CSA was performed using a 20G epidural catheter through an 18G Tuohy needle. The CSA was preplanned, or followed inadvertent dural puncture. Small LA boluses were injected to achieve the desired sensory level of anaesthesia. Demographic data, anaesthetic duration, LA doses, the most cephalad sensory level to pinprick, arterial blood pressure, heart rate, use of systemic sympathomimetics and complications were recorded.ResultsMean age was 66.2 ± 9.9 (SD). The ASA status was III–IV in 54.1 % and 5.5% of the preplanned and inadvertent patients, respectively. In 85 anaesthetics, hyperbanc bupivacaine 0.1% (9.7 ± 7.5 mg) was used as the sole anaesthetic. Sensory level was T4-T8. Maximal decrease in systolic and diastolic blood pressures and heart rate was 19.0 ± 9.8%, 13.4 ± 13.3%, and 7.2 ± 11.7 respectively. Intravenous sympathomimetics were used in nine of 82 (11.0%) preplanned, and in six of 18 (33.3%) inadvertent anaesthetics. Post dural puncture headache appeared following two of 82 (2.5%) preplanned, and four of 18 (22.2%) inadvertent anaesthetics. No postanaesthetic neurological deficit was detected.ConclusionContinuous spinal anaesthesia, using a standard epidural set and hyperbaric bupivacaine is feasible for ESWL in high risk patients. Inadvertent dural puncture does not preclude CSA under these circumstances.RésuméObjectifParce qu’elle permet de trtrer l’anesthesie avec des doses minimes d’anésthesique local (AL), la rachianesthésie continue (RAC) offre des avantages considérables sur la rachianesthésie et l’épidurale à injection unique. Nous avons recherché s’il était possible d’administrer la RAC avec un plateau épidural standard pour la lithotnpsie extracorporelle par ondes de choc (LEOC).MéthodesL’étude a consiste à revoir rétrospectivement les dossiers de 100 interventions de LEOC consécutives. La rachianesthésie lombaire était réalisée avec un cathéter épidural 20G introduit à travers une Tuohy 18G. La RAC faisart partie de la planification originale ou suivait une ponction accidentelle de la dure-mère. Le niveau sensoriel d’anesthésie désiré étart atteint par l’injection de petits bolus d’AL. Les données démographiques, la durée de l’anesthésie, les doses d’AL, le niveau céphalique maximal déterminé par piqûre. la pression artérielle, la fréquence cardiaque, l’utilisation de sympathicomimétiques et les complications ont été enregistrées.ResultatsL’âge moyen était 66,2 ± 9,9 (ÉT). Le pourcentage d’état physique ASA III-IV representart 54, 1% des patients prévus et de 5,5% chez les patients imprévus. Quatre-vingt-dnq patients n’ont reçu que de la bupivacaïne hyperbare à 0,1 % (9,7 ± 7,5 mg). Le niveau sensoriel atteint se situait entre T4 et T8. Les chutes maximales des pressions systolique et diastolique et de la fréquence cardiaque étaient de 19 ± 9,8%, 13,4 ± 13,3% et 7,2 ± 11,7 bpm. Il a fallu administrer des sympathicomimétiques intraveineux à 9 des 82 (11,0%) des patients prévus et à six des 18 (33,3%) des imprévus. Une céphalée postrachianesthésie s’est manifestée après 2 des 82 (2,5%) RAC prévues et quatre de 18 (22,2%) imprévues. Il n’y a pas eu de déficit neurologique.ConclusionIl est possible d’administrer une rachianesthésie continue avec un plateau épidural standard et de la bupivacaïne hyperbare pour la LEOC chez des patients à haut risque. Une ponction accidentelle de la duremère n’exclut pas la RAC dans ces circonstances.


Critical Care Medicine | 1976

The effect of PEEP on oxygenating capacity in acute respiratory failure with sepsis.

S. Cotev; Azriel Perel; Ruth Katzenelson; Dan Eimerl

We report an evaluation of the effect of positive-end-expiratory-pressure (PEEP) on improving pulmonary oxygenating capacity in the adult respiratory distress syndrome (ARDS), when the latter is associated with generalized gram-negative sepsis. Fifty-seven cases treated in our RICU with PEEP ventilation (April 1972 to January 1975) were retrospectively reviewed. Oxygenating capacity improvement was evaluated in terms of the changes in Pao2/Fio2 and AaDO2 (Fio2 = 1.0). Both the short term (2–3 hours from the initiation of PEEP) and the overall effects of PEEP were evaluated.A mean PEEP of 5.6 cm H2O initially increased Pao2/Fio2 by a mean of 94 torr and decreased AaDO2 (Fio2 = 1.0) by 105 torr in the 28 nonseptic patients. In the 29 septic patients, 5.1 cm H2O PEEP initially increased Pao2/Fio2 by 32 torr and decreased AaDO2 (Fio2 = 1.0) by 38 torr. The differences between the septic and nonseptic patients were statistically significant (P < 0.001). Likewise, the long-term effect of similar levels of PEEP was in increasing Pao2/Fio2 by 142 torr and by 75 torr in the nonseptic and septic patients, respectively. The final reduction in AaDO2 (Fio2 = 1.0) was 163 torr and 87 torr in the nonseptic and septic patients, respectively. These differences between patient groups were also statistically significant (P < 0.02).Mortality during PEEP was 15/29 and 3/28 in the septic and nonseptic patients, respectively. Overall mortality in the septic and nonseptic groups was 18/29 and 5/28, respectively.We conclude that ARDS with sepsis constitutes a more severe pulmonary insult than ARDS without sepsis, and/or that generalized sepsis creates a more prolonged pulmonary insult that makes it less amenable to PEEP. Thus, high levels of PEEP may be needed to treat ARDS associated with sepsis.


Canadian Journal of Anaesthesia-journal Canadien D Anesthesie | 1995

Patient data management systems in anaesthesia: an emerging technology

Yoram G. Weiss; S. Cotev; Benjamin Drenger; R. Katzenelson

The purpose of this review is to define the expectations of an on-line automatic patient data management system (PDMS) into anaesthesia work-stations in and around the operating room suite. These expectations are based on review of available information in the medical literature, and trials of several systems that are available commercially, three of them in a more detailed fashion (i.e. Informatics®, Datex® and North American Drager®). The ideal PDMS should:- communicate with and capture the information from different monitors, anaesthesia machines and electronic gadgets (e.g., infusion pumps) used in the operating room (OR), while presenting selected relevant values and trends on a screen.- inform the anaesthetist of deviations from preselected limits of physiological and technical values. In the future, the system will hopefully be upgraded to include an algorithm-based decision support system.- communicate with the hospital mainframe computer, and automatically transfer demographic data, laboratory and imaging results, and records obtained during preoperative consultations.- at the end of each anaesthetic procedure, create an anaesthetic record with relevant data automatically collected by the system, as well as that which was entered manually by the physician during the procedure. A copy of this anaesthesia file must be kept on a computerized archive system. None of the systems so far evaluated fulfilled all our expectations. We have therefore adopted an approach for the gradual introduction of such a system into our OR environment over the next two to five years, during which expected improvements may be incorporated to upgrade the system.RésuméCette présentation vise à déterminer s’il est possible de recueiller avec un seul ordinateur et de rassembler automatiquement toutes les données médicales fournies par les systèmes accessibles à notre poste de travail du bloc opératoire (système de gestion des données médicales: SGDM). Notre approche est basée sur des informations extraites de la littérature médicale à partir de plusieurs systèmes déjà commercialisés. Trois d’entre eux ont été plus particulièrement étudiés (Informatics®, Datex® et North American Drager®). Le SGDM devrait:- capter et communiquer les renseignements obtenus de moniteurs et appareils utilisés en salle d’opération pour l’anesthésie, tout en affichant les chiffres et tendances sur un écran.- avertir l’anesthésiste de toute donnée anormale. A l’avenir, on devrait être en mesure à partir des données recueillies et d’un algorithme de créer un système qui permettra à l’anesthésiste de prendre des décisions.- pouvoir communiquer avec l’ordinateur central de l’hôpital et transmettre automatiquement les données démographiques, les résultats de laboratoires et les dossiers de la visite préopératoires.- A la fin de chaque opération, constituer un dossier comprenant les paramètres spécifiques à l’anesthésie recueillies automatiquement par le système ainsi que ceux que le médecin a introduits pendant l’intervention; une copie de ce dossier serait conservée dans des archives informatisées. Aucun des systèmes évalués ne remplit les conditions de notre SGDM. Les auteurs annoncent leur décision d’introduire ce système graduellement dans nos blocs opératoires en deux à cinq ans.

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J.T. Davidson

Hebrew University of Jerusalem

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Esther Shohami

Hebrew University of Jerusalem

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Azriel Perel

Hebrew University of Jerusalem

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Y. Shapira

Hebrew University of Jerusalem

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G. Yadid

Hebrew University of Jerusalem

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Leonid A. Eidelman

Hebrew University of Jerusalem

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R. Katzenelson

Hebrew University of Jerusalem

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Yoram Shapira

Hebrew University of Jerusalem

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A. Perel

Hebrew University of Jerusalem

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A. Sidi

Hebrew University of Jerusalem

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