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Biomedical subjects

L Roytblat

Publications and source records attributed to L Roytblat.

15 recordsLinked to original sources
PubMed2000

Raised interleukin-6 levels in obese patients.

OBJECTIVE: Obese patients demonstrate a variety of biochemical, metabolic, and pulmonary abnormalities. Inflammatory mediators such as tumor necrosis factor-alpha and interleukin-6 (IL-6) may have a direct effect on glucose and lipid metabolism. Hypoxemia in itself induces release of IL-6. The aim of this study was to examine the relationship between IL-6 levels in healthy volunteers (control group) and three different groups of obese patients: patients without obstructive sleep apnea syndrome (OSAS), patients with OSAS, and patients with obesity hypoventilation syndrome (OHS) (daytime baseline oxygen saturation of <93%). RESEARCH METHODS AND PROCEDURES: We measured serum IL-6 levels in 25 obese patients (body mass index of >35 kg/m2) and 12 healthy women. RESULTS: The results demonstrate statistically significant differences in serum IL-6 levels between the control group (1.28 +/- 0.85 pg/mL) and obese patients without OSAS (7.69 +/- 5.06 pg/mL, p < 0.05) and with OSAS (5.58 +/- 0.37 pg/mL, p < 0.0005). In the patients with OHS, IL-6 concentrations were highest (43.13 +/- 24.27 pg/mL). DISCUSSION: We conclude that serum IL-6 is increased in obese patients. The highest IL-6 levels were found in the patients with OHS.

Adult↗
PubMed2000

NPS 1506: a novel NMDA receptor antagonist: neuroprotective effects in a model of closed head trauma in rats.

We examined whether NPS 1506, a novel uncompetitive N-methyl-D-aspartate receptor antagonist, influences neurological outcome following closed head trauma (CHT) in rats. One hundred ten rats were divided into 11 groups: CHT (yes/no), treatment with NPS 1506 (yes/no), and time of euthanization (24 h/48 h). The dose of NPS 1506 was 1 mg/kg IV at 1 and 4 hours following CHT or sham operation. Closed head trauma induced the following changes in the injured hemisphere: Decreased specific gravity (sg) (1.036 +/- 0.006) and magnesium (Mg) (0.042 +/- 0.005 microg/mg) at 24 hours, and potassium (K) at 24 (1.145 +/- 0.376 microg/mg) and 48 hours, and increased water content (W) (84.9 +/- 2.5%) and sodium (Na) (2.135 +/- 0.699 microg/mg) at 24 hours, and calcium (Ca) at 24 (0.543 +/- 0.157 microg/mg) and 48 hours. These were reversed by NPS 1506; sg of 1.043 +/- 0.004, Mg of 0.077 +/- 0.009 microg/mg, K of 1.930 +/- 0.238 microg/mg, W of 81.5 +/- 1.9%, Ca of 0.043 +/- 0.023 microg/mg, and Na of 0.688 +/- 0.110 microg/mg. In groups not given NPS 1506, a nonsignificant decrease in neurological severity score (NSS) occurred at 24 and 48 hours as compared to NSS at 1 hour after CHT. In groups given NPS 1506, NSS at 24 and 48 hours decreased significantly (improved) compared to NSS at 1 hour, but not compared to NSS at 24 and 48 hours in groups not given NPS 1506. NPS 1506 caused no significant change in ischemic tissue volume or hemorrhagic necrosis volume in the injured hemisphere at 24 hours or 48 hours. These findings indicate that NPS 1506 improved measures of brain tissue edema (at 24 hours but not at 48 hours) and ion homeostasis, and this improvement was not related to other measures of outcome.

Animals↗
PubMed1999

Treatments to support blood pressure increases bleeding and/or decreases survival in a rat model of closed head trauma combined with uncontrolled hemorrhage.

UNLABELLED: Hemorrhagic hypotension may aggravate the detrimental effects of head trauma on neurologic outcome. Our study examined whether using phenylephrine or large volumes of saline IV to increase mean arterial blood pressure (MAP) to 70, 80, or 90 mm Hg during the combination of head trauma and uncontrolled hemorrhage would improve neurologic outcome. Rats were assigned to one of 17 groups. In Groups 1-5, the variables were head trauma (yes/no), hemorrhage (yes/no), 0 or 3 mL saline per milliliter of blood lost, and no target MAP. In Groups 6-11, hemorrhage was or was not combined with head trauma, and large volumes of saline were given IV to achieve target MAPs of 70, 80, or 90 mm Hg. Groups 12-17 were similar to Groups 6-11 except that phenylephrine was used rather than saline to achieve target MAPs. Saline increased blood loss at 2 h to approximately 16 and 25 mL at a MAP of 80 and 90 mm Hg respectively, increased (worsened) the neurodeficit score but not cerebral edema at 24 h, and decreased survival rate at 2 and 24 h. Because phenylephrine was fatal for 62 of 63 rats, group mean values for blood loss, neurodeficit score, and brain tissue specific gravity could not be calculated. We conclude that supporting MAP with either phenylephrine or large volumes of saline worsened the neurodeficit score and/or survival and did not affect cerebral edema formation in our rat model of head trauma combined with hemorrhage. IMPLICATIONS: The results of this study indicate that maintaining mean arterial blood pressure at 70, 80, or 90 mm Hg with either phenylephrine or large volumes of saline worsened the neurodeficit score and/or survival and did not affect cerebral edema formation in our rat model of head trauma combined with hemorrhage.

Analysis of Variance↗
PubMed1999

Albumin or hetastarch improves neurological outcome and decreases volume of brain tissue necrosis but not brain edema following closed-head trauma in rats.

The present study examined whether hemodilution with 20% human serum albumin (HSA) or 10% hydroxyethyl starch (HES) improved the outcome from closed-head trauma (CHT) in rats. Rats anesthetized with halothane were given one of three hemodilution solutions (i.e., 20% HSA, 10% HES, or control [0.9% saline]) after CHT or sham surgery. CHT was delivered using a weight drop impact of 0.5 J onto the closed cranium. The hemodilution solution (volume = 1% of body weight) was given just after determining the neurological severity score (NSS) at 1 hour following CHT. The NSS was determined again at 24, 48, and 72 hours following CHT. At 72 hours, brains were removed, and brain edema and brain tissue necrosis volume were determined. Solutions of 20% HSA and 10% HES significantly improved brain tissue necrosis volume (143 +/- 72 mm3 and 104 +/- 53 mm3 as compared to 271 +/- 65 mm3 in controls, mean +/- SD) and NSS (12 +/- 2 and 9 +/- 2 as compared to 15 +/- 2 in controls at 72 hours, median +/- range) but not brain edema. The hematocrit decreased similarly in all groups during hemodilution. Hemodilution with 20% HSA and 10% HES following CHT in rats did not decrease brain edema but did decrease brain tissue necrosis volume and NSS (improved neurological function), suggesting that the beneficial effect of hemodilution resulted not from decreased edema formation but rather from effects not measured in this study such as improved perfusion of the salvageable brain tissue surrounding the core injury.

Animals↗
PubMed1998

Ketamine attenuates the interleukin-6 response after cardiopulmonary bypass.

UNLABELLED: Cardiopulmonary bypass (CPB) has been proposed as a model for studying the inflammatory cascade associated with the systemic inflammatory response syndrome. Serum interleukin-6 (IL-6) concentration seems to be a good indicator of activation of the inflammatory cascade and predictor of subsequent organ dysfunction and death. Prolonged increases of circulating IL-6 are associated with morbidity and mortality after cardiac operations. In the present study, we compared the effects of adding ketamine 0.25 mg/kg to general anesthesia on serum IL-6 levels during and after elective coronary artery bypass grafting (CABG). Thirty-one patients undergoing elective CABG were randomized to one of two groups and prospectively studied in a double-blind manner. The patients received either ketamine 0.25 mg/kg or a similar volume of isotonic sodium chloride solution in addition to large-dose fentanyl anesthesia. Blood samples for analysis of serum IL-6 levels were drawn before the operation; after CPB; 4, 24, and 48 h after surgery; and daily for 6 days beginning the third day postoperatively. Ketamine suppressed the serum IL-6 response immediately after CPB and 4, 24, and 48 h postoperatively (P < 0.05). During the first 7 days after surgery, the serum IL-6 levels in the ketamine group were significantly lower than those in the control group (P < 0.05). On Day 8 after surgery, IL-6 levels were no different from baseline values in both groups. A single dose of ketamine 0.25 mg/kg administered before CPB suppresses the increase of serum IL-6 during and after CABG. IMPLICATIONS: In this randomized, double-blind, prospective study of patients during and after coronary artery bypass surgery, we examined whether small-dose ketamine added to general anesthesia before cardiopulmonary bypass suppresses the increase of the serum interleukin-6 (IL-6) concentration. Serum IL-6 levels correlate with the patient's clinical course during and after coronary artery bypass. Ketamine suppresses the increase of serum IL-6 during and after coronary artery bypass surgery.

Aged↗
PubMed1998

Phenylephrine-induced hypertension does not improve outcome after closed head trauma in rats.

UNLABELLED: Phenylephrine-induced hypertension (increase of 30-35 mm Hg for 15 min) is reported to increase cerebral perfusion pressure and collateral flow to ischemic areas of the brain in a rat model of focal cerebral ischemia. In the present study, we examined whether phenylephrine-induced hypertension of similar magnitude and duration was beneficial in a rat model of closed head trauma (CHT). Forty-eight rats were randomized into four experimental conditions: CHT at time 0 min (yes/no), plus phenylephrine-induced hypertension (increase of 30-35 mm Hg for 15 min) at 65 min (yes/no). CHT was delivered using a weight-drop device (0.5 J). Outcome measures were neurological severity score (NSS) at 1, 4, and 24 h, and brain tissue specific gravity (microgravimetry) and injury volume (2,3,5-triphenyltetrazoium chloride) at 24 h. After CHT, NSS at 24 h (median +/- range) and brain tissue specific gravity (mean +/- SD, injured hemisphere) were 7+/-2 and 1.033+/-0.007 without phenylephrine and 8+/-2 and 1.035+/-0.005 with phenylephrine (P = 0.43), respectively. Tissue injury volume (mean +/- SD) was 335+/-92 mm3 without phenylephrine and 357+/-154 mm3 with phenylephrine (P > 0.62). The results of our study indicate that postinjury treatment with 15 min of phenylephrine-induced hypertension does not attenuate brain edema, reduce tissue injury volume, or improve neurological outcome after CHT in rats. IMPLICATIONS: Phenylephrine-induced hypertension is reported to increase cerebral perfusion pressure and blood flow in a rat model of focal cerebral ischemia. In our study, phenylephrine-induced hypertension did not decrease brain edema or tissue injury volume or improve neurological outcome in a rat model of closed head trauma.

Animals↗
PubMed1993

Postoperative pain: the effect of low-dose ketamine in addition to general anesthesia.

In a randomized, double-blind study, postoperative pain was assessed in 22 patients undergoing elective open cholecystectomy with two types of anesthesia: standardized general anesthesia (control group), and low-dose ketamine as an addition to the same method of general anesthesia, before surgical incision (ketamine group). After the operation we found that the time from the end of surgery to the first request for analgesic was longer in the ketamine group. Postoperatively, patients in both groups were treated with patient-controlled analgesia (PCA) in exactly the same way. The major difference in the study was the reduced dose requirement of morphine in the ketamine group compared with the control group after the operation. The mean dose of morphine given in patients of the control group during the first 24 h was 48.7 mg vs 29.5 mg in the ketamine group. Mean visual analog scale (VAS) and verbal rating scale (VRS) were higher in patients in the control group during the first 5 h after surgery (P < 0.02), but between 5 and 24 h after surgery VAS and VRS were not significantly different (P > 0.05). Our results indicate that postoperative pain can be decreased when ketamine in low doses is added to general anesthesia before surgical stimulation.

Adult↗
PubMed1992

Anaesthetic interaction between thiopentone and ketamine.

The anaesthetic effect of thiopentone, ketamine and their combinations were studied in 150 patients of ASA Grades I and II. The ability to open eyes on command and purposeful motor response to noxious pressure on the trapezius muscle were used as endpoints of anaesthesia. Dose-response curves for thiopentone, ketamine and their combinations were determined with a probit procedure and compared with isobolographic analysis. The interaction between thiopentone and ketamine was found to be additive for both endpoints of anaesthesia.

Adult↗
PubMed1991

H1 and H2 receptor antagonists and hepatic oxygen supply-demand relationship in pigs.

The hypothesis that histamine receptor (H1 and H2) blockade beneficially affects the hepatic oxygen supply-demand relationship was tested during experiments performed on 13 miniature pigs. Hepatic arterial and portal blood flows were measured with electromagnetic flowmeters. Cardiac output was determined by thermodilution. H1 and H2 receptor blockade was achieved with promethazine, 5 mg.kg-1 and cimetidine 30 mg.kg-1 IV, respectively. The study demonstrated no significant effect of H1 and H2 receptor blockade on hepatic oxygen uptake and no noticeable effects of cimetidine on hepatic circulation. However, promethazine decreased total hepatic blood flow, primarily by decreasing portal blood flow; this resulted in an increase in oxygen extraction as reflected in a decreased oxygen content in hepatic venous blood. The results reject the posed hypothesis: H1 receptor antagonist promethazine decreased, while H2 receptor antagonist cimetidine did not affect hepatic blood flow and oxygen supply; hepatic oxygen demand remained unaffected during H1 and H2 receptor blockade.

Animals↗
PubMed1991

Humoral factors and hemodynamics during cross-clamping of the thoracic aorta.

The present study was designed to test the hypothesis that vasoactive compounds produced in the ischemic part of the body below an occluded aorta are responsible for the hemodynamic changes observed during cross-clamping of the thoracic aorta. The experiments were performed on 32 rabbits anesthetized with halothane that underwent experiments with cross-circulation; the blood from the inferior caval veins of rabbits A was pumped into the inferior caval veins of rabbits B. Simultaneously, exactly the same amount of blood was pumped from the jugular vein of rabbits B into the jugular vein of rabbits A. The aorta and inferior vena cava were exposed and then simultaneously cross-clamped directly below the diaphragm. The cross-clamping of the aorta and inferior vena cava in rabbits A was associated with a 29% to 44% increase in mean arterial pressure in rabbits B. The experiments support the hypothesis and suggest that endogenously produced humoral factors are responsible for at least one third to one half of the arterial hypertension that usually develops during aortic cross-clamping.

Anesthesia, Inhalation↗
PubMed1990

Dopamine and hepatic oxygen supply-demand relationship.

The present study examined the effect of small, vasodilating doses of dopamine on the hepatic oxygen supply--uptake ratio. Thirteen miniature pigs weighing 18-27 kg were studied under sodium pentobarbital anesthesia. Hepatic arterial and portal blood flows were measured. Oxygen content in arterial, portal, and hepatic venous blood was determined. Dopamine was infused in doses of 5, 10, and 15 micrograms.kg-1.min-1. Dopamine infusion was associated with a dose-related increase in hepatic oxygen uptake and a dose-independent increase in hepatic oxygen delivery with a maximal increase (30%) in the hepatic oxygen delivery at 10 micrograms.kg-1.min-1. The hepatic oxygen delivery--uptake ratio remained unchanged during dopamine infusion in doses of 5 and 10 micrograms.kg-1.min-1 and significantly decreased during the dose of 15 micrograms.kg-1.min-1. The study demonstrated that an increase in cardiac output and hepatic oxygen delivery during dopamine administration was not associated with an improvement in hepatic oxygen supply--demand relationship since hepatic oxygen uptake also increased.

Animals↗
PubMed1986

Seizures after pentazocine overdose.

A patient with seizures, coma and respiratory depression after pentazocine overdose was treated successfully with naloxone and artificial ventilation. Pentazocine is an antagonist of the mu opioid receptors and a partial agonist of the kappa and sigma receptors. Because naloxone has less affinity for kappa and sigma receptors than for mu receptors, larger doses of naloxone are frequently required in the treatment of pentazocine overdose. Our case lends support to the view that large doses of the narcotic antagonist naloxone may be effective in pentazocine overdose.

Adolescent↗