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Biomedical subjects

P Talke

Publications and source records attributed to P Talke.

At least 19 recordsLinked to original sources
PubMed2003

Effects of intrathecally administered dexmedetomidine, MPV-2426 and tizanidine on EMG in rats.

BACKGROUND: When administered intrathecally, alpha-2 adrenergic agonists produce spinally mediated antinociception, but also rapidly redistribute to supraspinal sites. This investigation the compared EMG effects of intrathecally administered dexmedetomidine, MPV-2426 (fadolmidine), and tizanidine in Sprague-Dawley rats, which has not been previously described. METHODS: We studied electromyographic (EMG) responses of the head and gastrocnemius muscles, antinociception using the tail-flick test, and sedation by using observer assessment. Saline, dexmedetomidine (0.5 microg, 2.5 microg and 12.5 microg), MPV-2426 (2 microg, 10 microg and 50 microg) and tizanidine (2 microg, 10 microg and 50 microg) were administered intrathecally. RESULTS: Tizanidine 50 microg, MPV-2426 10 microg and 50 microg, and dexmedetomidine 2.5 microg and 12.5 microg, decreased EMG activity (P < 0.005). Dexmedetomidine 12.5 microg, MPV-2426 50 microg, and tizanidine 10 microg and 50 microg increased tail-flick latencies (P < 0.01). Dexmedetomidine alone significantly increased the magnitude of observer-assessed sedation (P < 0.0001). CONCLUSION: We conclude that in rats, intrathecally administered dexmedetomidine, MPV-2426 and tizanidine have dose-dependent effects on EMG. At antinociceptive doses, the EMG effects of these three alpha-2 adrenergic agonists differ (dexmedetomidine > MPV-2426 > tizanidine).

Adrenergic alpha-Agonists↗
PubMed2000

The hemodynamic and adrenergic effects of perioperative dexmedetomidine infusion after vascular surgery.

UNLABELLED: We tested dexmedetomidine, an alpha(2) agonist that decreases heart rate, blood pressure, and plasma norepinephrine concentration, for its ability to attenuate stress responses during emergence from anesthesia after major vascular operations. Patients scheduled for vascular surgery received either dexmedetomidine (n = 22) or placebo (n = 19) IV beginning 20 min before the induction of anesthesia and continuing until 48 h after the end of surgery. All patients received standardized anesthesia. Heart rate and arterial blood pressure were kept within predetermined limits by varying anesthetic level and using vasoactive medications. Heart rate, arterial blood pressure, and inhaled anesthetic concentration were monitored continuously; additional measurements included plasma and urine catecholamines. During emergence from anesthesia, heart rate was slower with dexmedetomidine (73 +/- 11 bpm) than placebo (83 +/- 20 bpm) (P = 0.006), and the percentage of time the heart rate was within the predetermined hemodynamic limits was more frequent with dexmedetomidine (P < 0.05). Plasma norepinephrine levels increased only in the placebo group and were significantly lower for the dexmedetomidine group during the immediate postoperative period (P = 0.0002). We conclude that dexmedetomidine attenuates increases in heart rate and plasma norepinephrine concentrations during emergence from anesthesia. IMPLICATIONS: The alpha(2) agonist, dexmedetomidine, attenuates increases in heart rate and plasma norepinephrine concentrations during emergence from anesthesia in vascular surgery patients.

Adrenergic alpha-Agonists↗
PubMed1999

Amount of air infused to patient increases as fluid flow rates decrease when using the Hotline HL-90 fluid warmer.

OBJECTIVE: The intraoperative use of fluid warming devices has been recommended to avoid perioperative hypothermia and related adverse outcomes. To evaluate whether these devices might introduce risks of their own, we measured the volume of air escaping from a warmed intravenous solution that might be delivered to a patient. METHODS: In an operating room maintained at 19-19.5 degrees C, we tested an HL-90 Hotline fluid warmer with the L-70 fluid-warming set. One liter of lactated Ringer's solution was infused at flow rates of 150, 300, 500 and 3400 ml/h. The air that formed within the L-70 tubing during infusion was collected in a bubble trap placed at the end of the L-70 tubing. The volume of air in the bubble trap was measured. Twelve separate measurements were obtained at each flow rate. One additional study (n = 8) was performed using the L-10 Gas Vent to determine whether this equipment might reduce the volume of air infused when fluid flow rate was 300 mL/h. The volume of air collected at each flow rate was compared using ANOVA. RESULTS: Volume of air increased significantly from 1.0 +/- 0.2 mL to 2.9 +/- 0.4 ml as flow rate decreased from 3400 ml/h to 150 ml/h (p < 0.0001). The L-10 gas eliminator was ineffective in reducing the amount of air infused. CONCLUSIONS: We conclude that the use of the Hotline fluid warmer can result in infusion of air into the patient, introducing possible risk of air embolism.

Embolism, Air↗
PubMed1999

Sevoflurane increases lumbar cerebrospinal fluid pressure in normocapnic patients undergoing transsphenoidal hypophysectomy.

BACKGROUND: The data on the effect of sevoflurane on intracranial pressure in humans are still limited and inconclusive. The authors hypothesized that sevoflurane would increase intracranial pressure as compared to propofoL METHODS: In 20 patients with no evidence of mass effect undergoing transsphenoidal hypophysectomy, anesthesia was induced with intravenous fentanyl and propofol and maintained with 70% nitrous oxide in oxygen and a continuous propofol infusion, 100 microg x kg(-1) x min(-1). The authors assigned patients to two groups randomized to receive only continued propofol infusion (n = 10) or sevoflurane (n = 10) for 20 min. During the 20-min study period, each patient in the sevoflurane group received, in random order, two concentrations (0.5 times the minimum alveolar concentration [MAC] and 1.0 MAC end-tidal) of sevoflurane for 10 min each. The authors continuously monitored lumbar cerebrospinal fluid (CSF) pressure, blood pressure, heart rate, and anesthetic concentrations. RESULTS: Lumbar CSF pressure increased by 2+/-2 mmHg (mean+/-SD) with both 0.5 MAC and 1 MAC of sevoflurane. Cerebral perfusion pressure decreased by 11+/-5 mmHg with 0.5 MAC and by 15+/-4 mmHg with 1.0 MAC of sevoflurane. Systolic blood pressure decreased with both concentrations of sevoflurane. To maintain blood pressure within predetermined limits (within+/-20% of baseline value), phenylephrine was administered to 5 of 10 patients in the sevoflurane group (range = 50-300 microg) and no patients in the propofol group. Lumbar CSF pressure, cerebral perfusion pressure, and systolic blood pressure did not change in the propofol group. CONCLUSIONS: Sevoflurane, at 0.5 and 1.0 MAC, increases lumbar CSF pressure. The changes produced by 1.0 MAC sevoflurane did not differ from those observed in a previous study with 1.0 MAC isoflurane or desflurane.

Anesthetics, Inhalation↗
PubMed1997

Effect of dexmedetomidine on lumbar cerebrospinal fluid pressure in humans.

UNLABELLED: Dexmedetomidine's potential for analgesia without respiratory depression and its opioid- and anesthetic-sparing properties make it an attractive choice as an anesthetic adjunct for patients undergoing neurosurgery. However, the effects of dexmedetomidine on intracranial pressure are not known. We therefore studied the effect of dexmedetomidine on lumbar cerebrospinal fluid (CSF) pressure in patients after transphenoidal pituitary tumor surgery. Sixteen transphenoidal pituitary tumor surgery patients were randomized to receive placebo (n = 9) or dexmedetomidine (n = 7) for 60 min in the postanesthesia care unit. The study drug was administered by a continuous computer-controlled infusion to achieve an estimated plasma dexmedetomidine concentration of 600 pg/mL, the highest plasma concentration that has been used for clinical purposes. Patient-controlled analgesia was used to administer morphine for postoperative discomfort. Lumbar CSF pressure (via lumbar intrathecal catheter), intraarterial blood pressure, and heart rate were monitored continuously. There was no change in lumbar CSF pressure in either group. The highest values obtained were 19 mm Hg in the dexmedetomidine group and 20 mm Hg in the placebo group. During infusion, mean arterial pressure decreased from 103 +/- 10 mm Hg to 86 +/- 6 mm Hg (P < 0.05), heart rate decreased from 77 +/- 12 bpm to 64 +/- 7 bpm (P < 0.05), and cerebral perfusion pressure decreased from 95 +/- 8 mm Hg to 78 +/- 6 mm Hg (P < 0.05) in the dexmedetomidine group, but not in the placebo group. We conclude that dexmedetomidine does not have an effect on lumbar CSF pressure in patients with normal intracranial pressure who have undergone transphenoidal pituitary hypophysectomy. IMPLICATIONS: The effects of dexmedetomidine (an alpha2-agonist) or placebo on lumbar cerebrospinal fluid pressure, measured via an intrathecal catheter, were studied postoperatively in 16 patients. Dexmedetomidine had no effect on lumbar cerebrospinal fluid pressure. We will continue to investigate the potential utility of dexmedetomidine for neurosurgical anesthesia.

Adjuvants, Anesthesia↗
PubMed1997

Postoperative pharmacokinetics and sympatholytic effects of dexmedetomidine.

UNLABELLED: Dexmedetomidine is a selective alpha2-adrenoceptor agonist with centrally mediated sympatholytic, sedative, and analgesic effects. This study evaluated: 1) pharmacokinetics of dexmedetomidine in plasma and cerebrospinal fluid (CSF) in surgical patients; 2) precision of a computer-controlled infusion protocol (CCIP) for dexmedetomidine during the immediate postoperative period; and 3) dexmedetomidine's sympatholytic effects during that period. Dexmedetomidine was infused postoperatively by CCIP for 60 min to eight women, targeting a plasma concentration (Cp) of 600 pg/mL. Before, during, and after infusion, blood was sampled to determine plasma concentrations of norepinephrine, epinephrine, and dexmedetomidine, and CSF was sampled to determine dexmedetomidine concentrations (C[CSF]). Heart rate and arterial blood pressure were measured continuously from 5 min before until 3 h after the end of infusion. During the infusion, Cp values generally exceeded the target value: median percent error averaged 21% and ranged from -2% to 74%; median absolute percent error averaged 23% and ranged from 4% to 74%. After infusion, C(CSF) was 4% +/- 1% of Cp. Because C(CSF) barely exceeded the assay's limit of quantitation, CSF pharmacokinetics were not determined. During the infusion, norepinephrine decreased from 2.1 +/- 0.8 to 0.7 +/- 0.3 nmol/L; epinephrine decreased from 0.7 +/- 0.5 to 0.2 +/- 0.2 nmol/L; heart rate decreased from 76 +/- 15 to 64 +/- 11 bpm; and systolic blood pressure decreased from 158 +/- 23 to 140 +/- 23 mm Hg. We conclude that infusion of dexmedetomidine by CCIP using published pharmacokinetic parameters overshoots target dexmedetomidine concentrations during the early postoperative period. Hemodynamic and catecholamine results suggest that dexmedetomidine attenuates sympathetic activity during the immediate postoperative period. IMPLICATIONS: We studied the pharmacokinetic and sympatholytic effects of dexmedetomidine during the immediate postoperative period and found that during this period, the published pharmacokinetic data slightly overshoot target plasma dexmedetomidine concentrations. We also found that heart rate, blood pressure, and plasma catecholamine concentrations decrease during dexmedetomidine infusion.

Adrenergic alpha-Agonists↗
PubMed1997

The effect of clonidine on cerebral blood flow velocity, carbon dioxide cerebral vasoreactivity, and response to increased arterial pressure in human volunteers.

BACKGROUND: Because patients may be taking clonidine chronically or may be receiving it as a premedication before surgery, the authors investigated its effect on cerebral hemodynamics. METHODS: In nine volunteers, middle cerebral artery mean blood flow velocity (Vm) was measured using transcranial Doppler ultrasonography (TCD). CO2 vasoreactivity was measured before clonidine administration (preclonidine), 90 min after clonidine, 5 microg/kg orally, then following restoration of mean arterial pressure (MAP) to the preclonidine level. In addition, Vm was measured after a phenylephrine-induced 30-mmHg increase in MAP. RESULTS: After clonidine administration, Vm decreased from 62 +/- 9 to 48 +/- 8 cm/s (P < 0.01), and MAP decreased from 86 +/- 10 to 63 +/- 5 mmHg (P < 0.01; mean +/- SD). Clonidine decreased the CO2 vasoreactivity slope from 2.2 +/- 0.4 to 1.2 +/- 0.5 cm x s(-1) x mmHg(-1) (P < 0.05); restoring MAP to the preclonidine level increased the slope to 1.60 +/- 0.5 cm x s(-1) x mmHg(-1), still less than the preclonidine slope (P < 0.05). CO2 vasoreactivity expressed as a percentage change in Vm, decreased after clonidine, 3.5 +/- 0.8 versus 2.4 +/- 0.8 %/mmHg (P < 0.05); this difference disappeared after restoration of MAP, 3.1 +/- 1.2 %/mmHg. With a 30-mmHg increase in MAP, Vm increased by 13% before and after clonidine (P < 0.05). CONCLUSIONS: Clonidine, 5 microg/kg orally, decreases Vm and slightly attenuates cerebral CO2 vasoreactivity, therefore decreased cerebral blood flow and mildly attenuated CO2 vasoreactivity should be anticipated.

Adrenergic alpha-Agonists↗
PubMed1997

Dexmedetomidine does not alter the sweating threshold, but comparably and linearly decreases the vasoconstriction and shivering thresholds.

BACKGROUND: Clonidine decreases the vasoconstriction and shivering thresholds. It thus seems likely that the alpha2 agonist dexmedetomidine will also impair control of body temperature. Accordingly, the authors evaluated the dose-dependent effects of dexmedetomidine on the sweating, vasoconstriction, and shivering thresholds. They also measured the effects of dexmedetomidine on heart rate, blood pressures, and plasma catecholamine concentrations. METHODS: Nine male volunteers participated in this randomized, double-blind, cross-over protocol. The study drug was administered by computer-controlled infusion, targeting plasma dexmedetomidine concentrations of 0.0, 0.3, and 0.6 ng/ml. Each day, skin and core temperatures were increased to provoke sweating and then subsequently reduced to elicit vasoconstriction and shivering. Core-temperature thresholds were computed using established linear cutaneous contributions to control of sweating, vasoconstriction, and shivering. The dose-dependent effects of dexmedetomidine on thermoregulatory response thresholds were then determined using linear regression. Heart rate, arterial blood pressures, and plasma catecholamine concentrations were determined at baseline and at each threshold. RESULTS: Neither dexmedetomidine concentration increased the sweating threshold from control values. In contrast, dexmedetomidine administration reduced the vasoconstriction threshold by 1.61 +/- 0.80 degrees C x ng(-1) x ml (mean +/- SD) and the shivering threshold by 2.40 +/- 0.90 degrees C x ng(-1) x ml. Hemodynamic responses and catecholamine concentrations were reduced from baseline values, but they did not differ at the two tested dexmedetomidine doses. CONCLUSIONS: Dexmedetomidine markedly increased the range of temperatures not triggering thermoregulatory defenses. The drug is thus likely to promote hypothermia in a typical hospital environment; it is also likely to prove an effective treatment for shivering.

Adrenergic alpha-Agonists↗
PubMed1996

Effects of dexmedetomidine on hypoxia-evoked glutamate release and glutamate receptor activity in hippocampal slices.

BACKGROUND: The selective alpha(2) agonist dexmedetomidine may improve neurologic outcome after incomplete ischemia in animals when it is administered either before or after the start of the ischemic insult. To clarify further the mechanisms by which alpha(2) agonists may provide neuroprotective effects, the authors tested the hypotheses that dexmedetomidine decreases synaptic and extrasynaptic glutamate release stimulated by potassium chloride or hypoxia, and decreases postsynaptic glutamate receptor activity during aerobic or hypoxic conditions. METHODS: Glutamate released from brain slices (300-microns thick) from rat hippocampus was measured in a cuvette during two experimental stresses: (1) potassium chloride-evoked depolarization (30 mM) with and without 10 nM, 100 nM, or 1,000 nM dexmedetomidine; and (2) hypoxia (95% N2 - 5% CO2) with and without 100 nM dexmedetomidine. Glutamate release was quantified by fluorescence assay using 1 mM nicotinamide adenine dinucleotide, and 5 international units per ml glutamate dehydrogenase. The formation of nicotinamide dinucleotide reduced from nicotinamide adenine dinucleotide by glutamate dehydrogenase was measured fluorometrically (excitation light 340 nm, emission intensity 460 nm) in the solution above the slice. Glutamate receptor activity was determined by the change in cytosolic calcium concentration in CA1 neurons in the presence and absence of 100 nM dexmedetomidine during administration of N-methyl-D-aspartate (100 microM) and during simulated ischemic penumbra conditions (PO2 = 20 mmHg, glutamate 3 mM). Calcium concentration was measured using a microscope fluorometer in fura 2-loaded rat hippocampal brain slices. RESULTS: Dexmedetomidine attenuated potassium chloride-evoked glutamate release by 37%, 51%, (P = 0.03) and 27%, respectively, for the 10 nM, 100 nM, and 1,000 nM concentrations, and decreased (at 100 nM) the increase in glutamate release in response to hypoxia by 61% (P < 0.0001). Dexmedetomidine (100 nM) had no effect on N-methyl-D-aspartate or hypoxia plus 3 mM L-glutamate-mediated calcium changes. CONCLUSIONS: The selective alpha(2)-adrenergic agonist dexmedetomidine decreases evoked glutamate release from hippocampal rat brain slices during depolarization or hypoxic stress, but does not alter calcium changes mediated by the stimulation of glutamate receptors during aerobic or hypoxic conditions.

Adrenergic alpha-Agonists↗
PubMed1996

Desflurane and isoflurane increase lumbar cerebrospinal fluid pressure in normocapnic patients undergoing transsphenoidal hypophysectomy.

BACKGROUND: Rapid emergence from anesthesia makes desflurane an attractive choice as an anesthetic for patients having neurosurgery. However, the data on the effect of desflurane on intracranial pressure in humans are still limited and inconclusive. The authors hypothesized that isoflurane and desflurane increase intracranial pressure compared with propofol. METHODS: Anesthesia was induced with intravenous fentanyl and propofol in 30 patients having transsphenoidal hypophysectomy with no evidence of mass effect, and it was maintained with 70% nitrous oxide in oxygen and a continuous 100 micrograms.kg-2.min-1 infusion of propofol. Patients were assigned to three groups randomized to receive only continued propofol infusion (n = 10), desflurane (n = 10), or isoflurane (n = 10) for 20 min. During the 20-min study period, each patient in the desflurane and isoflurane groups received, in random order, two concentrations (0.5 minimum alveolar concentration [MAC] and 1.0 MAC end-tidal) of desflurane or isoflurane for 10 min each. Lumbar cerebrospinal fluid (CSF) pressure, blood pressure, heart rate, and anesthetic concentrations were monitored continuously. RESULTS: Lumbar CSF pressure increased significantly in all patients receiving desflurane or isoflurane. Lumbar CSF pressure increased by 5 +/- 3 mmHg at 1-MAC concentrations of desflurane and by 4 +/- 2 mmHg at 1-MAC concentrations of isoflurane. Cerebral perfusion pressure decreased by 12 +/- 10 mmHg at 1-MAC concentrations of desflurane and by 15 +/- 10 mmHg at 1-MAC concentrations of isoflurane. Heart rate increased by 7 +/- 9 bpm with 0.5 MAC desflurane and by 8 +/- 7 bpm with 1.0 MAC desflurane, and by 5 +/- 11 bpm with 1.0 MAC isoflurane. Systolic blood pressure decreased in all but the patients receiving 1.0 MAC desflurane. To maintain blood pressure within predetermined limits, phenylephrine was administered to six of ten patients in the isoflurane group (range, 25 to 600 micrograms), two of ten patients in the desflurane group (range, 200 to 500 micrograms), and in no patients in the propofol group. Lumbar CSF pressure, heart rate, and systolic blood pressure did not change in the propofol group. CONCLUSION: Desflurane and isoflurane, at 0.5 and 1.0 MAC, increase lumbar CSF pressure.

Adult↗
PubMed1995

Effects of perioperative dexmedetomidine infusion in patients undergoing vascular surgery. The Study of Perioperative Ischemia Research Group.

BACKGROUND: Dexmedetomidine, a highly selective alpha 2-adrenergic agonist, increases perioperative hemodynamic stability in healthy patients but decreases blood pressure and heart rate. The goal of this study was to evaluate, in a preliminary manner, the hemodynamic effects of perioperatively administered dexmedetomidine in surgical patients at high risk for coronary artery disease. METHODS: Twenty-four vascular surgery patients received a continuous infusion of placebo or one of three doses of dexmedetomidine, targeting plasma concentrations of 0.15 ng/ml (low dose), 0.30 ng/ml (medium dose), or 0.45 ng/ml (high dose) from 1 h before induction of anesthesia until 48 h postoperatively. All patients received standardized anesthesia and hemodynamic management. Blood pressure, heart rate, and Holter ECG were monitored; additional monitoring included continuous 12-lead ECG preoperatively, anesthetic concentrations and myocardial wall motion (echocardiography) intraoperatively, and cardiac enzymes postoperatively. RESULTS: Preoperatively, there was a decrease in heart rate (low dose 11%, medium dose 5%, high dose 20%) and systolic blood pressure (low dose 3%, medium dose 12%, high dose 20%) in patients receiving dexmedetomidine. Intraoperatively, dexmedetomidine groups required more vasoactive medications to maintain hemodynamics within predetermined limits. Postoperatively, demedetomidine groups had less tachycardia (minutes/monitored hours) than the placebo group (placebo 23 min/h; low dose 9 min/h, P = 0.006; medium dose 0.5 min/h, P = 0.004; high dose 2.3 min/h, P = 0.004). Bradycardia was rare in all groups. There were no myocardial infarctions or discernible trends in the laboratory results. CONCLUSIONS: Infusion of dexmedetomidine up to a targeted plasma concentration of 0.45 ng/ml appears to benefit perioperative hemodynamic management of surgical patients undergoing vascular surgery but required greater intraoperative pharmacologic intervention to support blood pressure and heart rate.

Blood Pressure↗
PubMed1993

Treatment of postoperative nausea and vomiting after outpatient surgery with the 5-HT3 antagonist ondansetron.

BACKGROUND: Postoperative nausea and vomiting following outpatient surgery can significantly delay discharge. This study evaluates the safety and efficacy of ondansetron (a new 5-HT3 antagonist) in the treatment of postoperative nausea and vomiting in patients following outpatient surgery. METHODS: Five hundred outpatient surgical patients (53 male and 447 female), receiving general endotracheal anesthesia, were studied at ten centers. Patients were stratified by gender and received, in a randomized, double-blind manner, 1, 4, or 8 mg ondansetron or placebo in response to nausea and/or vomiting postoperatively. Episodes of vomiting, nausea scores, adverse events, vital signs, and laboratory values were evaluated before and during the 24 h after study drug administration. RESULTS: Complete response to study medication (no vomiting and/or retching, and no rescue antiemetic over the initial 0-2-h period) was more frequent in the ondansetron groups (1 mg 57%, 4 mg 61%, and 8 mg 57%) than in the placebo group (30%, P < .001). For the 0-24-h study a complete response occurred in only 15% of the placebo group compared to 41%, 47%, and 47% of the 1-, 4-, and 8-mg ondansetron groups, respectively (P < .001 for all comparisons with placebo). Median nausea scores (range 0-10) during the initial observation period (0-2 h) were significantly lower for all doses of ondansetron (1.3, 0.8, 1.8 for 1, 4, and 8 mg, respectively) as compared with placebo (2.3). No significant differences occurred in hemodynamic stability, incidence of adverse events, or changes in laboratory values in the ondansetron groups compared to the placebo group. CONCLUSIONS: Ondansetron, in doses less than 8 mg, is a safe, effective antiemetic for treating postoperative nausea and vomiting.

Adult↗
PubMed1992

Ondansetron in the treatment of postoperative nausea and vomiting in ambulatory outpatients: a dose-comparative, stratified, multicentre study.

The safety and efficacy of ondansetron were evaluated in the treatment of postoperative nausea and vomiting. Five hundred patients who experienced nausea or vomiting in the Post-Anaesthesia Care Unit within the first 2 h of recovery were randomized to receive either 1, 4, or 8 mg of ondansetron, or placebo. All patients had undergone ambulatory surgery with general endotracheal anaesthesia. Episodes of emesis, nausea scores, adverse events, vital signs, and laboratory values were assessed before and during the 24 h after study drug administration. Patients were evaluated for the first 2 h in the Post-Anaesthesia Care Unit then followed up for the next 22 h. Complete response was defined as no emetic episodes, no nausea or no rescue anti-emetic medication. For the 0-24 h study period, complete response occurred in only 15% of the placebo group compared to 41%, 47%, and 47% in the 1, 4, and 8 mg ondansetron groups, respectively. Mean nausea scores (scale of 0-10) during the initial observation period (0-2 h) were significantly lower for all doses of ondansetron [2.2 (1 mg), 1.7 (4 mg), and 2.1 (8 mg)] compared to placebo (3.0). The optimal dose of ondansetron for the treatment of postoperative nausea and vomiting was found to be 4 mg. All doses of ondansetron were well tolerated. No clinically significant increases in laboratory parameters or alterations in haemodynamic stability occurred in the ondansetron groups compared to placebo.

Adolescent↗
PubMed1990

Monitoring patients during helicopter flight.

In 11 patients being transported via helicopter we monitored heart rate, arterial oxygen saturation, and systolic blood pressure with a pulse oximeter. We were able to obtain vital signs in 10 of 11 patients. The pulse oximeter was a useful tool in monitoring vital signs intraflight.

Adolescent↗
PubMed1990

Does measurement of systolic blood pressure with a pulse oximeter correlate with conventional methods?

The pulse oximeter is commonly used in the operating room. We evaluated the use of a pulse oximeter to monitor systolic blood pressure in 20 healthy volunteers and 42 anesthetized patients. We compared the pulse oximeter method of measuring systolic blood pressure with the cuff methods using Korotkoff sounds and Doppler ultrasound as well as with direct pressure measurement through an intraarterial cannula. Systolic blood pressure values obtained by pulse oximeter correlated well with values obtained by other conventional methods. The best correlation was found with Doppler ultrasound (r = 0.996) and the worst with arterial cannulation (r = 0.880). We conclude that this method can be used intraoperatively to measure systolic blood pressure.

Adolescent↗
PubMed1990

Effects of allopurinol on smoke inhalation in the ovine model.

We hypothesized that the pulmonary damage induced by smoke inhalation is the result of ischemic reperfusion injury. We determined the effect of allopurinol (xanthine oxidase inhibitor) on the pulmonary microvascular fluid flux in an ovine model after inhalation of cotton smoke (n = 13) and compared these data with those from untreated similarly smoke-injured (n = 7), as well as sham- (air, n = 9) smoked, animals and sheep given an equivalent dose of CO (n = 7). Smoke injury resulted in an increased lung lymph flow, lymph-to-plasma protein ratio, lung content of polymorphonuclear cells, and extravascular lung water (gravametric), in addition to histological evidence of tissue (pulmonary) edema and destruction. No significant difference was found in these variables between the sheep that were injured with smoke whether or not they were pretreated with allopurinol. The sham-smoked and CO-insufflated animals showed no significant changes in cardiopulmonary function or morphology. We conclude that there are few data to support a role of ischemic reperfusion injury in the pulmonary damage seen after smoke inhalation.

Allopurinol↗
PubMed1985

A model of ovine endotoxemia characterized by an increased cardiac output.

High cardiac output sepsis is a major clinical problem. We have designed a sheep endotoxin model to simulate this condition and have evaluated how closely it approximates the clinical situation. The animals were prepared for chronic study by the implantation of cardiopulmonary catheters. One week later, endotoxin (0.75 microgram/kg/30 min) was administered following baseline measurements, and the animals were studied for an additional 15 hr. From 6-15 hr after the administration of endotoxin, there was a statistically significant twofold increase in cardiac output. Simultaneously, the total peripheral vascular resistance and mean arterial pressure was reduced. Eicosanoid measurements made at this time indicated that the vasodilator prostanoid, prostacyclin, was not elevated. A high cardiac output (hyperdynamic) model of sepsis has thus been established by the 30 min infusion of a small quantity of endotoxin. Prostacyclin is not a mediator of this response.

Animals↗