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At least 1,189 records · Page 66Linked to original sources
PubMed1998

[Value of orally administered retard morphine for therapy of severe pulmonary emphysema of the pink-puffer type. A pilot study].

BACKGROUND AND OBJECTIVE: In severe "pink puffer" emphysema the patients' physical capacity is limited by dyspnoea despite maximal application of established treatment. This pilot study investigated the effect of retarded morphine, taken orally for 10 days, on ventilation, dyspnoea, walking capacity and wakefulness. PATIENTS AND METHODS: Twenty clinically stable patients (11 men, 9 women, mean age 68.5 [50-81] years) with "pink puffer" emphysema were studied over a period of 10 days in a prospective, non-controlled trial of cross-over design. Criteria for inclusion in the study were: 1-second forced expiratory volume (FEV1) < 1 I, vital capacity < 50% and normocapnia. In addition to their existing therapy patients received either no further therapy or retarded morphine. Morphine dosage was increased to maximally 3 x 30 mg daily, depending on effectiveness and side effects, dyspnoea at rest and immediately after a 6-min walk (assessed with Borg's visual analog scale), maximal walking capacity were determined, as well as blood gases, respiratory minute volume and the respiratory drive (airway occlusion pressure [P0.1]), responsiveness of the respiratory pathways to CO2 and wakefulness (concentration, fatigue, interest in surroundings). RESULTS: Twelve patients completed the study (group A). In the remaining patients (group B) the test had to be stopped prematurely because of undesirable side effects or an exacerbation of the underlying infection. In group A, morphine (mean dosage: 49.2 +/- 28.4 mg/d) caused a reduction of PaO2, dyspnoea on activity, the resting minute respiratory volume, respiratory drive and CO2 response, and an increase in PaCO2, HCO3- and the 6-min walking distance. Morphine did not produce a change in subjectively evaluated vigilance and the blood pH. CONCLUSION: After strict patient selection oral morphine produced a reduction of exercise dyspnoea and an increase in walking capacity in half of the patients with severe pulmonary emphysema. There also occurred a slight rise in PaCO2 without any relevant respiratory acidosis or significant decrease in wakefulness.

Administration, Oral↗
PubMed1990

[Persistent pulmonary hypertension of newborn. The PFC syndrome].

Persistent pulmonary hypertension of the newborn (PPHN), initially described by Gersony et al as persistent foetal circulation (PFC syndrome), results from a flawed transition from foetal to extrauterine pulmonary circulation. It is characterised by the maintenance of a high pulmonary vascular resistance and right-to-left shunting through the ductus arteriosus and foramen ovale. Infants with a wide variety of underlying clinical conditions develop PPHN. According to Rudolph three main anatomic types of PPHN can be identified: normal pulmonary vascular development increased pulmonary vascular smooth muscle development decreased cross-sectional area of pulmonary vascular bed. It is important to realize that several pathophysiologic mechanisms may coexist and interact. Besides metabolic and respiratory acidosis, hypercapnia and hypoxaemia some other factors induce pulmonary vasoconstriction. Thromboxane, leukotrienes and prostaglandins play a decisive role. Since PPHN can be associated with a broad spectrum of clinical conditions, a specific clinical picture is lacking. The baby is usually term or post-term, cyanotic immediately after birth or some hours later. Birth asphyxia, hyperviscosity, sepsis and aspiration of meconium have been recognized as predisposing factors. The diagnosis can be confirmed by echocardiography. Contrast echo will indicate right-to-left shunting with normal anatomy. Currently hyperventilation, tolazolin, chlorpromazin and dopamine/dobutamine have been advocated as central foci for clinical therapy. Recently prostacyclin was introduced as a specific pulmonary vasodilatator.(ABSTRACT TRUNCATED AT 250 WORDS)

Echocardiography↗
PubMed1996

[Purulent pericardial effusion with tamponade: a rare initial manifestation of o pneumococcal infection].

HISTORY AND FINDINGS: A 70-year-old man, admitted for a haemorrhoid operation, suddenly went into circulatory shock (heart rate 150/min, blood pressure 100/70 mm Hg), necessitating transfer to an intensive care unit. His neck veins were prominent and he had a paradoxical pulse. Heart sounds were distant and there was an arrhythmia (atrial fibrillation in the ECG). No murmurs were heard. Breath sounds were decreased, especially in the lung bases. INVESTIGATIONS: Differential blood count showed 30% stab cells with 12,200 white cells per microliter. Erythrocyte sedimentation rate was 118 mm in the first hour, C-reactive protein was raised to 11.8 mg/dl. There was a partially compensated respiratory acidosis (pH 7.12; pO 93.4 mm Hg; pCO 16.3 mm Hg; base deficit -22.6 mmol/l). In the chest radiogram the cardiac silhouette was greatly enlarged bilaterally. The echocardiogram demonstrated a large pericardial perfusion with a "swinging heart". TREATMENT AND COURSE: At pericardial needle puncture 700 ml of amber-coloured fluid, containing pneumococci, were aspirated with immediate circulatory improvement. Penicillin, 10 mill.U twice daily for 13 days, was administered intravenously, followed by amoxycillin, 1 g three times daily by mouth, for a further 15 days. In addition he was given anti-inflammatory treatment with diclofenac and methylprednisolone. Despite this pericardial effusion recurred after 14 days and 600 ml of sterile fluid were removed. Subsequently the inflammatory signs disappeared. Three months later no effusion was present and there were no signs of constrictive pericarditis.

Administration, Oral↗
PubMed1984

Effect of carbon dioxide on diaphragmatic function in human beings.

We studied the effects of acute changes in the partial pressure of arterial carbon dioxide on diaphragmatic contractility and performance in four normal men. To study contractility we measured the ability of the diaphragm to generate pressure at a given level of excitation by determining the relation between the electrical activity of the diaphragm and transdiaphragmatic pressure during a voluntary quasi-isometric inspiratory effort carried out at different levels of end-tidal carbon dioxide. Our results show that contractility was reduced with hypercapnia (when end-tidal carbon dioxide was 7.5 per cent or higher), although hypocapnia (end-tidal carbon dioxide, 3 per cent) had no effect on diaphragmatic contractility. We also studied the development of diaphragmatic fatigue before and during carbon dioxide breathing. Subjects were studied at the same diaphragmatic tension-time index, a value analogous to the more familiar myocardial tension-time index, while the same inspiratory flow was maintained. Electromyographic signs of fatigue appeared at a lower tension-time index during hypercapnia than during normocapnia, indicating that endurance is diminished during hypercapnia. These findings show that acute respiratory acidosis equivalent to an arterial carbon dioxide tension of about 54 mm Hg decreases the contractility and endurance time of the diaphragm in human beings.

Carbon Dioxide↗
PubMed2005

Evidence from renal proximal tubules that HCO3- and solute reabsorption are acutely regulated not by pH but by basolateral HCO3- and CO2.

Respiratory acidosis, a decrease in blood pH caused by a rise in [CO(2)], rapidly triggers a compensatory response in which the kidney markedly increases its secretion of H(+) from blood to urine. However, in this and other acid-base disturbances, the equilibrium CO(2) + H(2)O HCO(3)(-) + H(+) makes it impossible to determine whether the critical parameter is [CO(2)], [HCO(3)(-)], and/or pH. Here, we used out-of-equilibrium CO(2)/HCO(3)(-) solutions to alter basolateral (BL) [HCO(3)(-)], [CO(2)], or pH, systematically and one at a time, on isolated perfused S2 rabbit proximal tubules. We found that increasing [HCO(3)(-)](BL) from 0 to 44 mM, at a fixed [CO(2)](BL) of 5% and a fixed pH(BL) of 7.40, caused HCO(3)(-) reabsorption (J(HCO(3))) to fall by half but did not significantly affect volume reabsorption (J(V)). Increasing [CO(2)](BL) from 0% to 20%, at a fixed [HCO(3)(-)](BL) of 22 mM and pH(BL) of 7.40, caused J(HCO(3)) to rise 2.5-fold but did not significantly affect J(V). Finally, increasing pH(BL) from 6.80 to 8.00, at a fixed [HCO(3)(-)](BL) of 22 mM and [CO(2)](BL) of 5%, did not affect either J(HCO(3)) or J(V). Analysis of the J(HCO(3)) and J(V) data implies that, as the tubule alters J(HCO(3)), it compensates the reabsorption of other solutes to keep J(V) approximately constant. Because the cells cannot respond acutely to pH changes, we propose that the responses of J(HCO(3)) and the reabsorption of other solutes to changes in [HCO(3)(-)](BL) or [CO(2)](BL) involve sensors for basolateral HCO(3)(-) and CO(2).

Absorption↗
PubMed1998

Hypoxia stimulates insulin-like growth factor binding protein 1 (IGFBP-1) gene expression in HepG2 cells: a possible model for IGFBP-1 expression in fetal hypoxia.

IGFBP-1 is elevated in fetuses with long-term, chronic hypoxia and intrauterine growth restriction. We investigated the hypothesis that hypoxia regulates IGFBP-1 in the human fetus in vivo and IGFBP-1 gene expression and protein in vitro. Umbilical artery IGFBP-1 levels (mean +/- SEM) from term babies with respiratory acidosis (acute hypoxia), normal babies, and those with mixed respiratory/metabolic acidosis (more profound and prolonged hypoxia) were measured using an immunoradiometric assay. IGFBP-1 levels were similar in normal (n = 12) and acutely hypoxic (n = 6) babies (189.1 +/- 71.8 vs. 175.8 +/- 45.9 ng /ml, respectively, P = 0.789). However, with more profound and prolonged hypoxia (n = 19), IGFBP-1 levels were markedly elevated (470.6 +/- 80.0 ng /ml, P = 0.044). To investigate IGFBP-1 regulation by hypoxia in vitro, HepG2 cells were incubated under hypoxia (pO2 = 2%) and normoxia (pO2 = 20%). IGFBP-1 protein and mRNA increased 8- and 12-fold, respectively, under hypoxic conditions. Hypoxia did not affect protein or mRNA levels of IGFBP-2 or -4. IGFBP-5 and -6 mRNAs, undetectable in control cells, were not induced by hypoxia, whereas minimally expressed IGFBP-3 mRNA increased twofold. Investigation into IGFBP-1 gene structure revealed three potential consensus sequences for the hypoxia response element (HRE) in the first intron. To investigate functionality, a 372-bp fragment of IGFBP-1 intron 1, containing putative HREs, was placed 5' to a heterologous hsp70 promoter in a plasmid using luciferase as a reporter gene. Under hypoxia, reporter gene activity increased up to 30-fold. Mutations in the middle HRE abolished reporter activity in response to hypoxia, suggesting that this HRE is functional in the IGFBP-1 hypoxia response. Cotransfection of HRE reporter genes with a constitutively expressing hypoxia-inducible factor 1 plasmid in HepG2 cells resulted in a fourfold induction of reporter activity, suggesting a role for hypoxia-inducible factor 1 in hypoxia induction of IGFBP-1 gene expression. These data support the hypothesis that hypoxia regulation of IGFBP-1 may be a mechanism operating in the human fetus to restrict insulin-like growth factor-mediated growth in utero under conditions of chronic hypoxia and limited substrate availability.

Animals↗
PubMed2005

Combined metabolic gas analyser and dGPS analysis of performance in cross-country skiing.

The purpose of this study was to provide a more detailed analysis of performance in cross-country skiing by combining findings from a differential global positioning system (dGPS), metabolic gas measurements, speed in different sections of a ski-course and treadmill threshold data. Ten male skiers participated in a freestyle skiing field test (5.6 km), which was performed with dGPS and metabolic gas measurements. A treadmill running threshold test was also performed and the following parameters were derived: anaerobic threshold, threshold of decompensated metabolic acidosis, respiratory exchange ratio = 1, onset of blood lactate accumulation and peak oxygen uptake (VO2peak). The combined dGPS and metabolic gas measurements made detailed analysis of performance possible. The strongest correlations between the treadmill data and final skiing field test time were for VO2peak (l x min(-1)), respiratory exchange ratio = 1 (l x min(-1)) and onset of blood lactate accumulation (l x min(-1)) (r = -0.644 to - 0.750). However, all treadmill test data displayed stronger associations with speed in different stretches of the course than with final time, which stresses the value of a detailed analysis of performance in cross-country skiing. Mean oxygen uptake (VO2) in a particular stretch in relation to speed in the same stretch displayed its strongest correlation coefficients in most stretches when VO2 was presented in units litres per minute, rather than when VO2 was normalized to body mass (ml x kg(-1) x min(-1) and ml x min(-1) x kg(-2/3)). This suggests that heavy cross-country skiers have an advantage over their lighter counterparts. In one steep uphill stretch, however, VO2 (ml x min(-1) x kg(-2/3)) displayed the strongest association with speed, suggesting that in steep uphill sections light skiers could have an advantage over heavier skiers.

Adolescent↗
PubMed1989

The effect of voluntary ventilation on acid-base responses to a Moo Duk Tkow form.

Voluntary control of breathing is taught in Moo Duk Tkow in order to maximize force during striking, kicking, and blocking. Form, a formalized practice routine which incorporates these techniques, is a short predetermined sequence of arm and leg movements performed at high intensity which includes a number of pauses. The purpose of this study was to investigate the acid-base and lactate responses to a beginning level form, Ki Cho I. Nine subjects, five black belts and four brown belts, were asked to perform Ki Cho I at competitive intensity. Arterialized finger capillary blood was drawn prior to and immediately after the form for the determination of pH, bicarbonate, base excess, and PCO2 by use of the Siggaard-Anderson Nomogram. Heart rate was obtained by ECG, and lactate was measured by enzymatic assay. Statistically significant differences (p less than .05) were found for all variables. Mean pre and post values (+/- standard deviations) were: pH 7.39 +/- .04 to 7.34 +/- .03; base excess -.3 +/- 1.2 to -2.8 +/- 1.7 mEq/L; bicarbonate 23.7 +/- 1.0 to 21.8 +/- 1.4 mEq/L; PCO2 39.9 +/- 3.9 to 45.1 +/- 5.4 mmHg; lactate 1.51 +/- .71 to 3.23 +/- 1.56 mM; and heart rate 74.9 +/- 12.6 to 132.1 +/- 17.0 bpm. The mean form time was 17.2 +/- 1.8 s. It was concluded that respiratory compensation does not occur and that respiratory acidosis may contribute to the metabolic acidosis.

Acid-Base Equilibrium↗
PubMed1989

On the role of sodium ions in the regulation of the inward-rectifying potassium conductance in cat ventricular myocytes.

The conductance of the inward-rectifying K+ current (IK1) in isolated cat ventricular myocytes is decreased by reducing the extracellular Na+ concentration. Using a whole-cell patch-clamp technique, possible mechanisms underlying this Na+ dependence were investigated. These included (a) block of inward K+ current by the Na+ substitute, (b) changes in membrane surface charge associated with removal of extracellular Na+, (c) increases of intracellular Ca2+ due to suppression of Na-Ca exchange, (d) reduction of a Na+-dependent K+ conductance due to a subsequent decrease of intracellular Na+, (e) reduction of IK1 conductance (gK1) associated with reduction of intracellular pH due to suppression of Na-proton exchange. The findings support the hypothesis that the effect of removing Na+ is mediated through a decrease in intracellular pH. These include observations that: (a) reducing internal pH by reducing external pH caused a decrease in gK1, and the conductance changes caused by reducing extracellular pH and removing extracellular Na+ were not additive: (b) the effect of reducing pHo was attenuated by dialyzing with a low pH internal solution; (c) gK1 was reduced by exposure to the Na-proton exchange inhibitor dimethylamiloride, and this effect was absent in the absence of Na+. These findings imply that physiological or pathological processes such as ischemia and metabolic or respiratory acidosis which can produce intracellular acidosis should be expected to affect K+ permeation through the IK1 channel.

Animals↗
PubMed2005

Extracellular and intracellular acid-base status with regard to the energy metabolism in the oyster Crassostrea gigas during exposure to air.

The acid-base status of extra- and intracellular fluids was studied in relation to the anaerobic energy metabolism in the adductor muscle, mantle, gills, and heart of the marine bivalve Crassostrea gigas after exposure to air for periods of 2, 4, 8, 12, 24, and 48 h. Such exposure was found to cause a significant reduction in the pH in the hemolymph (pH(e)) within the first 4 h. The decrease in the pHe was accompanied by elevated Pco2 values, causing [HCO3-] to rise (respiratory acidosis). Thereafter, the pHe fell at a lower rate, and this fall was partially compensated for by a further increase in [HCO3-] in the hemolymph. The increase in the [Ca] levels in the hemolymph indicates a mobilization of Ca2+ from CaCO3 and the involvement of bicarbonates in the buffering of pHe. The main anaerobic end-products that accumulated in the tissues during the first stages of anaerobiosis were alanine and succinate, at a ratio of about 2 : 1. Later on, propionate and acetate were also accumulated at significant rates. In contrast to the adductor muscle, gills, and mantle, opine production in the heart was significant after 12-24 h of exposure to air. Determination of intracellular pH (pHi) revealed that there is a close relationship between the rate of anaerobic end-product accumulation and the extent of intracellular acidosis in the adductor muscle, mantle, and gills. On the contrary, accumulation of anaerobic end-products in the heart did not cause any significant change in its pHi. The intracellular nonbicarbonate, nonphosphate buffering value (beta (NB,NPi)) was determined to be higher in the heart than in the other three tissues and thus probably plays a crucial role in stabilizing heart pHi during exposure to air.

Acid-Base Equilibrium↗
PubMed2004

Pneumothorax masked by subcutaneous emphysema after laparoscopic nephrectomy.

An 81-year-old man with an enhancing upper-pole renal mass underwent laparoscopic nephrectomy via a retroperitoneal approach. Postoperatively, his systolic blood pressure declined to 72 mm Hg, and arterial blood gas analysis suggested acute respiratory acidosis. Chest radiography suggested subcutaneous emphysema, but a CT scan showed tension pneumothorax. This case illustrates the difficulties in interpretation of chest films caused by the subcutaneous air that is routinely present after laparoscopic procedures.

Aged↗
PubMed1985

pH-dependent accumulation of fentanyl, lofentanil and alfentanil by beating guinea pig atria.

The influence of the pH of the incubation medium on the cellular accumulation of tritiated fentanyl, lofentanil, and alfentanil was investigated in isolated guinea pig atria. Fentanyl and lofentanil accumulated in atrial tissue up to about 30- and 50-fold, respectively. The amount of drug bound when equilibrium was attained was found to be dependent upon the pH of the medium. By plotting binding equilibria v. pH of the bath, curves were obtained which resembled titration curves. Half-maximal binding was attained at pH values close to the pKa values of fentanyl and lofentanil. Alfentanil was found to accumulate less. The uptake by the tissue was strongly proportional to the extracellular concentration. Atria equilibrated with fentanyl at pH 8.5 released the compound rapidly when exposed to a pH of 7.0, even in the continuous presence of fentanyl in the bath. The consequences of the findings for in vivo conditions are discussed with respect to a possible augmentation of the actions of fentanyl by respiratory acidosis.

Alfentanil↗
PubMed2004

Suspected GHB overdoses in the emergency department.

Blood specimens from 146 suspected gamma-hydroxybutyrate (GHB) overdose cases, presenting to an emergency department in Washington State over a 12-month period, were analyzed for GHB and other drugs. Of these 146 patients, GHB was confirmed in approximately one-third of the patients (N = 54), sometimes in potentially toxic concentrations. These patients were aged between 17 and 59 years (median 28 years), and 83% were male. Blood GHB concentrations ranged from 29 to 490 mg/L (mean 137 mg/L; median 103 mg/L). In 36 (67%) of the 54 patients, other drugs were additionally detected. Ethanol was measured in 22 (41%) patients, with concentrations ranging from 0.01 to 0.26 g/100 mL (median 0.04 g/100 mL). Other commonly co-administered drugs included 3,4-methylenedioxymethamphetamine, marijuana, methamphetamine, cocaine, and citalopram. Frequently observed clinical symptoms on admission for the GHB overdose group included copious vomiting, ataxia, lack of gag reflex, respiratory depression, mild acute respiratory acidosis, unconsciousness, and sudden altered states of consciousness. Many patients required intubation, and several became combative and required restraints. The majority of patients were discharged within 6 h of hospital admission. However, despite presenting with similar clinical symptoms on admission, GHB was not confirmed in 92 of the 146 overdose patients, suggesting that GHB overdose cases may frequently be indistinguishable from other drug overdoses or medical conditions.

Adolescent↗
PubMed1997

Near-fatal but reversible acute renal failure after massive ibuprofen ingestion.

Adverse effects of nonsteroidal antiinflammatory drugs are frequently seen because of the extremely widespread use of these agents. Nephrotoxicity is relatively uncommon with the drug ibuprofen and, when present, is usually rapidly reversible. Fatal acute renal failure from ibuprofen has never been reported. This is the case of a patient with multiple medical problems who had near-fatal acute renal failure after the ingestion of 36 g ibuprofen, and who required dialysis for several months, at which point renal function improved. He did not admit to ibuprofen ingestion at the time of admission, and some of the clinical manifestations, including anion gap metabolic acidosis, respiratory alkalosis, and mental status abnormalities, could be accounted for by renal failure. Hence, this diagnosis was not considered during admission. However, the patient admitted to ibuprofen ingestion after his mental status improved with hemodialysis. A number of other variables were present that probably contributed to the development of acute renal failure, such as the presence of long-term renal insufficiency, hypotension, and possibly other drug ingestion. Acute renal failure with massive ibuprofen ingestion may be fatal or may show delayed reversibility even after necessitating dialysis for several months.

Acute Kidney Injury↗
PubMed1995

Detection of tissue hypoxia by arteriovenous gradient for PCO2 and pH in anesthetized dogs during progressive hemorrhage.

The present study tested the hypothesis that, during acute bleeding, the development of tissue hypoxia might be reflected by an abrupt widening in arteriovenous gradient for PCO2 (AV PCO2) and for pH (AV pH) as accurately as by an increase in blood lactate levels. Twenty-four anesthetized (isoflurane 1.4% end-tidal), paralyzed, and mechanically ventilated dogs submitted to progressive hemorrhage were studied. Oxygen uptake (VO2) was derived from expired gas analysis and oxygen delivery (DO2) was calculated by the product of the thermodilution cardiac index and the arterial O2 content. During the first part of the protocol, VO2 remained stable as the progressive reduction in DO2 was associated with a corresponding increase in O2 extraction (O2ER). Blood lactate increased slightly but not significantly. AV PCO2 and AV pH increased significantly, essentially related to venous respiratory acidosis. The critical value of DO2 below which VO2 decreased was 8.95 +/- 1.60 mL.min-1.kg-1. Below this value, there was a marked increase in blood lactate and an abrupt widening in AV PCO2 and AV pH gradients. The critical value of DO2 obtained from blood lactate, AV PCO2 and AV pH were similar to those obtained from VO2 (8.60 +/- 1.12; 8.73 +/- 1.40; 8.78 +/- 1.37, respectively; P = not significant). A significant correlation was found, during the hemorrhage protocol, between blood lactate and AV PCO2 (r = 0.84; P < 0.001) or AV pH (r = 0.78; P < 0.001). Therefore, AV PCO2 and AV pH represent simple but reliable indicators of tissue hypoxia during hemorrhagic shock.

Animals↗
PubMed2002

Target-controlled versus manually-controlled infusion of propofol for direct laryngoscopy and bronchoscopy.

UNLABELLED: Few studies have compared the clinical profile of target-controlled infusions of propofol with that of manually-controlled infusions. Fifty-four ASA physical status I or II patients scheduled for an elective otorhinolaryngology endoscopy performed under general anesthesia with spontaneous ventilation were enrolled in this prospective randomized study to compare the clinical outcome of such administrations. Before induction, all patients received a single alfentanil bolus dose (10 microg/kg). Propofol administration was adapted to maintain absence of movement, hemodynamic stability, and efficient spontaneous ventilation. When compared with the Manually-Controlled Infusion group, in the Target-Controlled Infusion group there were fewer movements at insertion of the laryngoscope (14.8% vs. 44.4%), improved hemodynamic stability (largest variations of mean arterial blood pressure <10% of control values, versus 20%), fewer episodes of apnea, and less respiratory acidosis after endoscopy (pH = 7.37 +/- 0.05 and PaCO(2) = 50 +/- 7 mm Hg versus pH = 7.28 +/- 0.06 and PaCO(2) = 58 +/- 9 mm Hg); the recovery was also shorter (time to opening eyes or verbal response, 4.6 +/- 2.0 min and 6.8 +/- 2.5 min versus 10.8 +/- 7.3 min and 15.7 +/- 7.1 min). Propofol consumption was comparable in the two groups. Targeting the effect-site concentration improved the time course of the propofol drug effect during direct laryngoscopy performed during spontaneous ventilation when compared with manual infusion. IMPLICATIONS: This study compares the clinical profile of propofol anesthesia for direct laryngoscopy with spontaneous ventilation when the drug is administered either as a manually controlled infusion or by targeting the effect-site concentration through a target-controlled infusion (TCI) device. TCI improves the time course of propofol effects.

Adult↗
PubMed1989

Fentanyl-induced muscle rigidity in unanesthetized and ketamine- or thiopental-anesthetized rats.

This study was undertaken to search for an alternative experimental model in the evaluation of fentanyl-induced muscle rigidity. Unanesthetized, spontaneously ventilating Sprague-Dawley rats, and rats anesthetized with either ketamine or thiopental whose ventilation was mechanically controlled, were studied. Intravenous administration of fentanyl (25, 50, or 100 micrograms/kg) caused an increase in electromyographic (EMG) activity in both unanesthetized and ketamine-anesthetized, but not in thiopental-anesthetized, animals. Muscle rigidity was more prominently manifested in the gastrocnemius muscle, when compared with the rectus abdominis muscle. Hypoxemia was exhibited during the course of rigidity by both spontaneously ventilating and ketamine-anesthetized rats, but not by thiopental-anesthetized animals. In addition, unanesthetized, spontaneously ventilating rats developed hypercarbia and respiratory acidosis. The authors suggest that, in addition to using unanesthetized animals, EMG activity in the gastrocnemius muscle of rats anesthetized with ketamine in whom ventilation is controlled may provide an alternative approach in the evaluation of fentanyl-induced muscle rigidity.

Anesthesia↗
PubMed1991

Cerebral blood flow response to PaCO2 during hypothermic cardiopulmonary bypass in rabbits.

Differences in cerebral blood flow (CBF) between alpha-stat and pH-stat management depend on preserved responsiveness of the cerebral vasculature to changes in arterial carbon dioxide tension (PaCO2). We tested the hypothesis that hypothermia-induced reductions in CBF would decrease the CBF response to changing PaCO2 (delta CBF/delta PaCO2). Anesthetized New Zealand white rabbits were randomly assigned to one of three temperature groups--group 1 (37 degrees C, n = 9); group 2 (31 degrees C, n = 10); or group 3 (25 degrees C, n = 10)--and were cooled using cardiopulmonary bypass. After esophageal temperature equilibration (approximately 40 min), oxygenator gas flows were serially varied to achieve PaCO2 values of 20, 40, and 60 mm Hg (temperature-corrected). All animals were studied at all three PaCO2 levels in random order. At each level of PaCO2, CBF and masseter blood flow were determined using radiolabeled microspheres. There were no significant differences between groups with respect to mean arterial pressure (approximately 80 mmHg), central venous pressure (approximately 4 mmHg), or hematocrit (approximately 22%). Prior normothermic studies have found delta CBF/delta PaCO2 to be proportional to CBF. Nevertheless, in this study, with hypothermia-induced reductions in CBF, delta CBF/delta PaCO2 was not significantly different between temperature groups. Thus, hypothermia either increased the sensitivity of the cerebral vasculature to carbon dioxide and/or increased the effective level of cerebrospinal fluid respiratory acidosis produced by each increment of temperature-corrected PaCO2.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗