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Biomedical subjects

L Fagraeus

Publications and source records attributed to L Fagraeus.

At least 19 recordsLinked to original sources
PubMed1991

Rapid reduction of intestinal cytochrome a,a3 during lethal endotoxemia.

In vivo near-infrared spectrophotometry was used to determine whether lethal endotoxemia impairs small intestinal oxidative phosphorylation as reflected by the redox state of mitochondrial cytochrome a,a3 (AA3). Adult male Sprague-Dawley rats were anesthetized with 2.1% isoflurane in 30% O2:70% N2O, and the small intestine was partially exteriorized for spectrophotometric monitoring (OMNI-3). By 5 min after an iv bolus of Escherichia coli endotoxin (40 mg/kg, LD90, n = 7) a significant shift toward reduction in intestinal AA3 had occurred in association with hypotension and a marked fall in both superior mesenteric artery blood flow (SMAF) and cardiac output. In a separate group (n = 7) SMAF was kept at the baseline level by periodic infusions of donor rat plasma begun 1 min after endotoxin injection, and the reduction in AA3 was again found despite the fluid loading intervention which successfully maintained not only organ blood flow, but also cardiac output and mean arterial pressure in their normal ranges. Further experiments (n = 34) measuring SM vascular bed oxygen consumption indicated that intestinal VO2 remained unchanged during early endotoxemia. These findings suggest a rapid impairment of oxidative phosphorylation by endotoxin which seems to occur through direct (and/or indirect) toxic cellular effects rather than through impaired tissue perfusion.

Animals↗
PubMed1990

Evaluation of thyrotropin releasing hormone as a therapeutic intervention for endotoxemia.

Thyrotropin releasing hormone (TRH) has been reported to reduce endotoxin-induced hypotension and mortality rate in conscious rats. Limited data are available to explain these effects. We evaluated hemodynamic parameters, metabolic function, tissue injury, and survival rate in three groups of instrumented conscious rats following intravenous endotoxin (20 mg/kg, LD/90-24 h) challenge. Pretreatment with TRH (2.0 mg/kg, i.v.) was administered 10 min before endotoxin (n = 10) and control (n = 10) animals were given an equivalent volume of saline. The post-treated group (n = 7) was given TRH at the nadir of the hypotensive response following endotoxin to duplicate published protocols. 5 min after endotoxin blood pressure and cardiac output were significantly higher in the post and pre-treatment groups, respectively, compared to the untreated group. There were no differences at other times. Systemic vascular resistance was not affected by either treatment mode at any time. TRH treatment following endotoxin resulted in transient increases in heart and respiration rates and decreased central venous pressure during the first 30 min. Metabolic function indicated by measurements of glucose, lactate, hematocrit, pH, PO2, and PCO2 at 60 and 240 min after endotoxin was not modified by TRH. The hemorrhagic small intestine characteristic of this model was not improved by either treatment mode. Mortality rates at 4 h after endotoxin were 20% for the untreated, 40% for the pre-treated, and 43% for the post-treated. These results suggest TRH exerts early transient effects on cardiovascular responses evoked by endotoxin in the conscious rat but no lasting beneficial effects were found to support the use of TRH as a mono-therapy for endotoxemia.

Animals↗
PubMed1990

Anesthetic considerations in geriatric patients.

The increasing number of geriatric patients presenting for surgical procedures provides continuing anesthetic challenges. With an understanding of each patient's situation and communication among all the participants in the procedural chain (patient, family, and the anesthesia, surgical, and nursing teams), a well-planned and well-executed anesthetic should help ensure a favorable outcome. The complexities outlined demonstrate that there is not one best way for every patient; rather, an individualized approach is necessary.

Aged↗
PubMed1989

Respiratory and cardiovascular effects of thyrotropin-releasing hormone as modified by isoflurane, enflurane, pentobarbital and ketamine.

Thyrotropin-releasing hormone (TRH) possesses significant arousing and cardio-respiratory stimulant actions. The effects of a 2 mg/kg i.v. bolus dose of TRH on respiration and systemic hemodynamics were compared in conscious, freely-moving rats and during anesthesia with 4 different anesthetics. Fifty-four male Sprague-Dawley rats weighing 285 +/- 4 g (mean +/- S.E.M.) were divided into 5 groups: conscious, enflurane (2%), isoflurane (1.4%), pentobarbital (8 mg/kg/h i.v.), and ketamine (60 mg/kg/h i.v.). Anesthetized rats were intubated and breathed oxygen or anesthetic/oxygen spontaneously. Aortic blood pressure, heart rate, cardiac output, respiratory rate, arterial blood pH, blood gases, lactate and glucose were measured, and data were collected over a 20 min baseline period and for 130 min post-TRH. TRH increased respiratory rate in all groups; concomitant changes in arterial PCO2 indicated increased minute ventilation in the inhalation agent groups but not in the i.v. anesthetic groups or in the awake group. Significant respiratory depression in the enflurane group was rapidly reversed by TRH. The respiratory stimulant and arousing effects of TRH were smallest with ketamine anesthesia. The hemodynamic responses to TRH were consistent with a pattern of sympathoadrenalmedullary activation and were relatively uniform across groups despite anesthetic-induced alterations in baseline values. TRH or its analogues may prove useful as an analeptic in clinical anesthesia.

Animals↗
PubMed1989

Arterial oxygen saturation in sedated patients undergoing gastrointestinal endoscopy and a review of pulse oximetry.

The pulse oximeter is a widely used noninvasive monitor which provides a continuous reading of arterial oxygen saturation. We sought to determine if patients with cardiopulmonary disease were at higher risk of oxygen unsaturation than controls during gastrointestinal endoscopy. Patients presenting for upper gastrointestinal endoscopy and/or colonoscopy were placed into one of two groups: A. control population:patients with no history of cardiac and/or pulmonary disease (N = 11); B. test population:patients with a history of cardiac and/or pulmonary disease (N = 39). The procedure was performed by one of 14 equally experienced physicians. The Nellcor N-100 Pulse Oximeter and D-25 finger probe were used to monitor arterial oxygen saturation which was recorded at five minute intervals from commencement of intravenous sedation analgesia to 15 minutes post-procedure. In both groups, the oxygen saturation fell to statistically significant. A: 98.3% to 90.2%; B: 97.7% to 89.5%. However, the amount of unsaturation which occurred in Group B was not statistically different from Group A. Therefore, history of prior cardiac and/or pulmonary disease does not increase the degree of unsaturation from that occurring in patients with no such history. In addition, the effects of age, procedure, duration, I.V. sedation, and individual tolerance on oxygen unsaturation were studied by regression analysis and analysis of variance (ANOVA). Only the upper GI endoscopy patients showed a dependence of oxygen unsaturation upon one of the variables, specifically patient tolerance. It is concluded that patients at risk for hypoxemia during endoscopy or colonoscopy cannot be determined prior to the initiation of the procedure, and it is recommended that all of these patients be given supplemental oxygen as well as monitored with a pulse oximeter.

Endoscopy↗
PubMed1988

Improved techniques for cardiovascular monitoring in rats as applied during endotoxemia.

We describe a new combination of techniques for measurements of systemic blood pressure, central venous pressure, pulmonary arterial (PA) pressure, PA wedge pressure, and cardiac output in the rat. Application of the method to the conscious rat in a septic shock (Escherichia coli endotoxin iv injection) model demonstrated a response pattern of decreased cardiac output and stroke volume, increased total peripheral vascular resistance and heart rate, and transiently decreased systemic arterial pressure. In the pulmonary circulation, a very brief hypertension and a sustained increase in pulmonary vascular resistance were observed, but changes in PA wedge pressure were small. The soft PA catheter (0.3 mm ID, 0.6 mm OD) had no undue effects on cardiovascular function. We suggest that this combined technique could be useful for many cardiovascular studies in the rat, not only as related to shock research.

Animals↗
PubMed1987

Dose-related effects of isoflurane on superior mesenteric vasoconstriction induced by endotoxemia in the rat.

To investigate the interplay between endotoxin-induced circulatory shock and the cardiovascular effects of different doses of isoflurane, mean aortic pressure (MAP), central venous pressure (CVP), mean pulmonary arterial pressure (MPAP), heart rate (HR), cardiac output and superior mesenteric artery flow (SMAF), were monitored in rats anesthetized with either 1.4% or 2.0% isoflurane in oxygen. Cardiac index (Cl), total peripheral vascular resistance (TPR) and superior mesenteric vascular resistance (SMVR) were derived. During continuous administration of isoflurane, endotoxin (LD90, 40 mg X kg-1 iv) was given after a 30-min baseline period, and data were collected for an additional 2-h period. Sham-challenged (saline) animals served as controls. The response to endotoxin in the systemic circulation showed a decrease in Cl and MAP, while HR and TPR increased. MPAP and CVP were essentially unchanged. There were no significant differences in the systemic circulation variables between endotoxin groups, apart from a more pronounced HR increase during 1.4% isoflurane. Regionally, however, SMAF was lower and SMVR was higher in the 2.0% versus the 1.4% isoflurane group following endotoxin. To conclude, the degree of mesenteric vasoconstriction during endotoxemia was dependent on the dose of isoflurane. This dose-related effect seems to be mediated through interaction with intrinsic vascular control, a higher dose allowing a more pronounced local blood flow reduction.

Animals↗
PubMed1987

Choice of anesthetic alters the circulatory shock pattern as gauged by conscious rat endotoxemia.

A standardized rat endotoxin shock model was used to assess the differential effects of four commonly used anesthetics upon hemodynamics before and during endotoxin shock. Forty-nine male Sprague-Dawley rats weighing 307 +/- 4 g were divided into five groups:freely-moving conscious, enflurane (2%), isoflurane (1.4%), pentobarbital (6 mg.kg-1.h-1 i.v.), and ketamine (45 mg.kg-1.h-1 i.v.). Anesthetic doses were chosen as 1.0 MAC equivalent. Anesthetized rats were intubated and ventilated with oxygen. The right carotid artery was cannulated with a thermocouple-catheter for aortic blood pressure, heart rate, and thermodilution cardiac output measurements. The right jugular vein was cannulated for measurement of central venous pressure and for i.v. injections. Data were collected over a 30-min baseline period and for 4 h after an i.v. bolus of endotoxin (40 mg.kg-1, LD100 within 24 h). Gross small intestinal pathology was rated on a 0-4 scale. Anesthetic effects were judged in terms of significant deviations from the awake data on each parameter. Despite differing patterns, total deviations were similar for enflurane, ketamine, and pentobarbital, although the latter drug was the least preferable due to particularly high systemic vascular resistance. Significantly less hemorrhagic small intestinal pathology occurred with enflurane. Ketamine offered no advantage over the inhalation anesthetics. Among the four anesthetics tested, results were closest to the awake pattern with isoflurane anesthesia, thus making it the logical choice for hemodynamic studies in experimental shock research.

Anesthetics↗
PubMed1986

Safety and efficacy of epidural analgesia in spine surgery.

Over the last 4 years, the authors have had experience with epidural analgesia for a variety of spinal operations in 24 patients. It has proved to be safe, reliable, and effective. No patient has had a new neurological deficit as a result of the epidural technique, and 18 of 22 patients with neurological deficit improved. Thus, epidural analgesia should not be excluded from the anesthesiologist's consideration simply because of the presence of spine disease or neurological deficit.

Adult↗
PubMed1985

Evaluation of cardiac output, total peripheral vascular resistance, and plasma concentrations of vasopressin in the conscious, unrestrained rat during endotoxemia.

To eliminate the influence of anesthesia while investigating the role of vasoactive hormones during shock, we have developed an unanesthetized rat model that provides information on key cardiovascular parameters pertinent to shock. Enfluane anesthesia was used while the animals were being catheterized. After recovery from anesthesia, endotoxin (40 mg/kg) was given, and after 4 hr of measurements, animals (11) were killed. Cardiac index (CI) fell significantly 5 min after endotoxin and remained depressed for 4 hr. Mean blood pressure (MBP) decreased from 121 +/- 5.7 mmHg to 79 +/- 5.6 at 5 and 15 min, and increased to 113 +/- 3.0 at 180 min. Central venous pressure (CVP) was decreased from 30 min to the end of the study. Heart rate (HR) increased from 357 +/- 13 to a high of 448 +/- 14 at 5 min and remained at well over 400 for the 4-hr monitoring period. Total peripheral vascular resistance (TPVR) was twice that of the control at 30 min and remained elevated. Stroke volume decreased to 37% of that of the control at 15 and 30 min and remained at 50% of that of the control until sacrifice. Plasma concentrations of vasopressin measured by radioimmunoassay increased from 14 pg/ml (+/- 2.2, SEM) to 144 (+/- 56) and 144 (+/- 66) at 15 and 240 min after endotoxin. Pathological examination at the end of the study revealed extensive hemorrhage in all areas of the small intestine. We conclude that in the conscious endotoxic rat decreases in CI, MBP, and CVP are accompanied by compensatory increases in HR and TPVR; plasma vasopressin concentrations are greatly elevated; and severe small intestinal hemorrhage occurs. The control animals (12) were stable throughout the entire study period, establishing the conscious, instrumented, unrestrained rat presented here as an attractive model for the study of shock without the bias of anesthesia.

Animals↗
PubMed1984

Myocardial depression by anesthetic agents (halothane, enflurane and nitrous oxide): quantitation based on end-systolic pressure-dimension relations.

The end-systolic pressure-diameter relation of the left ventricle was used to examine the effect of halothane, enflurane and nitrous oxide on left ventricular (LV) contractility in 10 dogs chronically instrumented with dimension transducers to measure LV diameter and micromanometers to measure LV transmural pressure. Contractility was assessed by the slope (EES) of the end-systolic pressure-diameter relation. A new index that identifies the dose of anesthetic necessary to depress the inotropic state by 20% (ID20) was calculated to be 0.63% for halothane and 1.55% for enflurane, indicating a greater apparent myocardial depressant effect of halothane than enflurane. However, when these agents were compared at equi-anesthetic concentrations by normalizing the ID20 to the minimal alveolar concentration of each drug, they had comparable degrees of myocardial depressant effects. This measurement technique was used in 7 patients undergoing coronary artery bypass grafting conducted under narcotic anesthesia showing that halothane induced a similar depression of contractility. The use of ID20 should allow reclassification of anesthetic agents according to their myocardial depressant effects.

Anesthesia↗
PubMed1983

The influence of time on the response to dopamine after coronary artery bypass grafting: assessment of left ventricular performance and contractility using pressure/dimension analyses.

Pressure and dimension analyses were used to quantitate the changing cardiac response to dopamine over a 24-hour interval after coronary artery bypass grafting (CABG). Ultrasonic dimension transducers were utilized to measure the minor-axis diameter of the left ventricle, and matched micromanometers were inserted to measure intracavitary left ventricular pressure and intrathoracic pressure. Pressure and dimension data were recorded and analysed by computer during dopamine infusion at 0, 2.5, 5.0, and 10.0 micrograms per kilogram per minute, at periods designated as early (2 to 4 hours after CABG) and late (18 to 24 hours after CABG). Myocardial contractile responses to dopamine (peak velocity of minor-axis shortening, maximal excursion) were similar at each dose in the early and late studies. However, overall hydraulic performance, as reflected by cardiac outputs and the areas of the pressure/diameter work loops, had augmented late dose responses. This study suggests a major change in the relationship between the heart and peripheral control mechanisms that may partially explain diminishing inotropic requirements over time, in addition to the generally accepted occurrence of improvement in contractile state and functional reserve following cardiac operation.

Angina Pectoris↗
PubMed1983

The mechanism of halothane-induced myocardial depression. Altered diastolic mechanics versus impaired contractility.

Although halothane has been shown to depress left ventricular function, it remains a common alternative to narcotic anesthesia in cardiac operations. To clarify the mechanism by which this functional depression occurs (direct decrease in contractility versus altered diastolic compliance), we studied seven dogs in the closed-chest state following instrumentation with ultrasonic dimension transducers to measure left ventricular anteroposterior diameter and micromanometers to measure transmural left ventricular pressure. Ventricular volumes were varied with transient vena caval occlusions in the awake state and following general anesthesia with halothane at 1% and 2% end-tidal concentrations. Ventricular contractility was assessed by the slope of the end-systolic pressure-diameter relationship (EES). Following normalization of end-diastolic diameters with a Lagrangian strain definition (E), diastolic compliance was assessed by fitting end-diastolic pressure-strain data to the exponential: P = alpha (e beta E -1), where alpha and beta are nonlinear elastic coefficients. Halothane was found to produce a significant, dose-dependent decrease in EES from 10.6 +/- 0.6 control to 6.7 +/- 0.4 at 1% halothane and 4.2 +/- 0.5 at 2% halothane (p less than 0.05, control versus both 1% and 2% halothane). Furthermore, halothane at the concentrations studied did not significantly alter alpha and beta nor significantly shift the exponential end-diastolic pressure-strain curve from control. These data indicate that halothane produces a direct, severe depression of left ventricular contractility without primarily altering the diastolic mechanical properties of the myocardium.

Animals↗
PubMed1982

The effect of PEEP on left ventricular diastolic dimensions and systolic performance following myocardial revascularization.

To quantitate the alterations in left ventricular (LV) dimensions and performance at successive levels of positive end-expiratory pressure (PEEP), 16 patients undergoing coronary artery bypass grafting (CABG) underwent instrumentation with ultrasonic dimension transducers to measure the minor-axis diameter of the left ventricle. Matched micromanometers were placed to measure intracavitary LV pressure and intrathoracic pressure. LV pressure and dimension data were recorded and computer analyzed during continuous positive-pressure ventilation at 0, 5, 10, and 15 cm H2O of PEEP 4 to 8 hours postoperatively. Preload was determined by the end-diastolic minor-axis diameter, cardiac output was measured by thermodilution, and indices of LV contractility assessed included the maximal velocity of minor-axis shortening and the slope of the end-systolic pressure-diameter relationship. PEEP produced a progressive increase in intrathoracic pressure associated with a fall in cardiac output; this was associated with a decrease in LV end-diastolic diameter and no significant change in the maximal velocity of minor-axis shortening or the slope of the end-systolic pressure-diameter relationship. Our results indicate that PEEP of 10 cm H2O or greater will produce a significant fall in cardiac output in patients following CABG, due to a decrease in preload rather than impaired LV contractility.

Angina Pectoris↗