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Biomedical subjects

R D Fitzgerald

Publications and source records attributed to R D Fitzgerald.

At least 37 records · Page 2Linked to original sources
PubMed1997

Transfusing red blood cells stored in citrate phosphate dextrose adenine-1 for 28 days fails to improve tissue oxygenation in rats.

OBJECTIVE: To determine whether the time that red blood cells are stored in citrate phosphate dextrose adenine-1 solution before transfusion alters the ability to improve tissue oxygenation. DESIGN: Prospective, randomized, controlled study. SETTING: University research institute laboratory. SUBJECTS: Male Sprague-Dawley rats (350 to 450 g). INTERVENTIONS: Twenty-four hours after randomization to sham laparotomy (n = 21) or cecal ligation and perforation (n = 16)1 supply-dependency of systemic oxygen uptake (VO2) was induced in rats by isovolemic hemodilution. Rats were then re-randomized to receive either rat red blood cells stored in citrate phosphate dextrose adenine-1 for 3 days ("fresh" n = 17) or rat red blood cells stored in citrate phosphate dextrose adenine-1 for 28 days ("old" n = 20). MEASUREMENTS AND MAIN RESULTS: Changes in systemic VO2 were measured for 90 mins to determine the efficiacy of the treatment. Statistical analysis included a fully factorial repeated-measures, generalized linear model. No significant interaction was found between cecal ligation and perforation or sham animals and transfusion with fresh or old red blood cells. However, comparing the combined groups of animals receiving either fresh or old red blood cells, we found that after the transfusion of old red blood cells, systemic VO2 was not significantly improved (after hemodilution 1.68 +/- 0.27 mL/100 g/min, after transfusion 1.86 +/- 0.17 mL/100 g/min; p > .05). In contrast, transfusion with fresh red blood cells acutely increased systemic VO2 (after hemodilution 1.62 +/- 0.06 mL/100 g/min, after transfusion 2.10 +/- 0.09 mL/100 g/min; p = .049). CONCLUSION: Storage of rat red blood cells for 28 days in citrate phosphate dextrose adenine-1 impaired their ability to improve tissue oxygenation when transfused into either control or septic rats placed into supply dependency of systemic VO2.

Adenine↗
PubMed1997

Animal models for blood transfusion: a model for sterile blood sampling in the rat.

Rat blood is frequently used for experimental transfusion. However, no data are available concerning the quality of the blood used, although bacterial contamination could severely alter results. To obtain large quantities of sterile rat blood for a transfusion study, we tested carotid artery cannulation, known as a standard procedure. Blood cultures from the collected blood showed polymicrobial overgrowth even after sterility measures were improved. In contrast, the puncture of the abdominal aorta proved to be a simple and reliable method for the collection of sterile blood. We conclude that studies using blood collected from donor rats should be controlled and the quality of such blood be tested before transfusion.

Animals↗
PubMed1996

Endocrine stress reaction to surgery in brain-dead organ donors.

We studied the course of plasma levels of the stress markers adrenocorticotropic hormone (ACTH), cortisol, human growth hormone (h-GH), beta-endorphin, and prolactin during retrieval surgery in eleven brain-dead organ donors scheduled for multiple organ explantation. Donors were divided into two groups according to hemodynamic stability. Hormones demonstrated a great variability in plasma levels and in the pattern of reaction, revealing a different degree of remaining pituitary function. Beta-Endorphin was the only stress hormone that showed a response to surgical stimuli in six patients. Only three of them developed a concomitant rise in ACTH. Cortisol, prolactin, and h-GH plasma levels did not change during the observation period. In the three cases with a slight elevation in ACTH, no subsequent change in cortisol was detectable. Beta-Endorphin showed greater variability and a tendency to higher levels in the group presenting with a higher arterial pressure, which resulted in a significant difference (P < 0.005) when distributions were compared using the Mann-Whitney U-test. No correlation was found between hypotensive episodes and deficiencies of other stress hormones. We conclude that pituitary function varies considerably in brain-dead organ donors without demonstrating a correlation to the onset of hypotension. Thus, we feel no need for a substitution treatment with any of the hormones investigated prior to organ explanation.

Adrenocorticotropic Hormone↗
PubMed1996

The acute respiratory distress syndrome: definitions, severity and clinical outcome. An analysis of 101 clinical investigations.

OBJECTIVE: To determine possible changes in outcome from acute respiratory distress syndrome (ARDS) and to compare severity of lung injury and methods of treatment from 1967 to 1994. DATA SOURCES: Computerized (Medline, Current Contents) and manual (Cumulated Index Medicus) literature search using the key word and/or title ARDS. STUDY SELECTION: Only clinical studies published as full papers reporting data on both patient mortality (survival) and oxygenation index (PaO2/FIO2) were included. Single case reports, abstracts, reviews and editorials were excluded from evaluation. DATA EXTRACTION: Relevant data were extracted in duplicate, followed by quality checks on approximately 80% of data extracted. DATA SYNTHESIS: 101 papers reporting on 3264 patients were included: 48 studies (2207 patients) were performed in the USA, 43 studies (742 patients) in Europe and 10 studies (315 patients) elsewhere. Mortality reported in these studies was 53 +/- 22% (mean +/- SD), with no apparent trend towards a higher survival (1994: 22 studies, mortality 51 +/- 19%). The mean PaO2/FIO2 ratio remained unchanged throughout the observation period (118 +/- 47 mmHg). No correlation could be established between outcome and PaO2/FIO2 or lung injury score. Patients who underwent pressure-limited ventilation had a significantly lower mortality (35 +/- 20%) than patients on volume-cycled ventilation (54 +/- 22%) or patients for whom there was no precise information on ventilatory support (59 +/- 19%). Significantly lower PaO2/FIO2 ratios (61 +/- 17 mmHg) were observed in patients prior to extracorporeal lung assist, together with mortality rates in the range of those for conventionally treated patients (55 +/- 22%). CONCLUSIONS: The mortality of ARDS patients remained constant throughout the period studied. Therefore, the standard for outcome in ARDS should be a mortality in the 50% range. Neither PaO2/FIO2 ratio nor lung injury score was a reliable predictor for outcome in ARDS. Patients might benefit from pressure-limited ventilatory support, as well as extracorporeal lung assist. Since crucial data were missing in most clinical studies, thus preventing direct comparison, we emphasize the importance of using standardized definitions and study entry criteria.

APACHE↗
PubMed1996

Traumatizing effects of blind oral intubation using the Augustine Guide.

PURPOSE: This study evaluated whether the Augustine Guide, a device enabling blind oral intubation, carries a high risk for laryngopharyngeal trauma in routine airway management. PATIENTS AND METHODS: Telescopic laryngoscopic or microlaryngoscopic examinations were performed in 20 patients before and immediately after blind oral intubation, as well as 24 hours postoperatively. RESULTS: Intubation using the Augustine Guide was successful in all but one patient. However, 18 of 20 patients showed evidence of considerable trauma to the laryngopharyngeal region. Vallecular edema, epiglottic swelling, mucosal lacerations, and vocal cord hematomas, causing a high percentage of postoperative discomfort, occurred in a very uniform pattern. CONCLUSIONS: It was concluded that blind oral intubation using the Augustine Guide should not be used in routine airway management but should only be used in special indications.

Adult↗
PubMed1996

Effectiveness of nitric oxide inhalation in septic ARDS.

STUDY OBJECTIVE: To evaluate the percentage of nitric oxide (NO) responders in septic shock patients with ARDS. Additionally, to investigate long-term NO effects on cardiac performance and oxygen kinetic patterns in NO responders vs nonresponders. DESIGN: Prospective cohort study. SETTING: ICU of a university hospital. PATIENTS: Twenty-five consecutive patients with a diagnosis of septic shock and established ARDS requiring inotropic and vasopressor support. INTERVENTIONS: After diagnosis of ARDS, NO was administered at 18 or 36 ppm. Patients demonstrating a NO-induced rise of arterial oxygen tension of 20% or more and/or a fall in mean pulmonary artery pressure of 15% or more were grouped as NO responders; others were grouped as nonresponders. MEASUREMENTS AND RESULTS: Ten patients (40%) were NO responders, while 15 patients (60%) were nonresponders. Mortality was 40% in NO responders and 67% in nonresponders (NS). NO responders developed a significantly lower mean pulmonary artery pressure (28 +/- 6 vs 33 +/- 6 mm Hg; p < 0.05), lower pulmonary vascular resistance (PVR: 258 +/- 73 vs 377 +/- 163 dyne.s.cm-5.m-2; p < 0.05), and higher PaO2/FIO2 ratio (192 +/- 85 vs 144 +/- 74 mm Hg; p < 0.05) within the study period. In responders, NO-induced afterload reduction resulted in increased right ventricular ejection fraction (RVEF: 40 +/- 7 vs 35 +/- 9%; p < 0.05), significantly higher cardiac index (CI: 4.5 +/- 1.1 vs 4.0 +/- 1.2 L.min-1.m-2; p < 0.05) and oxygen delivery (DO2: 681 +/- 141 vs 599 +/- 160 mL.min-1.m-2; p < 0.05) compared with nonresponders. In NO nonresponders, RVEF was correlated with PVR, CI, DO2, mixed venous oxygen saturation (SvO2), and oxygen extraction ratio (O2ER) (r = +/- 0.60 to +/- 0.69; p < 0.05). No significant correlation between RVEF and any of these parameters was observed in responders. SvO2 (75 +/- 7 vs 69 +/- 8%; p < 0.05) and O2ER (0.24 +/- 0.06 vs 0.27 +/- 0.06; p < 0.05) were significantly different between responders and nonresponders, while no difference in oxygen consumption was observed (161 +/- 41 vs 153 +/- 43 mL.min.m-2). CONCLUSIONS: Inhaled NO is effective in only a subgroup of septic ARDS patients, with a higher, but insignificantly different percentage of survivors in the responder group. NO responders were characterized by increased RVEF accompanied by higher CI, DO2, and lower O2ER. In nonresponders, RVEF remained depressed, with a close correlation between RVEF and CO as well as DO2 and O2ER. Thus, nonresponders seem to suffer from impaired cardiac reserves and correspondingly lower oxygen transport variables.

Administration, Inhalation↗
PubMed1995

Learning versus performance effects of cocaine on discriminative heart rate conditioning in rats.

The study examined the effects of cocaine on learning and performance of a classically conditioned heart rate (HR) discrimination in rats involving two auditory conditioned stimuli (CSs). In the discrimination protocol, one CS (CS+) was paired with the shock unconditioned stimulus (US) on a consistent basis and the other CS (CS-) was always presented alone. Four groups received an IP injection of 1, 3, 10, or 30 mg/kg cocaine and a fifth group received saline. Shortly after the injections, all groups were given six CS-alone trials, followed by 24 randomly sequenced discrimination conditioning trials (12 CS+ and 12 CS-). Approximately 72 h later, all groups were given six test trials with each CS in the absence of cocaine to evaluate the presence or absence of discrimination learning. All cocaine groups showed impaired discrimination performance on the discrimination conditioning trials, reductions in early pretest CS-alone responses, and reductions in resting HR. However, on the non-drug test trials discrimination performance was normal in all cocaine groups. The results established that in spite of major changes in HR dynamics, learning of the HR discrimination was not affected by cocaine but that cocaine did interfere with the performance of the discrimination. Except for the highest 30 mg group, the performance decrement appeared to be related to a cocaine-produced reduction in the capacity to inhibit bradycardia responding to the safe CS-. It was suggested that this loss of inhibitory control may have been due to cocaine changes in a corticothalamic pathway that controls inhibition of bradycardia to a safe CS-.

Animals↗
PubMed1995

Stress response to tracheal intubation: direct laryngoscopy compared with blind oral intubation.

Haemodynamic and hormonal responses to tracheal intubation can be profound and associated with serious cardiovascular and cerebral side effects. The Augustine Guide, a device enabling blind oral intubation, has been introduced recently. The aim of our study was to compare the haemodynamic and hormonal stress response of this method with direct laryngoscopy. Thirty five patients (ASA 1 and 2) were randomly assigned to undergo either direct laryngoscopy (n = 17), or blind oral intubation (n = 18). Haemodynamic responses and concentrations of adrenaline, noradrenaline and prolactin were determined prior to induction, before intubation and 5 min after intubation. The median duration of intubation was 22s for direct laryngoscopy vs 46s for blind oral intubation (p < 0.05). Between the groups, no significant differences were observed for heart rate, systolic or mean arterial blood pressure. Serum levels of adrenaline decreased slightly after induction and remained unaltered after intubation in both groups. Noradrenaline (1.01 vs 0.66 nmol.l-1) and prolactin (5.2 vs 2.9 nmol.l-1) levels were significantly higher after direct laryngoscopy compared to blind oral intubation. Although blind oral intubation took significantly longer to perform than direct laryngoscopy, hormonal stress response was less pronounced. Blind oral intubation should therefore not be withheld from patients with impaired cardiovascular reserve.

Adolescent↗
PubMed1995

Cardiovascular and catecholamine response to surgery in brain-dead organ donors.

Eleven brain-dead organ donors were studied during surgery. Plasma levels of adrenaline and noradrenaline were measured before and after skin incision, upon sternotomy and 15, 30 and 45 min thereafter. Haemodynamic changes were measured continuously throughout the observation period. Blood pressure and heart rate increased after skin incision, remained high at sternotomy then decreased towards the end of the observation period in six of the 11 patients. Plasma catecholamines increased promptly with the onset of surgical stimuli. We conclude that surgical stress can evoke an excessive rise of plasma adrenaline and noradrenaline and thus could impair allograft function.

Adult↗
PubMed1994

Excursions of the cervical spine during tracheal intubation: blind oral intubation compared with direct laryngoscopy.

The most appropriate technique for performing tracheal intubation in patients with cervical spine injury is debatable. Recently, a new device enabling blind oral intubation (Augustine Guide) with the patient's head and neck in the neutral position has been introduced. The aim of this study was to compare the extent of upper cervical spine movement during intubation with this device compared to direct laryngoscopy. Twelve patients (Mallampati I and II), without a cervical spine injury, were intubated using the Augustine Guide and afterwards by direct laryngoscopy. Both procedures were viewed radiographically. Extension in the upper cervical spine was determined at the point of the maximum excursion. By evaluating the joints occiput-C3 together as a functional unit, blind oral intubation caused 17 degrees (median) less extension compared to direct laryngoscopy (p < 0.01). The median differences observed for the individual joints were: 7 degrees in occiput-C1 (p < 0.05), 5 degrees in C1-2 (p < 0.01) and 6 degrees in C2-3 (p < 0.01) respectively. Since we assume that intubation-induced excursions of the injured spine are even higher, blind oral intubation might be a safe alternative for airway management in this special group of trauma victims.

Adult↗
PubMed1991

Effects of centrally administered anxiolytic agents on classically conditioned bradycardia.

Rats received infusions of the opioid peptide D-Ala2-Met-enkephalinamide (DALA, 10 micrograms), the alpha 2-noradrenergic agonist clonidine (CLON, 3 micrograms), UK14,304 (UK, 5 micrograms), the corticotropin-releasing factor (CRF) antagonist alpha-helical CRF (9-41) (alpha-HEL, 25 micrograms), or saline in the rostral fourth ventricle. The DALA, CLON, and UK groups showed no evidence of a heart rate (HR) conditioned response (CR) during conditioning, after antagonist administration, or on a nondrug test 48 hr after conditioning. These three groups showed the development of normal CRs when later retrained without drugs. The alpha-HEL group showed an enhanced CR. During a subsequent startle test, the presence of a conditioned stimulus resulted in a pronounced suppression of startle in the SAL and alpha-HEL groups but had no effects on startle in the DALA, CLON, and UK groups. The results indicate an important role for fourth ventricle structures containing opioid and alpha 2 receptors in the learning of an HR CR.

Animals↗
PubMed1991

Locus coeruleus involvement in the learning of classically conditioned bradycardia.

Opioid agonists are known to inhibit the activity of locus coeruleus (LC) neurons. In this study, microinjections of the mu-opioid agonist [D-Ala2, N-Me-Phe4, Gly5-ol]-enkephalin (DAMGO; 1.6 microM) bilaterally into the LC caused a significant impairment in the development of a heart-rate (HR) conditioned response (CR). The adverse effect of DAMGO on the HR CR could be reversed with naltrexone pretreatment. Microinjections of DAMGO into the periaqueductal gray, parabrachial nucleus, or fourth ventricle structures 1-2 mm away from the LC had no effects on the development of an HR CR. We conclude that central noradrenergic activity as mediated by the LC is critically involved in the learning and retention of conditioned cardiovascular responses.

Analysis of Variance↗
PubMed1989

Impaired learning of classically conditioned bradycardia in rats following fourth ventricle administration of D-Ala2-methionine-enkephalinamide.

Prior to differential classical conditioning on two successive days, three groups of rats received an infusion (10 micrograms) of either the opioid peptide D-alanine2-methionine-enkephalinamide (DALA), DALA plus naltrexone (5 micrograms), or saline into the rostral region of the fourth ventricle. A fourth group, which served as a control to help localize DALA's site of action, received an infusion of DALA (10 micrograms) into the brain stem area on the floor of the ventricle. The group given DALA alone in the ventricle showed no evidence of a heart rate conditioned response (CR) either during conditioning or during a nondrug test session given 2 days after conditioning. Interference with the CR by DALA was reversed by the concomitant infusion of naltrexone. The control group given DALA in the brain stem developed a normal CR. It was suggested that DALA-induced opioid-receptor activity in the region of the periaqueductal/periventricular gray or locus coeruleus region of the ventricle may have prevented the learning of a CR. This could have occurred through a blunting of the emotional aftereffects of the unconditioned stimulus or through interference with projection pathways to other areas.

Animals↗
PubMed1988

Morphine influences on classical aversive conditioned heart rate in rats.

The present series of three experiments was concerned with the effects of morphine and the morphine antagonist naloxone on the development of a classical aversive heart rate (HR) conditioned response (CR) to a tone conditioned stimulus (CS) paired with an electric shock unconditioned stimulus (US). In the first study, separate groups of rats received preconditioning sc injections of either 0.25 mg/kg, 5 mg/kg, or 10 mg/kg of morphine. Three other groups were given 0.1 mg/kg, 5 mg/kg, or 10 mg/kg of naloxone alone. All of the morphine groups showed attenuation HR responses to the CS on preconditioning CS-alone trials. During conditioning, the 10-mg/kg morphine group showed a markedly decremented bradycardia CR and tachycardia unconditioned response (UR), whereas the 5-mg/kg morphine group showed a normal CR in combination with a decremented UR. Naloxone had no measurable effects on HR. In the second study, naloxone (1 mg/kg) given after conditioning failed to reverse the CR and UR losses produced by 10 mg/kg of morphine given prior to conditioning. Administration of 10 mg/kg of morphine produced only a minor reduction in a HR CR established in a drug-free state, but the tachycardia UR was severely reduced. The results of the third study showed that 1 mg/kg of naloxone was effective in reversing analgesia induced by 10 mg/kg of morphine, as indexed by the tail-flick test. Taken together, the results suggest that the 10-mg/kg dose of morphine interfered with the learning of a HR CR, perhaps principally by reducing the aversive or emotional consequences of the shock US. Direct cardiovascular effects of morphine seemed to interfere with the performance of the tachycardia UR, but not with the performance of the bradycardia CR.

Acoustic Stimulation↗
PubMed1986

Opposing heart rate reactions associated with behavioral states of excitation and inhibition.

Following the development of an excitatory bradycardia conditioned response (CR) to a CS+ paired with a shock US on Day 1, three groups of rats were given one of three inhibitory training procedures on Day 2 with a different CS (CS-). Then on Day 3 the inhibitory capacity of each CS- was examined on a modified combined cue test in which CS- was given slightly before CS+ and on a reversal conditioning test in which CS- was now paired with the US. The three inhibitory procedures consisted of CS- alone (CSA) trials, explicitly unpaired (EUP) CS- and US trials, and truly random (TR) CS- and US trials. During inhibitory training, the bradycardia CR to CS+ was replaced with a tachycardia reaction to CS- in the EUP group but not in the other groups. Subsequent to inhibitory training the EUP group and to some extent also the TR group showed a decrement in the excitatory bradycardia response to CS+ when compared to the robust HR slowdowns displayed by the CSA group. It was suggested, within the context of opponent process theory, that the separate USs given the EUP and TR groups (especially the former) during inhibitory training may have led to conditioning of inhibitory tendencies to CS- and that these in turn generalized and decremented previous established bradycardia responding to CS+ and the development of a new bradycardia to CS- during reversal conditioning.

Animals↗
PubMed1984

Baroreceptor involvement in classically conditioned heart rate responses of restrained rats.

A group (N = 8) of restrained, baroreceptor denervated rats and a sham-operated-control group (n = 8) received discriminated classical conditioning consisting of 30 reinforced trials in which a CS+ was paired with an electric shock US and 30 non-reinforced trials in which a different CS (CS-) was presented alone. The control group displayed a decelerative heart rate CR and a biphasic pressor-depressor blood pressure CR. The denervated group failed to show a heart rate CR but did show a pressor-only blood pressure CR. The URs of the denervated group consisted of a major depressor change in blood pressure and a slight tachycardia whereas the URs of the control group consisted of a slight pressor response and tachycardia. The results indicated that centrally initiated activity in the efferent vagal pathways mediating the decelerative HR CR in rats may be blocked by the absence of normal afferent baroreceptor neural discharge. An integrating role of baroreceptor input was also suggested for the URs.

Animals↗
PubMed1984

Effects of drug-induced changes in resting blood pressure on classically conditioned heart rate and blood pressure in restrained rats.

Subsequent to receiving aversive classical conditioning, which led to a decelerative heart rate (HR) conditioned response (CR) and a pressor-depressor blood pressure (BP) CR, three separate groups of restrained rats received intravenous infusion of sodium nitroprusside (40 micrograms/mg/min) to lower baseline BP, phenylephrine (17 micrograms/mg/min) to raise baseline BP, or an equivalent volume of saline. Conditioning test trials during infusion revealed that hypotension produced by sodium nitroprusside eliminated the HR CR and transformed the BP CR into a pressor-only reaction. Hypertension produced by phenylephrine facilitated the HR CR and changed the BP CR to a pressor-only response on selected trials in which baseline BP increases and baseline HR decreases were within restricted limits. Following drug withdrawal, the HR CRs of both drug groups and the BP CR of the phenylephrine group were attenuated. The unconditioned responses to the shock unconditioned stimulus under phenylephrine were exaggerated and consisted of tachycardias and depressor BP changes, whereas under sodium nitroprusside reduced tachycardias and depressor activity occurred. The results suggested that the loss of the vagally mediated HR CR under sodium nitroprusside was due to baroreceptor-controlled inhibition of vagal discharge and that the enhancement of the HR CR under phenylephrine was due to baroreceptor-influenced facilitation of vagal discharge.

Animals↗