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Biomedical subjects

P Allen

Publications and source records attributed to P Allen.

At least 127 records · Page 7Linked to original sources
PubMed1989

Noncardiogenic pulmonary edema after abdominal aortic aneurysm surgery.

Limb ischemia in experimental animals leads to white blood cell (WBC) and thromboxane (Tx)A2 dependent pulmonary dysfunction. This study examines the pulmonary sequelae of lower torso ischemia in 20 consecutive patients aged 63 +/- 5 years (mean +/- SEM) who underwent elective abdominal aortic aneurysm surgery. After 30 minutes of aortic cross-clamping, plasma TxB2 levels had risen from 77 +/- 26 pg/ml to 359 +/- 165 pg/ml (p less than 0.01) and was temporally related to increases in mean pulmonary artery pressure (MPAP) from 18 +/- 1 to 23 +/- 3 mmHg (p less than 0.01), as well as to increases in pulmonary vascular resistance (PVR) from 0.07 +/- 0.02 to 0.12 +/- 0.02 mmHg sec/ml (p less than 0.01). Each time that the aortic clamp was repositioned and with final declamping, after 83 +/- 10 minutes, there were further increases in MPAP to a peak of 32 +/- 2 mmHg (p less than 0.01) and in PVR to 0.26 +/- 0.030 mmHg sec/ml (p less than 0.01), corresponding to a plasma TxB2 level of 406 +/- 177 pg/ml (p less than 0.01). MPAP and PVR returned to baseline values within 30 minutes of declamping. Ten minutes after removal of the aortic clamp, platelet levels had fallen from 180 +/- 41 to 97 +/- 17 X 10(3)/mm3 (p less than 0.01) and WBC levels from 8900 +/- 1100 to 4700 +/- 400/mm3 (p less than 0.01). Both platelets and WBC returned towards normal levels, but at 24 hours, while WBC was elevated at 13000 +/- 900/mm3 (p less than 0.01), platelets were 44% of baseline at 135 +/- 14 X 10(3)/mm3 (p less than 0.01). Four to 8 hours after surgery, pulmonary dysfunction was manifest by increases in physiologic shunt from 9 +/- 2% to 16 +/- 2% (p less than 0.01), and peak inspiratory pressure (PIP) from 23 +/- 2 to 33 +/- 2 cmH2O (p less than 0.01). Chest radiography demonstrated interstitial pulmonary edema in all patients, whereas pulmonary artery wedge pressure was 12 +/- 2 mmHg, excluding the possibility of left ventricular failure. After 24 hours, pulmonary edema had resolved, and the PIP and PaO2 had both returned to baseline. These data indicate that reperfusion of the ischemic lower torso leads to the synthesis of TxA2, an event temporally related to pulmonary hypertension and transient leukopenia with subsequent pulmonary microvascular injury manifest by interstitial edema.

Aged↗
PubMed1989

Pulmonary edema after aneurysm surgery is modified by mannitol.

Abdominal aortic aneurysmectomy (AAA) results in thromboxane (Tx)A2 generation, a rise in mean pulmonary artery pressure (MPAP), leukopenia, and noncardiogenic pulmonary edema. This study tests whether mannitol, a hydroxyl radical scavenger, modifies these events. Patients received mannitol 0.2 g/kg (n = 14) or saline (n = 12) intravenously before infrarenal aortic clamping. With saline, 30 minutes after clamping, plasma TxB2 levels rose from 124 to 290 pg/mL (p less than 0.01), and MPAP rose from 19 to 27 mmHg (p less than 0.01). Aortic clamp release led to further increases in plasma TxB2 to 378 pg/mL (p less than 0.01) and MPAP to 34 mmHg (p less than 0.01). The white blood count (WBC) fell from 9800 to 4400/mm3 (p less than 0.01). Four to eight hours after surgery, physiologic shunting (Q[sc]S[xsc]/Q[sc]T[xsc]) rose from 9% to 20% (p less than 0.01) and peak inspiratory pressure (PIP) increased from 22 to 32 cmH2O (p less than 0.01). Chest radiography demonstrated pulmonary edema while the pulmonary wedge pressure was 12 mmHg, excluding left ventricular failure. By 24 hours pulmonary edema resolved and the PIP and PaO2 returned to baseline. Mannitol treatment relative to saline, during and after aortic clamping reduced plasma TxB2 levels to 155 and 198 pg/mL, respectively (p less than 0.01); MPAP to 21 and 26 mmHg (p less than 0.01); minimized the decline in WBC to 5850/mm3 (p less than 0.01), and the postoperative rise in Q[sc]S[xsc]/Q[sc]T[xsc] to 12%, and PIP to 28 cmH2O (both p less than 0.01). Chest radiography showed no pulmonary edema. Finally in vitro studies documented that mannitol 1 to 10(-4)M, but not dextrose, in a dose-dependent manner inhibited Tx synthesis by ADP-activated platelets. These data indicate that mannitol maintains pulmonary function after AAA by limiting ischemia-induced thromboxane synthesis.

Aged↗
PubMed1989

Temporal resolution in children.

The auditory temporal resolving power of young children was measured using an adaptive forced-choice psychophysical paradigm that was disguised as a video game. 20 children between 3 and 7 years of age and 5 adults were asked to detect the presence of a temporal gap in a burst of half-octave-band noise at band center frequencies of 400 and 2,000 Hz. The minimum detectable gap (gap threshold) was estimated adaptively in 20-trial runs. The mean gap thresholds in the 400-Hz condition were higher for the younger children than for the adults, with the 3-year-old children producing the highest thresholds. Gap thresholds in the 2,000-Hz condition were generally lower than in the 400-Hz condition and showed a similar age effect. All the individual adaptive runs were "adult-like," suggesting that the children were generally attentive to the task during each run. However, the variability of threshold estimates from run to run was substantial, especially in the 3-5-year-old children. Computer simulations suggested that this large within-subjects variability could have resulted from frequent, momentary lapses of attention, which would lead to "guessing" on a substantial portion of the trials.

Attention↗
PubMed1988

The Carpentier-Edwards supra-annular porcine bioprosthesis: new generation low pressure glutaraldehyde fixed prosthesis.

The Carpentier-Edwards supra-annular porcine bioprosthesis was implanted in 1,576 operations (1,536 patients with 1,704 valves) between 1981 and 1987. The mean age of the patients was 61.9 years (range 13 to 87 years). During the years 1981 and 1987, approximately 90% of the total valvular surgery population received the prosthesis. The early mortality was 7.0% (included patients with concomitant procedures including coronary artery bypass and ascending aortic aneurysm resection). Late mortality was 4.0% per patient-year. The total cumulative follow-up was 4,237 years. Thromboembolism (TE) was 2.4% per patient-year (fatal 0.4% per patient-year) (minor 1.2%; major 1.3%); antithromboembolic therapy-related hemorrhage (ATH) 0.5% (fatal 0.07%); prosthetic valve endocarditis (PVE) 0.5% (fatal 0.2%); periprosthetic leak (PPL) 0.3% (fatal 0%); clinical valve dysfunction (CVD) 0.3% (fatal 0.02%); and structural valve deterioration/primary tissue failure (SVD) 0.2%/patient-year (fatal 0%). Thromboembolism and structural valve deterioration were the significant complications, SVD occurring primarily between the fourth and fifth year of evaluation. The overall patient survival was 77.1% +/- 1.4% at five years. The patients were classified as 89.6% NYHA functional Class III and IV preoperatively and 96.1% Class I and II postoperatively. The freedom at five years from TE was 90.6% +/- 1.0%; SVD 98.9% +/- 0.5%; and reoperation 95.9% +/- 0.9%. Freedom from all valve-related complications at five years was 84.1% +/- 1.3%; valve-related mortality 96.8% +/- 0.7%; mortality and reoperation (valve failure) 92.9% +/- 1.1%; mortality and residual morbidity (treatment failure) 93.7% +/- 0.9%; and mortality, residual morbidity, and reoperation (valve failure and dysfunction) 90.0% +/- 1.2%. There were 28 valve-related deaths of a total 280 deaths (early 4, late 24) (TE 17; ATH 3; CVD 1; PVE 7; PPL 0; and SVD 0). Valve-related reoperations were performed in 32 patients (TE 2; CVD 4; PVE 7; PPL 11; and SVD 8). The supra-annular Carpentier-Edwards porcine bioprosthesis has provided very satisfactory clinical performance and afforded patients an excellent quality of life. The long-term durability of this low pressure glutaraldehyde fixed prosthesis will be determined by observation over the next five to seven years.

Adolescent↗
PubMed1988

The Carpentier-Edwards standard porcine bioprosthesis: long-term evaluation of the high pressure glutaraldehyde fixed prosthesis.

The Carpentier-Edwards standard porcine bioprosthesis was implanted in 1,000 operations (988 patients with 1,092 valves) between 1975 and 1981. The mean age of the patients was 56.8 years (range 8 to 85 years). During the years 1975 and 1981, approximately 97% of the total valvular surgery population received the prosthesis. The early mortality was 7.8% (including patients with concomitant procedures including coronary artery bypass and ascending aortic aneurysm resection). Late mortality was 3.8% per patient-year. The total cumulative follow-up was 5,937 years. Thromboembolism (TE) was 1.3% per patient-year (fatal 0.4%/patient-year) (minor 0.4%; major 0.9%); antithromboembolic therapy-related hemorrhage (ATH) 0.5% (fatal 0.1%); prosthetic valve endocarditis (PVE) 0.5% (fatal 0.2%); periprosthetic leak (PPL) 0.4% (fatal 0.2%); clinical valve dysfunction (CVD) 0.2% (fatal 0.02%); and structural valve deterioration (SVD)/primary tissue failure 1.6% per patient-year (fatal 0.2%/pt-yr). Thromboembolism and SVD occurring primarily between the sixth and tenth year of evaluation, were the significant complications. The overall patient survival was 60.5% +/- 2.4% at 10 years. The patients were classified as 93.5% NYHA functional Class III and IV, preoperatively and 93.1% Class I and II, postoperatively. The freedom at 10 years from TE was 82.9% +/- 2.7%; SVD 76.9% +/- 2.9%; and reoperation 70.8% +/- 3.1%. Freedom from all valve-related complications at 10 years was 54.3% +/- 3.1%; valve-related mortality 86.4% +/- 2.3%; mortality and reoperation (valve failure) 64.0% +/- 3.2%; mortality and residual morbidity (treatment failure) 82.3% +/- 2.6%; and mortality, residual morbidity, and reoperation (valve failure and dysfunction) 60.6% +/- 3.2%. There were 61 valve-related deaths of a total 352 deaths (early 7, late 54) (TE 21; ATH 7; CVD 1; PVE 12; PPL 9; and SVD 11). Valve-related reoperations were performed in 128 patients (TE 3; CVD 4; PVE 14; PPL 17; and SVD 90). The standard Carpentier-Edwards porcine bioprosthesis has provided very satisfactory clinical performance and afforded patients excellent quality of life. Primary tissue failure is the significant long-term complication.

Adolescent↗
PubMed1988

Sources of error in flow-volume curves. Effect of expired volume measured at the mouth vs that measured in a body plethysmograph.

The popularity of the maximum expiratory flow-volume curve (FVC) is in part due to the effort independence of expiratory flow. Of interest are expiratory flow rates at specific lung volumes, usually 50 and 25 percent of vital capacity (VC); Vmax50 and Vmax25, which make accurate assessment of lung volumes essential. Changes in lung volume during the test are due to both the volume of gas expired and the volume change due to gas compression (Vcomp). In normal subjects, Vcomp is small but may be considerable in those with airflow obstruction. When the FVC is measured in a plethysmograph (FVCp), both expired volume and Vcomp are measured. When the volume of the FVC is derived from gas expired at the mouth (FVCm), Vcomp is not considered and differences in Vmax25 or Vmax50 may occur. The magnitude of these errors was assessed in 30 children and young adults: nine normal subjects, ten with cystic fibrosis (CF) and 11 with asthma. For Vmax50, use of FVCm instead of FVCp resulted in an error of 8 +/- 7 percent (mean +/- 1 SD) in the normal subjects compared to 32 +/- 23 in those with CF (p less than 0.01) and 24 +/- 18 for those with asthma (p less than 0.05). For Vmax25, the errors were similar. These errors were not predictable from FEV1 or RV/TLC but were related to a combination of expiratory effort, the shape of the FVCp, and the absolute volume of gas that was being compressed (p less than 0.0001). These findings suggest that expiratory flows in the FVCm are not effort-independent in the face of significant airflow obstruction and that comparisons of values derived from an FVCp with those from an FVCm may not be valid.

Adult↗
PubMed1988

The Carpentier-Edwards supraannular porcine bioprosthesis. A new generation tissue valve with excellent intermediate clinical performance.

The Carpentier-Edwards supraannular porcine bioprosthesis, an investigational valve, was implanted in 1167 patients (1174 operations, 1274 valves) between November 1981 and December 1985 (age range 13 to 85 years, mean 61 years). The early mortality rate was 7.2% (with concomitant procedures 10.9%, without 4.8%; with previous operation 10.5%, without 6.6%). The late mortality rate was 4.5% per patient-year (aortic valve replacement, 4.0%; mitral valve replacement, 4.8%; multiple valve replacement, 5.6%). Total cumulative follow-up was 2272.3 years. The prevalence of thromboembolism was 2.6% per patient-year (fatal 0.4% per patient-year, major 1.4%, minor 1.2%); hemorrhage related to antithromboembolic therapy, 0.7% (fatal 0.1%); prosthetic valve endocarditis, 0.4% (fatal 0.2%); periprosthetic leak, 0.4% (fatal 0%); structural valve deterioration (primary tissue failure/structural failure), 0.1% per patient-year; and clinical valve dysfunction, 0.4%. The reoperation rate was 0.8% per patient-year (thromboembolism, 0.1%; clinical valve dysfunction, 0.1%; prosthetic valve endocarditis, 0.1%; periprosthetic leak, 0.4%; structural valve deterioration, 0.1%). Thromboembolism occurred throughout the observation period but with decreasing frequency, hemorrhage throughout the period in no predictable fashion, prosthetic valve endocarditis within 2 years, periprosthetic leak within 2 years, and structural valve deterioration occurred during the fourth year of assessment. The overall survival rate was 79.8% +/- 1.7% (4 years). Freedom (at 4 years) from thromboembolism was 92.2% +/- 1.2%; from structural valve deterioration, 98.8% +/- 0.8%; and from reoperation, 95.8% +/- 1.3%. Freedom from all complications (4 years) was 85.9% +/- 1.7%; from complication mortality, 98.4% +/- 0.4%; and from valve failure (mortality and reoperation), 94.3% +/- 1.3%. This investigational Carpentier-Edwards supraannular porcine bioprosthetic valve has provided excellent clinical performance and remains our overall prosthesis of choice.

Aged↗
PubMed1988

Carpentier-Edwards porcine bioprostheses: assessment of clinical performance.

Carpentier-Edwards porcine bioprostheses have been implanted since 1975, commencing with the previous generation standard prosthesis in that year and the new generation supra-annular prosthesis in 1981. The first 700 operations with each prosthesis were evaluated: Carpentier-Edwards standard porcine bioprosthesis (CE-S), 692 patients (772 valves) and Carpentier-Edwards supra-annular porcine bioprosthesis (CE-SA), 698 patients (756 valves). The incidence of thromboembolism was CE-S 1.4% per patient-year and CE-SA 2.1% per patient-year (hazard interval rates not considered). The rate of structural valve deterioration was CE-S 1.8% per patient-year (79 prostheses) and CE-SA 0.2% (four prostheses). The reoperation rate was 2.5% per patient-year (110 prostheses) for CE-S and for CE-SA it was 0.9% (six prostheses). The late mortality rate was 3.7% per patient-year and 4.2%, respectively. The 10-year freedom rates for CE-S were thromboembolism, 82.7 +/- 2.8%; prosthetic valve endocarditis, 93.5 +/- 1.6%; structural valve deterioration, 77.1 +/- 2.9%; reoperation, 69.9 +/- 3.1%; valve related mortality, 85.9 +/- 2.4%; valve failure, 62.8 +/- 3.2%; treatment failure, 82.0 +/- 2.7%; mortality, reoperation and residual morbidity, 59.5 +/- 3.2%; and all complications, 53.4 +/- 3.1%. The four-year freedom rates for CE-SA were thromboembolism, 93.0 +/- 1.3%; prosthetic valve endocarditis, 98.7 +/- 0.5%; structural valve deterioration, 98.3 +/- 1.0%; reoperation, 95.6 +/- 1.3%; mortality, 97.9 +/- 0.6%; valve failure, 93.6 +/- 1.4%; treatment failure, 94.6 +/- 1.1%; mortality, reoperation and residual morbidity, 90.9 +/- 1.6%; and all complications, 85.6 +/- 1.9%.(ABSTRACT TRUNCATED AT 250 WORDS)

Bioprosthesis↗
PubMed1987

Dantrolene prevents the malignant hyperthermic syndrome by reducing free intracellular calcium concentration in skeletal muscle of susceptible swine.

Malignant hyperthermia (MH) is a pharmacogenetic disorder of skeletal muscle triggered when susceptible subjects are exposed to volatile anesthetic agents and/or depolarizing muscle relaxants. We have used Ca2+ selective microelectrodes to measure in vivo the intracellular free [Ca2+] in skeletal muscle of MH susceptible swine before and after the administration of dantrolene. We have investigated the effectiveness of this muscle relaxant in preventing clinical MH and the relationship between the resting intracellular free [Ca2+] and the probability of inducing the MH syndrome. The resting intracellular free [Ca2+] was 0.41 +/- 0.01 microM (M +/- SEM), which agrees with our previous measurements in susceptible swine. The administration of 0.5, 1, 2, 2.5 and 3 mg/Kg Dantrolene, reduced the intracellular free [Ca2+] to 0.31, 0.21, 0.09, 0.08, 0.08 microM respectively. The 0.5 mg/Kg dose induced a moderate decrease of [Ca2+]i and failed to prevent the MH syndrome after exposure to halothane (2%). The 1 mg/Kg dose produced a further reduction in [Ca2+]i and was sufficient to prevent the clinical syndrome in 2 out of 3 animals. The 2.5 mg/Kg dose was uniformly protective in all animals. These results suggest that the mechanism by which dantrolene protects susceptible animals exposed to triggering agents is by reducing the intracellular free [Ca2+] in skeletal muscle.

Anesthetics↗
PubMed1987

Effects of halothane, isoflurane and enflurane on ventilation in children.

The ventilatory effects of halothane in eight children were compared with those of isoflurane in eight children and enflurane in six children. All studies were completed before surgery commenced, and the children received no preoperative medication. The depression of ventilation produced by the three agents increased in a dose-related fashion as the alveolar concentrations were increased, and the depression of ventilation that they produced in oxygen was greater than that produced by equipotent concentrations in nitrous oxide. While the increase in ventilatory frequency and the decrease in TE associated with increasing concentrations of halothane were statistically significant (P less than 0.05), the increase in frequency associated with isoflurane was not, although it was sufficient to maintain the end-tidal and arterialized venous PCO2 in the isoflurane group at a value which did not differ significantly from that in the halothane group. Profound depression of ventilation was produced in the children by enflurane, clearly because no increase in ventilatory frequency was associated with its use. It was evident that the ventilatory effects of the three volatile agents in unstimulated children are very similar to those described elsewhere in the adult. There was no difference of any clinical significance between the degree of depression of ventilation produced by halothane and isoflurane in children.

Anesthesia, Inhalation↗
PubMed1987

Isolation from Klebsiella and characterization of two rcs genes that activate colanic acid capsular biosynthesis in Escherichia coli.

Two genes, designated rcsA (regulation of capsule synthesis) and rcsB, that had been cloned from the chromosome of Klebsiella aerogenes (K. pneumoniae) capsular serotype K21 were capable of activating expression of colanic acid capsular polysaccharide in Escherichia coli K12. The Klebsiella rcsA gene encoded a polypeptide of 23 kDa that was required for the induction of a mucoid phenotype at less than or equal to 30 degrees C but not at greater than or equal to 37 C. The Klebsiella rcsB locus encoded no apparent polypeptides and was not capable by itself of causing the overproduction of colanic acid. However, when present in the same cell with rcsA, either in cis or in trans, rcsB caused expression of mucoidy in E. coli at all growth temperatures. These findings are best explained if the Klebsiella rcsA gene product acts as a positive regulator of colanic acid biosynthesis in E. coli and that activity of this protein is in turn subject to regulation by Lon protease. The Klebsiella rcsB locus may exert its effect by preferentially binding a negative regulator of capsular biosynthesis, possibly Lon itself. DNA sequences homologous to the Klebsiella K21b rcsA and rcsB genes were found in the genomes of all other capsular serotypes of klebsiellae examined, including K2, K12, K36 and K43. However, there was no homology between such genes and the chromosome of E. coli. The ability of these rcs genes to induce a mucoid phenotype explains the apparent conjugative transfer from klebsiellae to E. coli of the ability to produce K21 or other Klebsiella capsular polysaccharides that are structurally and antigenically related to colanic acid.

Base Sequence↗
PubMed1987

Effect of clot removal at 24 hours on chronic vasospasm after SAH in the primate model.

The efficacy of complete clot removal 24 hours after subarachnoid hemorrhage (SAH) in the prevention of chronic cerebral vasospasm was evaluated in monkeys in a blind randomized controlled trial. Twenty-four monkeys were randomized to one of three groups to undergo sham-operation (sham-operated group), clot placement only (clot group), or clot placement and removal (clot-removal group). By means of standard microsurgical techniques, the major cerebral vessels bilaterally were dissected free of arachnoid. An autologous hematoma averaging 5 gm was placed around the vessels in the subarachnoid spaces in the clot and clot-removal groups. Saline solution was instilled in the subarachnoid spaces of the sham-operated group. All animals underwent reoperation 24 hours after the first procedure. In the clot-removal group, the hematoma was evacuated. In the sham-operated and clot groups, the incision was simply closed again after 3 hours of anesthesia. Indices monitored before and 7 days after SAH induction included neurological status, angiographic cerebral vessel caliber, and arterial blood pressure. All animals were evaluated with magnetic resonance imaging (MRI); representative animals were evaluated with computerized tomography (CT) brain scans. There were no neurological deficits in either the sham-operated or the clot-removal groups. One animal in the clot group developed a progressive delayed ischemic deficit on Day 5 after SAH. A second animal in this group died suddenly on Day 4 post-SAH. An autopsy revealed a recent infarct in the territory of the superior cerebellar artery. Clinical findings correlated with MRI and CT images. Significant vasospasm (25% to 100% reduction in vessel caliber) was present on Day 7 in 100% of the clot animals (p less than 0.01). There was no significant vasospasm (p greater than 0.05) on Day 7 in either the sham-operated or the clot-removal groups. A large volume of clot placed bilaterally resulted in a 25% incidence of delayed ischemic deficit. Evacuation of subarachnoid hematoma within 24 hours of SAH prevented the development of chronic vasospasm and delayed ischemic deficit in the primate model.

Animals↗
PubMed1986

Effects of nitrous oxide on the respiratory pattern of spontaneously breathing children. A re-appraisal.

An increase in ventilation in spontaneously breathing children, when nitrous oxide was withdrawn from the nitrous oxide-halothane inspired mixture, was previously suggested to be a direct effect of decreased alveolar nitrous oxide concentration. To test whether a "gas effect" of oxygen inflow had caused a false increase in tidal volume signal, in the present study nitrous oxide was withdrawn in two stages, with equilibrium at each stage; there was a 7% increase in VT, to 3.88 ml kg-1. During that nitrous oxide withdrawal, despite a constant vaporizer setting for halothane, the alveolar concentration of halothane decreased (from 1.06% to 0.9%). When the alveolar halothane concentration was subsequently deliberately decreased from 1.06% to 0.9% with nitrous oxide maintained constant at 65%, there was a 14% increase in VT, again to 3.88 ml kg-1. It is concluded that nitrous oxide did not produce significant depression of ventilation in children, and that the observed increases in tidal volume were the result of decreases in end-tidal halothane concentration, produced by a decrease in its inspired concentration.

Anesthesia, General↗