Biomedical subjects

C L Rice

Publications and source records attributed to C L Rice.

At least 37 records · Page 2Linked to original sources

PubMed1994

Mild hemorrhagic shock does not enhance the risk of CD18 blockade to S. aureus skin inoculations.

Monoclonal antibody (MAb) 60.3 recognizes the leukocyte CD18 glycoprotein and ameliorates much of the injury after hemorrhagic shock in rabbits and nonhuman primates. This MAb blocks neutrophil emigration and has been shown to increase the risk of infection after high-dose inoculation of Staphylococcus aureus into skin. Hemorrhagic shock might also cause an increased sensitivity to bacterial injections. Therefore, we examined changes in host sensitivity to subcutaneous injections of 10(5)-10(8) colony-forming units (CFU) of S. aureus just before shock. Cardiac output was lowered to 40-45% of baseline by phlebotomy for 1 h. Intravenous saline or MAb 60.3 (2 mg/kg) treatment immediately preceded resuscitation with the shed blood. Cefazolin was given intravenously for 3 days, and the animals were killed after 7 days for analysis of infectious risk by measuring the incidence and surface area of skin abscess/necrosis. Bacteria injection resulted in no infections at 10(5) or 10(6) CFU and one abscess/necrotic region at 10(7) CFU (7% incidence) in the MAb-treated group. However, injection of 10(8) CFU resulted in more abscesses/necrotic regions in the MAb- vs. saline-treated group (86 vs. 25%; P < 0.05). The average size of these lesions was also larger in the MAb-treated group (4.6 +/- 7.1 vs. 0.5 +/- 0.6 cm2; P < 0.001). These results were similar to previously published results without shock (Sharar et al., Surgery St. Louis 110:213-220, 1991). We conclude that mild hemorrhagic shock does not enhance the infectious risk of MAb 60.3 after subcutaneous S. aureus injection.

Abscess↗

PubMed1994

The economic status of trauma centers on the eve of health care reform.

An in-depth understanding of the economic problems confronting trauma centers is essential for their continued development and to address impending changes of health care reform. A comprehensive financial and demographic survey was sent to 839 hospitals identified as potential trauma centers. A total of 313 surveys from 48 states were returned. Extensive information was collected in several areas including financial status (58% reported serious financial problems and 36% reported minor financial problems; 68% reported a financial loss), cost containment and management strategies, marketing, "halo" effect (53% reported positive effect), operational impacts, physician support (47% reported problems), malpractice (92% reported no special problem), role of auto insurance reimbursement, and access to rehabilitation. Detailed financial data of actual costs and reimbursements (95 respondents) were analyzed with the costing method used by the Health Care Financing Administration (HCFA). These data will allow us to develop better strategies to deal with the problems of uncompensated and underfunded trauma care and improve trauma center viability.

Catchment Area, Health↗

PubMed1993

Neutrophils contribute to hepatic ischemia-reperfusion injury by a CD18-independent mechanism.

Hepatic ischemia-reperfusion injury is reported to be modulated by neutrophils (PMNs). The adhesion and emigration of PMNs that precede tissue inflammation and necrosis in other organs are mediated, in part, by the leukocyte adhesion complex CD11/CD18. In this study, the role of PMN adhesion via CD11/CD18 in isolated liver ischemia-reperfusion injury was examined in rabbits using a blocking monoclonal antibody (mAb 60.3) specific for the CD18 receptor. Vinblastine-induced neutropenia provided significant protection, confirming participation of neutrophils in the pathogenesis of hepatic injury. Inhibition of PMN adherence with mAb 60.3 did not ameliorate injury, as measured by aminotransferase concentrations or a histologic scoring system for injury severity. Histologic sections were scored for pattern and extent of injury as well as neutrophil association with injury. These results suggest a CD18-independent mechanism of neutrophil adhesion in the evolution of isolated hepatic ischemia-reperfusion injury.

Animals↗

PubMed1993

Strength training alters contractile properties of the triceps brachii in men aged 65-78 years.

Voluntary and electrically evoked contractile properties were studied in the triceps brachii following a 24-week dynamic strength training program in ten men aged 65-78 years. Eight men of a similar age were control subjects. A resistance overload program was undertaken three times per week with subjects performing four sets of six to eight repetitions at 80% of their one repetition on maximum (1RM). Maximum voluntary contraction (MVC) and contractile properties were measured at 0, 12, and 24 weeks in the exercise group and at 0 and 24 weeks in the controls. The 1RM was used to assess dynamic strength at 0 and 24 weeks in the exercise group. Contractile measures consisted of supramaximal isometric twitch and post-activation twitch parameters. Muscle size was estimated from anthropometric measurements. Compared with the control group, the exercise group MVC increased by about 20% and time to peak tension was slowed by about 11%. Also in the exercise group the peak rate of torque development of the potentiated twitch was reduced by about 10%. Twitch potentiation was substantial in both groups (about 140%) and unaffected by training. The 1 RM increased by about 30%, and there was a non-significant positive change of 8.6% in the muscle plus bone cross-sectional area in the exercise group. The results show that the force generating capacity of the triceps brachii in these men can be significantly improved for up to 24 weeks using concentric overload training. Furthermore, the finding of slowed twitch properties and no change in peak twitch amplitude substantiate and extend the limited data currently available on intrinsic contractile changes in the elderly.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMed1993

Monitoring intensive care unit performance using statistical quality control charts.

This paper discusses results of a study in which mortality rates and APACHE II severity of illness scores of Intensive Care Unit (ICU) patients were monitored for a five-year period (1986-1990) using statistical quality control charts. The purpose of the study was to determine whether severity of illness of patients and mortality rates had changed significantly over this time horizon. The results show that the Intensive Care Unit process is stable and in statistical control. There is no apparent trend in the severity of illness scores nor mortality rates measured both at ten days and six months from the last ICU admission. Quality control charts, which have been used extensively to detect changes in industrial processes on a short term basis, provide a simple method of monitoring the ICU process over an extended time horizon.

Critical Care↗

PubMed1993

Health-care reform. Single-payer models.

Health-care reform is one of the most urgent issues facing the United States today. The current system is marked by enormous disparities between services available to those with virtually unlimited resources and those who must pay for services directly. Among the options being considered is that of a single-collector, state-based system with universal access, effective cost control, administrative simplicity, re-allocation of services toward primary and preventive care, and a reduction in unnecessary services. A key element in such a plan is a politically independent Federal Health Board, which would be responsible for making decisions about the definition of a standard benefit plan to be provided to each American.

Delivery of Health Care↗

PubMed1993

Inhibition of leukocyte adherence and aggregation for treatment of severe cold injury in rabbits.

We tested the hypothesis that blocking neutrophil adherence and/or aggregation reduces tissue injury that results when tissue is frozen and rewarmed. The left hindlimbs of three groups of New Zealand White rabbits were immersed in a -15 degrees C salt water bath for 30 min to freeze the foot. The foot was rewarmed in a 39 degrees C water bath. In two groups, adherence and aggregation were blocked with monoclonal antibody (MAb) 60.3, and the third group was treated with saline. Two of the groups were treated at the time of rewarming with either saline or MAb 60.3, and the third group received MAb 60.3 at the conclusion of rewarming. Tissue edema and tissue loss were significantly less in the two groups receiving MAb 60.3 than in the control group. Rabbits treated at the time of rewarming had less edema and tissue loss than those treated at the completion of rewarming. These studies indicate that a substantial component of severe cold injury is neutrophil mediated and occurs after rewarming.

Animals↗

PubMed1992

Liposome-encapsulated hemoglobin inhibits tumor necrosis factor release from rabbit alveolar macrophages by a posttranscriptional mechanism.

Macrophages contribute to the systemic inflammatory response that characterizes the sepsis syndrome through the production of inflammatory cytokines such as tumor necrosis factor (TNF). Liposome-encapsulated hemoglobin (LEH), a potential red cell substitute, is cleared by fixed tissue macrophages. In these studies, in vitro incubation of alveolar macrophages with stored LEH was shown to inhibit the expression of TNF induced by endotoxin (lipopolysaccharide, LPS) stimulation. This effect was dependent on LEH dose but independent of the period of exposure to the LEH. Despite inhibition of TNF expression, Northern blot analysis of total cellular RNA from LPS-stimulated macrophages revealed accumulations of TNF-specific transcripts in cells treated with or without LEH. Thus the mechanism of LEH inhibition of TNF expression appears to involve a posttranscriptional event. Although these results suggest a potential advantage of resuscitation with LEH when sepsis complicates hemorrhagic shock, immunomodulation in vivo remains to be defined.

Animals↗

PubMed1992

Neuromuscular responses of patients with multiple sclerosis.

Muscle weakness, studied in 4 patients with multiple sclerosis (MS), was compared with values from normal subjects. Twitch occlusion showed that normal subjects could activate their muscles maximally, but patients rarely achieved greater than 60% activation. In both groups, motoneuron firing rates increased linearly with force. Consistent with the reduced level of activation, MCV firing rates in MS muscles rarely exceeded 17 Hz (compared with approximately 24 Hz for normals). However, for right and left muscles of one patient, mean maximum firing rates were 14.2 +/- 2 Hz and 8.0 +/- 2 Hz, but her muscles, could be activated to levels greater than 92% and 60%, respectively. This patient's ability to achieve higher than expected forces at low firing rates was probably due to her slow muscle contractile speeds, especially 1/2-relaxation time (75 to 115 ms, cf. approximately 60 ms for normals), and high twitch/tetanus ratio (0.4, cf. 0.2).

Adult↗

PubMed1992

Sensitivity to endotoxin in rabbits is increased after hemorrhagic shock.

The immunoinflammatory response following trauma and hemorrhage may predispose to the development of sepsis and multiple-organ failure syndrome. Cardiac output (CO), arterial pressure, arterial PO2, and pulmonary permeability index were measured. We examined the sensitivity of rabbits to infusions of lipopolysaccharide (LPS) after hemorrhagic shock. Shock was produced by reducing CO to 40% of baseline for 90 min, followed by resuscitation with shed blood and then with lactated Ringer solution to maintain CO near baseline. Animals were assigned to three groups: 1) hemorrhagic shock only, 2) LPS only, and 3) hemorrhagic shock + LPS. Groups 1 and 3 were subjected to hemorrhagic shock on day 1. Escherichia coli LPS was infused (1.0 microgram/kg i.v.) into groups 2 and 3 on day 2. Fluid resuscitation with lactated Ringer solution was continued in an effort to maintain CO at baseline. Five hours after LPS infusion, 125I-albumin was injected intravenously, and rabbits were killed 1 h later for measurement of pulmonary permeability index. LPS infusion after shock (group 3) caused significant decreases in CO, arterial pressure, and PO2 and an increase in pulmonary permeability. These changes were not seen in the groups 1 and 2. We conclude that hemorrhagic shock and resuscitation result in a proinflammatory state, leading to increased sensitivity to subsequent exposure to LPS.

Animals↗

PubMed1992

Role of leukocyte CD11/CD18 complex in endotoxic and septic shock in rabbits.

Two models of sepsis were investigated using rabbits. In the first model, rabbits given lipopolysaccharide (LPS) were treated with saline (group II) or CD18 monoclonal antibody (MAb) 60.3 (group III). Group I animals received no LPS. Cardiac output was maintained by infusion of lactated Ringer solution with group II (95 +/- 68 ml/kg) requiring significantly more than group I (0 +/- 0 ml/kg) or group III (39 +/- 27 ml/kg). Lung permeability indexes in groups II (median 0.002, range 0.023) and III (median 0.0035, range 0.053) were not different but were significantly greater than group I (median 0.0007, range 0.001). In the second model, peritonitis was produced by devascularizing the appendix, leaving it in situ for 19 h, and then performing an appendectomy. Saline or MAb 60.3 treatment was at appendectomy and every 12 h for 3 days. Survival was significantly greater in the MAb 60.3-treated group at day 10 (90 vs. 40%). Lung permeability was increased at day 2 and was not different between groups. Day 1 fluid requirements were greater in the saline-treated group. These data are consistent with MAb 60.3 protection of systemic but not pulmonary circulation in two models of sepsis.

Animals↗

PubMed1992

Muscle temperature, contractile speed, and motoneuron firing rates during human voluntary contractions.

A study was made of motoneuron firing rates and mechanical contractile parameters during maximum voluntary contraction of human hand muscles. A comparison of muscles that had been fatigued after a 60-s maximum voluntary contraction (MVC) with muscles that were cooled by approximately 5 degrees C showed that the contractile properties, in particular the rates of contraction and relaxation, were similarly affected in both conditions. In contrast, the motoneuron firing rate was affected differently by the two treatments. In the case of the fatigued muscles the motoneuron firing rate was reduced by 36%, as was expected from previous studies, but in the case of the cooled muscles, there was no significant change in the motoneuron firing rate. We conclude that the reflex reduction in the motoneuron firing rate seen in the fatigued muscle is not triggered directly by a change in the mechanical properties of the muscle.

Adult↗

PubMed1991

Interferon gamma increases sensitivity to endotoxin.

Interferon-gamma (IFN-gamma) has been proposed for use following severe trauma to reverse depressed macrophage (M phi) function and thereby reduce infection, sepsis, and subsequent multiple organ failure syndrome (MOFS). However, an excessive inflammatory response by M phi s and other components of the inflammatory cascade is thought to be central to the underlying pathophysiology of MOFS. Endotoxin (LPS) has been implicated as a principal mediator of sepsis-induced MOFS by stimulating M phi s and leukocytes (WBC). This study addresses the following question: Does IFN-gamma predispose normal rabbits to a pathophysiologic response to LPS infusion? Four groups of New Zealand White rabbits (n = 6, each group) were prepared for measurement of cardiac output, arterial pressure, arterial PO2, and WBC counts over a 6-hr period. Group I (control) was instrumented alone, Group II (LPS alone) was given a subclinical dose of 1.0 micrograms/kg of Escherichia coli LPS iv, Group III (IFN-gamma alone) was given recombinant rabbit IFN-gamma (5.0 micrograms/kg subcutaneous) for 3 days prior to preparation for measurements, and Group IV (IFN-gamma + LPS) received 3 days of IFN-gamma followed by LPS. One hour prior to sacrifice 5.0 microCi of 125I-albumin was given and bronchoalveolar lavage was performed at death to determine the lavage/plasma 125I ratio as an index of pulmonary permeability. The results indicate that IFN + LPS animals had significant decreases in cardiac output, PO2, and WBC counts, and increased lavage/plasma ratio of 125I-albumin when compared to all other groups (P less than 0.05 by ANOVA, t test). Neither LPS alone nor IFN-gamma alone had a significant effect on measured variables.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1991

Reappraisal of emergency room thoracotomy in a changing environment.

The efficacy of resuscitative emergency room thoracotomy (ERT), particularly in blunt injury, has been questioned. Wide application of the procedure may not be cost effective. The risk of exposure and lethal infection to medical personnel during ERT is considerable. For the past decade, the policy at this institution has been to perform ERT on all moribund patients sustaining penetrating torso injury and all patients sustaining blunt injury with any evidence of cardiac electrical activity. To evaluate whether such a liberal policy is currently justified, the charts of all patients undergoing ERT over a 4-year period were reviewed. One hundred twelve patients underwent ERT; 24 (21%) sustained penetrating injury, 88 (79%) blunt injury. The overall survival rate was 1.8%. Penetrating injury had a 4.2% survival and blunt injury 1.1%. No patients with CPR initiated at the scene and required throughout transport survived. In those patients with both blood pressure and spontaneous respirations present in the field, survival rate was 11.8%. Survival rate in patients manifesting sinus rhythm or ventricular fibrillation upon arrival at the ER was 6.4%. No survivors were noted among patients coming to the hospital with an idioventricular rhythm or asystole. The total hospital charges for patients undergoing ERT exceeded reimbursement by $59,565. Screening for HIV and hepatitis could be documented in only two patients; both were negative. Liberal performance of ERT has dismal results, incurs monetary loss, and affords a greater potential for exposure to lethal infection. Emergency room thoracotomy is justified only when vital signs or a resuscitatible cardiac rhythm are present in the field or ER and deteriorate shortly before thoracotomy.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1991

An analysis of the critical problem of trauma center reimbursement.

There is a widespread perception that many trauma centers are poorly reimbursed, and many hospitals that once cared for trauma victims no longer do so, primarily for financial reasons. The problem is blamed on both uninsured and underinsured patients, but data supporting this perception are lacking. To determine the validity of these perceptions and to better understand the nature of trauma center reimbursement, a survey was conducted. A questionnaire on the volume of trauma seen annually and the reimbursement experience for trauma center (TC) and hospital (HO) patient populations was mailed to representative but nonrandomly chosen trauma centers. Seventy-one surveys were mailed and 25 were returned (35%). There were 15 Level I and 10 Level II centers; 16 were urban, seven were suburban, and two were rural. Eighteen centers (72%) reported significant underfunding of the TC in contrast to the HO, and 11 indicated that they would not be able to continue their current level of TC services with present reimbursement. For Medicare patients, HO cost recovery rates averaged 93%, but recovery rates were only 64% for TCs. For Medicaid beneficiaries, the HO cost recovery rate averaged 85%, but it was only 49% for TCs. Thirty-one percent of TC patients had no insurance coverage at all, in contrast to only 9% of HO patients. An aggregate loss equal to 19.9% of total costs was reported by respondents. This survey, while not representative of trauma centers as a whole throughout the United States, does suggest that there is a basis for the perception of underfunding of trauma care and indicates that such underfunding results from the combination of adverse selection and disproportionate share. We also describe a new method for assessing and comparing trauma center reimbursement.

Data Collection↗

PubMed1991

A CD18 monoclonal antibody increases the incidence and severity of subcutaneous abscess formation after high-dose Staphylococcus aureus injection in rabbits.

Monoclonal antibody (MAb) 60.3 blocks CD18-dependent polymorphonuclear neutrophil adherence to endothelium and has been shown to be of benefit in preventing tissue injury in a variety of inflammatory conditions. However, concern exists that interference with normal polymorphonuclear neutrophil host-defense functions may increase susceptibility to bacterial infection. We compared the development of subcutaneous Staphylococcus aureus abscesses in rabbits pretreated with MAb 60.3 to those pretreated with saline placebo. Bacterial inoculation with 10(6) or 10(7) colony-forming units (CFU) did not result in abscess formation in either control or antibody-treated groups. However, inoculation with 10(8) CFU resulted in more frequent and larger abscesses in antibody-treated rabbits than in controls. Abscess incidence was similar for inoculation with 10(9) CFU, although antibody-treated rabbits developed larger abscesses than did controls. The difference in abscess development is due to delayed leukocyte migration into inoculated tissue. The results of these experiments suggest that subjects treated with MAb 60.3 and exposed to massive S. aureus inocula may be at serious risk of infection. However, despite inhibited leukocyte adhesion, inocula of up to 10(7) CFU were well tolerated in this model. Whether these findings are clinically important remains to be determined, although exposure to bacterial concentrations of 10(8) CFU or greater occurs only rarely in clinical practice.

Abscess↗

PubMed1991

Mechanisms and consequences of leukocyte-endothelial interaction.

Leukocyte adhesion to endothelium is a critical event in host defense against microorganisms and in the repair of tissue damage. Under some circumstances, however, altered leukocyte-endothelial interactions may contribute to the pathogenesis of inflammatory and immune diseases. In a number of experimental models, the inhibition of leukocyte adherence to endothelium substantially reduces vascular and tissue injury. Antiadhesion therapy may represent a novel approach to the treatment of a wide spectrum of clinical disorders.

Animals↗

PubMed1991

Transient inhibition of neutrophil adherence with the anti-CD18 monoclonal antibody 60.3 does not increase mortality rates in abdominal sepsis.

Monoclonal antibodies (MAbs) that recognize the neutrophil (PMN) adherence complex CD11/CD18 inhibit PMN adherence to endothelium and attenuate PMN-mediated ischemia-reperfusion injury. One consideration regarding the clinical usefulness of such therapy is whether transient inhibition of PMN adherence or function will impede host defense and increase susceptibility to infection and sepsis. We studied susceptibility to sepsis in New Zealand white rabbits with an appendiceal devascularization model to answer the question: Does inhibition of PMN adherence with the anti-CD18 MAb 60.3 increase morbidity and mortality rates in abdominal sepsis? Four treatment groups of 10 animals each were studied: group 1 (controls) received no treatment, group 2 received MAb 60.3, group 3 was given the antibiotic cefazolin alone, and group 4 received both cefazolin and MAb 60.3. PMN emigration into the peritoneum was inhibited significantly in MAb 60.3-treated animals (groups 2 and 4). There was no difference in weight loss, incidence of infectious complications, or mortality rates when MAb 60.3-treated animals were compared with untreated animals. These results demonstrate that transient inhibition of PMN adherence does not increase morbidity or mortality rates in this model of abdominal sepsis. These results suggest that if MAb 60.3 or similar antibodies are used to prevent PMN-mediated injury, they will not increase susceptibility to sepsis.

Abdomen↗