Biomedical subjects

C Lalonde

Publications and source records attributed to C Lalonde.

At least 19 recordsLinked to original sources

PubMed1998

Modulation of the vascular smooth muscle angiotensin subtype 2 (AT2) receptor by angiotensin II.

The angiotensin subtype 2 (AT2) receptor is scarce in most adult vascular tissues except after injury. Since angiotensin II (AngII) is released upon injury, we examined the possibility that AngII governs AT2 receptor expression in smooth muscle cells (SMC). A polyclonal antiserum, raised to a peptide corresponding to the AT2 receptor C-terminus, recognized a approximately 45-kDa protein after transfection of cos-7 cells with AT2 receptor cDNA. Detection of a approximately 65-kDa band in extracts of SMC indicated that the AT2 receptor was glycosylated. Treatment of SMCs with AngII increased AT2 receptor levels fourfold over 24 h. This response was abrogated by losartan, but not by PD123319, indicating AT1 receptor involvement. AngII-dependent increases in AT2 receptor levels were also prevented by LY294002, an inhibitor of phosphatidyinositol 3-kinase, but not by rapamycin. These results indicate AngII influences AT2 receptor expression through the AT1 receptor via a signaling pathway that includes PI3K.

Angiotensin II↗

PubMed1998

Repression of phosphoenolpyruvate carboxykinase gene activity by insulin is blocked by 3-aminobenzamide but not by PD128763, a selective inhibitor of poly(ADP-ribose) polymerase.

Expression of the phosphoenolpyruvate carboxykinase (PEPCK) gene is induced by 3-aminobenzamide, an inhibitor of poly(ADP-ribose) polymerase. Synthesis of PEPCK mRNA is repressed by insulin, but remains detectable in H4IIE hepatoma cells exposed simultaneously to both 3-aminobenzamide and insulin. This capability of 3-aminobenzamide to block the inhibitory actions of insulin suggests that ADP-ribosylation is required for the regulation of PEPCK gene expression by insulin. Furthermore, neither changes in chromatin condensation nor cell growth status were linked to these events. The inability of 3,4-dihydro-5-methylisoquinolinone (PD128763), a selective inhibitor of poly(ADP-ribose) polymerase, to impede insulin-dependent repression of PEPCK gene expression, however, indicated that 3-aminobenzamide does not operate by inhibiting poly(ADP-ribosyl)ation. The potential involvement of mono(ADP-ribosyl)ation, a process that is also inhibited by 3-aminobenzamide, in the regulation of PEPCK gene activity was then evaluated. Analysis of poly(ADP-ribose) polymerase activity and poly(ADP-ribosyl)ation confirmed that there were no significant changes in response to insulin, while microsomal mono(ADP-ribosyl)transferase activity was elevated approximately fourfold. An increase in protein hydroxylamine-sensitive mono(ADP-ribosyl)ation was observed following insulin treatment. The sensitivity of the mono(ADP-ribosyl)transferase activity to 3-aminobenzamide but not PD128763 makes it plausible that mono(ADP-ribosyl)ation rather than poly(ADP-ribosyl)ation contributes to the regulation of PEPCK gene expression.

ADP Ribose Transferases↗

PubMed1998

Molecular cloning of rat cardiac sarcolemmal Ca2+/Mg2+ ectoATPase (Myoglein).

Rat cardiac sarcolemmal Ca2+/Mg2+ ectoATPase (Myoglein), a membrane-bound enzyme requiring millimolar concentrations of Ca2+ or Mg2+ for maximal hydrolysis of ATP, has been purified to apparent homogeneity. Tryptic digestion and amino acid sequencing was used to design an oligonucleotide probe for screening a rat heart cDNA library; this produced a partial cDNA clone (pND2.1), and sequencing of a 400 base pair portion revealed a 100% homology to human platelet CD36. Northern blotting with pND2.1 detected a 3.1 kb transcript in rat heart but not in other tissues. Interspecies expression analysis (cardiac tissue total RNA blot probed with pND2.1) detected a approximately 2.0 kb transcript in canine, rabbit and porcine heart, whereas transcripts of a 4.1 kb, approximately 3.0 kb and 2.1 kb were observed in human cardiac tissue. A rat genomic DNA Southern blot, probed with pND2.1, indicated that there was a single copy of the gene in the rat genome. Expression of the pND2.1 cDNA in E. coli produced an 89 kDa polypeptide recognized by anti-human CD36 antibody but not by anti-rat Ca2+/Mg2+ ectoATPase antibody. It is concluded that rat cardiac Ca2+/Mg2+ ectoATPase is tightly associated with a protein highly homologous to the adhesion molecule CD36.

Adenosine Triphosphatases↗

PubMed1997

Correlates of battering among 997 men: family history, adjustment, and attitudinal differences.

In order to identify the characteristics associated with physical abuse of female partners, a detailed questionnaire was administered to 997 men who were recruited from either a forensic out-patient clinic (780) or from a community based employment center (217). This questionnaire sampled family and personal history, criminal behavior, psychopathology, and attitudes towards violence. Based upon self-report, the sample was divided into 184 non-abusive men, 517 moderately abusive men, and 296 severely abusive men. The full sample (997) was randomly divided into two subsamples and then, using a cross-validation design, group differences were identified in both subsamples on 46 of the 93 variables examined in this study. All significant effects were linear, such that the average scores of the severely abusive men were worse than the scores of the abusive men who, in turn, scored worse than the non-abusive men. In general, both groups of abusive men reported high rates of violence during childhood (both as victims and perpetrators), antisocial personality disorder, subjective distress, marital maladjustment, attitudes tolerant of spouse assault, and a range of impulsive behaviors (impulsive violence, substance abuse, motor vehicle accidents). The factors that correlated with abuse in the total sample also correlated with abuse in the community sample.

Adult↗

PubMed1996

Attrition from a male batterer treatment program: client-treatment congruence and lifestyle instability.

Although patient compliance is a problem for almost all forms of therapy, treatment programs for male batterers face special concerns. Male batterers are often perceived as coming to therapy only because of the external pressures of courts or intimate partners. In the present study, we examined the rates at which male batterers failed to attend treatment following an initial assessment interview. Of the 526 men recommended for treatment, only 218 (41%) attended a single treatment session, and only 132 (25%) completed the brief (10-week) treatment program. The variables associated with attrition fell into two general categories: (a) those associated with lifestyle instability (e.g., moves, unemployment, youthfulness), and (b) those variables indicating a congruence between the clients' self-identified problems and the targets of treatment (e.g., self-admitted problems with spousal assault). Suggestions are provided as to how programs could reduce their attrition rates by attending to the issues of client-treatment congruence and lifestyle instability.

Adult↗

PubMed1995

Effect of graded increases in smoke inhalation injury on the early systemic response to a body burn.

OBJECTIVE: To study the early (first 24 hrs) effect of increasing lung exposure to smoke on the hemodynamic response to a modest body burn. DESIGN: A prospective randomized study. SETTING: Laboratory at a university medical center. SUBJECTS: Thirty-two adult yearling female sheep. INTERVENTIONS: Adult sheep (n = 32) were given an 18% of body surface burn; 24 sheep were then exposed to cotton toweling smoke using 12 breaths of a tidal volume of 5, 10, or 20 mL/kg. Animals were awakened, resuscitated to baseline oxygen delivery, and then killed at 24 hrs. MEASUREMENTS AND MAIN RESULTS: Vascular pressure, cardiac output, and oxygen consumption and delivery were measured, as well as blood gases, lung and soft tissue lymph flow, and fluid balance. We found that a 5-mL/kg tidal volume smoke exposure x 12 breaths did not produce significant airway inflammation or alter the cardiopulmonary response to a burn alone. Oxygen consumption (VO2) remained at baseline and the net 24-hr positive fluid balance of 1.5 L was comparable to a burn alone. Increasing the smoke exposure to 10 mL/kg tidal volume, which produced a moderate airway injury, resulted in a significant increase in early fluid requirements, a 40% early increase in VO2, a doubling of positive fluid balance, as well as a marked increase in burn edema. However, gas exchange was not impaired. The 20-mL/kg tidal volume exposure resulted in an early 100% increase in VO2, a three-fold increase in fluid requirements at 1 to 4 hrs, compared with burn alone, in addition to a severe airway inflammation with mucosal slough and resulting impaired gas exchange. CONCLUSIONS: The addition of a smoke exposure which produces airway inflammation and injury significantly increases early post burn systemic metabolic demands and fluid requirements, as well as the degree of burn edema and positive fluid balance compared with a burn alone. The magnitude of the accentuated response appears to correspond with the degree of airway inflammation and not with alveolar dysfunction.

Animals↗

PubMed1995

Increased early postburn fluid requirements and oxygen demands are predictive of the degree of airways injury by smoke inhalation.

The combination of burn and smoke inhalation was studied to determine if early hemodynamic and metabolic abnormalities would correspond with the degree of subsequent smoke-induced airways injury. Adult sheep (n = 45) given an 18% total body surface third-degree burn alone or with smoke exposures of 12 breaths of 5, 10, or 20 mL/kg tidal volume were continuously monitored with airways assessed at 4 or 24 hours. With increased smoke exposure (20 mL/kg tidal volume), oxygen consumption (VO2) in the first several hours and net positive fluid balance, especially in the first 6 hours, increased by 100% and 300%, respectively, over that seen with burn alone. The degree of increase in fluid requirement, net fluid retention, and VO2 with smoke, compared with burn alone, correlated best with the degree of airways damage quantitated at 24 hours, r = 0.83, 0.85, and 0.89, respectively. Airways damage at 4 hours did not predict the damage seen at 24 hours. Systemic changes were not caused by gas-phase toxins, such as carbon monoxide, because smoke filtered of particles had the same blood carbon monoxide control as whole smoke, but the systemic response was equal to burn alone, and there was no airways injury. The cause of the systemic changes is likely the result of the intense airways inflammation.

Animals↗

PubMed1994

Administration of large doses of vitamin C does not decrease oxidant-induced lung lipid peroxidation caused by bacterial-independent acute peritonitis.

Acute zymosan-induced peritonitis in rats produces lung inflammation and lipid peroxidation. The effect of this process on plasma and lung tissue ascorbic acid was determined, as was the effect of infusing 150 mg/kg of ascorbic acid immediately after zymosan on the degree of lung insult. Ascorbic acid levels were significantly decreased in plasma and lung tissue at 24 h after zymosan, and lung tissue conjugated diene and neutrophil content was also significantly increased. Vitamin C infusion increased postzymosan plasma levels by 50% over normal control levels. However, lung tissue ascorbic acid was still decreased, and no decrease in the lung injury process was noted. Added ascorbic acid also did not prevent a decrease in plasma vitamin E with the peritonitis. We conclude that the amount of ascorbic acid given in this study did not diminish the lung oxidant inflammatory changes. An insufficient dose or inadequate time for plasma ascorbic acid to equilibrate with the lung cytosol are possible explanations for the lack of attenuation of lung oxidant stress.

Acute Disease↗

PubMed1994

Laparoscopic Presacral Neurectomy Versus Neurotomy with the Argon Beam Coagulator

Presacral neurectomy is effective treatment for dysmenorrhea and midline pelvic pain. The purpose of this paper is to report the benefits of the argon beam coagulator (ABC) used laparoscopically to perform a presacral neurotomy compared with conventional techniques for presacral neurectomy. In 51 patients undergoing laparoscopic presacral neurectomy, 34 were performed using the ABC only without dissection or excision, and 17 underwent presacral neurectomy by conventional methods. Postoperative pain reduction was the same in both groups, 77% versus 73%, with average anesthesia time 64 minutes for the ABC neurotomy versus 92 minutes with conventional techniques. One major vascular complication requiring immediate laparotomy occurred in the ABC group. When properly applied laparoscopically, the ABC is an effective tool to rapidly coagulate and separate the presacral nerves with minimal smoke, excellent visualization and no retroperitoneal dissection.

Journal Article↗

PubMed1994

Changes in lung and systemic oxidant and antioxidant activity after smoke inhalation.

We determined the oxidant activity in lung airways, parenchyma, and systemic tissues in response to smoke inhalation, comparing lipid peroxidation with physiologic and histologic change. Adult sheep were given a controlled amount of cooled smoke from burned cotton toweling, containing a uniform particle diameter of 3-4 microns. The mean peak carboxyhemoglobin was 45 +/- 4%. Animals were monitored unanesthetized for 24 h and killed. Severe respiratory failure was noted, as a result of airways mucosal ulceration, submucosal edema, and atelectasis, along with increased airways fluid, but minimal alveolar edema. Airway fluid malondialdehyde (MDA) content was threefold greater than plasma. However, airways mucosa and lung parenchymal tissue, lipid peroxidation, and oxidized glutathione were not increased, suggesting the only direct oxidant activity was present only at the airways surface. Other factors besides oxidants are likely to be involved in the lung injury. However, a marked systemic oxidant stress was noted as evidenced by a significant increase in liver tissue MDA and decrease in reduced glutathione and catalase activity. The tissue oxidant stress also corresponded with a 75% increase in systemic oxygen consumption and an increase in soft tissue vascular permeability. We conclude that: 1) the only direct lung oxidant stress after smoke was noted in airways fluid, while lung tissue lipid peroxidation was not seen despite severe airways injury and atelectasis, and 2) major systemic physiologic changes, as evidenced by increased systemic oxygen demands and systemic microvascular permeability are seen with smoke exposure in addition to evidence of systemic tissue oxidant stress. The likely source of the oxidant activity was a smoke-induced systemic inflammation.

Animals↗

PubMed1994

Comparison of plasma reduced glutathione and oxidized glutathione with lung and liver tissue oxidant and antioxidant activity during acute inflammation.

We determined whether plasma levels of reduced glutathione (GSH) and oxidized glutathione (GSSG) accurately reflect the tissue GSH and GSSG levels in lung and liver during a progressive acute inflammation-induced increased oxidant activity. We also determined whether plasma GSH also reflected other antioxidant defenses. Male Wistar rats (n = 38) were given intraperitoneal zymosan (.75 mg/g body weight) producing an acute progressive peritonitis and generalized inflammation. Animals were resuscitated then killed at 4 or 24 h. Plasma and tissue levels of GSH, GSSG, vitamin C, alpha-tocopherol, and catalase were measured. Conjugated dienes and malondialdehyde were used as tissue markers of lipid peroxidation. We found lung and liver tissue GSH to be decreased significantly at 4 h while GSSG was increased. Lipid peroxidation was also present in the lung. At 24 h, GSH remained decreased in liver and GSSG remained increased in lung along with the lipid peroxides conjugated dienes and malondialdehyde. In addition, overall antioxidant defenses were decreased in both lung and liver. Plasma GSH remained decreased at 24 h corresponding with the decrease in liver GSH as well as the decrease in other plasma and tissue antioxidants. However, plasma GSSG levels were not significantly increased, at any time point, indicating plasma GSSG does not accurately reflect tissue oxidant activity.

Acute Disease↗

PubMed1994

Effect of increasing the tidal volume of smoke breaths on smoke-induced lung dysfunction.

We determined the effect of a graded increase in lung exposure to a toxic smoke by increasing smoke tidal volume (VT) or the number of smoke breaths. Sheep were anesthetized and then insufflated with cooled cotton toweling smoke; VT was 5, 10, or 20 ml/kg, and smoke breaths were varied from 12 to 48. The smoke had a uniform particle size (3 +/- 0.4 microns diam). Peak carboxyhemoglobin levels varied from 8 +/- 2 to 45 +/- 4% in the lowest to highest exposure groups, respectively. Animals were monitored unanesthetized for 24 h, and then they were killed. Oxygenation (ratio of arterial PO2 to fraction of inspire O2) decreased from 480 +/- 21 to 200 Torr, and compliance decreased by approximately 50% in the highest smoke exposure groups, whereas only a modest decrease in oxygenation and no compliance changes were seen with lesser exposures. A moderate tracheobronchitis, some atelectasis, and no alveolar edema were noted in the lower smoke exposure groups, whereas severe tracheobronchitis, airway edema, and alveolar atelectasis were observed in the highest exposure group. Only modest alveolar flooding was noted. Impaired oxygenation and anatomic injury correlated best with the total smoke delivered (r = 0.59). Increasing VT from 5 to 20 ml/kg did not increase airway or alveolar injury if the total smoke mass delivered was maintained constant. The degree of impaired oxygenation did not correlate with measured lung water (r = 0.27) or lung lymph flow (r = 0.31).

Aerosols↗

PubMed1994

Smoke inhalation injury in sheep is caused by the particle phase, not the gas phase.

The inhalation of smoke can produce severe lung injury, particularly to airways. We assessed the role of the toxic compounds in the particle phase vs. those in the gas phase of smoke in the injury process by filtering out all particles > 0.3 micron diam before exposure. Adult sheep (n = 16) were insufflated with a well-characterized cellulose smoke. Mean particle size was 3 +/- 0.4 micron diam. A standardized dose of 12 breaths of whole or filtered smoke (n = 8/group) was given to sheep under anesthesia with a tidal volume of 20 ml/kg. Sheep were awakened and monitored for 24 h and then killed. Peak carboxyhemoglobin levels were 40-45% in both groups. Severe respiratory failure occurred only in the whole-smoke group, as evidenced by an increase in shunt fraction from a control of 0.04 +/- 0.02 to 0.28 +/- 0.05, a decrease in lung compliance of 50%, and histological evidence of severe airway mucosal edema, ulceration, and bronchorrhea. No significant physiological, histological, or biochemical changes were noted in the filtered-smoke group.

Animals↗

PubMed1994

Lung and systemic oxidant and antioxidant activity after graded smoke exposure in the rat.

We wanted to determine the effect of a graded smoke inhalation on lung and systemic oxidant stress, and its relationship to physiological and histological change. Male Wistar rats were given 12 breaths of 10 ml/kg (n = 8) (group 1) or 20 ml/kg (n = 8) (group 2) tidal volume, using cotton toweling smoke through the trachea using positive pressure. Rats were monitored, then killed at 24 hr. Data were compared to controls (n = 8). Peak group 1 and group 2 carboxyhemoglobins were 22 +/- 6 and 46 +/- 6%, with a mortality prior to 24 hr of 14% and 50%, respectively. Group 1 rats showed only moderate lung dysfunction but with severe airway inflammation and edema, alveolar inflammation and atelectasis, with a decrease in PaO2 from the control of 96 +/- 4 to 72 +/- 5 torr. No increase in lung, liver, or kidney oxidant-induced lipid peroxidation, measured as malondialdehyde lung, liver, or kidney oxidant-induced lipid peroxidation, measured as malondialdehyde (MDA), or decrease in the antioxidant defenses catalase was noted. Group 2 rats demonstrated severe airways edema, alveolar atelectasis, and alveolar edema, and a PaO2 decreasing below 60 torr, corresponding with a 3-fold increase in lung tissue MDA and 35% decrease in catalase. In addition, liver and kidney tissue MDA doubled, and catalase activity decreased by 40%. Increased oxygen consumption was also demonstrated.(ABSTRACT TRUNCATED AT 250 WORDS)

Aerosols↗

PubMed1994

Physiologic support of the septic patient.

The patient's response to inflammation, referred to as sepsis, is a complex process involving the degree of the inflammatory insult and the host response. Ischemia, from blood flow abnormalities and direct cell injury from mediators, produces the physiologic response. The treatment is focused first on restoring and maintaining perfusion through maintenance of increased oxygen delivery. The second approach is first surgical then pharmacologic attenuation of the inflammation-induced injury.

Hemodynamics↗

PubMed1993

Relationship of burn-induced lung lipid peroxidation on the degree of injury after smoke inhalation and a body burn.

OBJECTIVE: We compared the effect of a modest smoke inhalation injury, a burn injury alone, and a smoke inhalation injury plus a body burn, on the degree of lung oxidant-induced lipid peroxidation and lung injury. DESIGN: Prospective animal study with concurrent controls. SETTING: An animal laboratory. SUBJECTS: Forty-four adult yearling female sheep (weight range 45 to 50 kg). INTERVENTIONS: Forty-four sheep were prepared with lung and prefemoral (soft tissue) lymph fistulas. Twelve breaths of cooled smoke with tidal volume of 10 mL/kg body weight were given to 24 sheep, producing a peak blood carboxyhemoglobin of 25% to 30%. Twelve sheep also received a 15% total body surface third-degree burn. Sheep were killed at 4 or 24 hrs. MEASUREMENTS AND MAIN RESULTS: Circulating lipid peroxidation was monitored as conjugated dienes and tracheobronchial mucosal and lung parenchyma as malondialdehyde. Antioxidant defenses were monitored by catalase activity. Lung physiologic and histologic changes were compared. We noted intense airways inflammation in both smoke inhalation groups and lung parenchymal inflammation in all groups. Lung lymph flow was modestly increased (two-fold) in the smoke inhalation groups. Alveolar water content was not significantly increased after any injury. PaO2 was decreased at 24 hrs after the smoke insult alone. Parenchymal malondialdehyde content did not increase with the smoke insult alone, but did increase from a control value of 110 +/- 20 to 270 +/- 24 nmol/g tissue by 4 hrs in the combined burn and smoke injury group, while catalase activity decreased. Airway mucosal malondialdehyde did not increase in any group. CONCLUSIONS: We conclude that alveolar capillary permeability is not increased early after a moderate smoke injury or smoke injury with burn. Lipid peroxidation is not increased in large airway or lung parenchyma with early after-smoke exposure. The addition of a burn significantly increases lung parenchymal lipid peroxidation, but the oxidant changes do not correspond with the degree of early lung dysfunction.

Animals↗

PubMed1993

The effect of acute nonbacterial dependent peritonitis on lung and liver oxidant stress and antioxidant activity.

BACKGROUND: The role of oxidant release and tissue antioxidant defenses on inflammation-induced organ injury is not clearly defined. METHODS: We determined the effect of acute zymosan peritonitis in rats on lung and liver tissue oxidant stress and antioxidant defenses during a 5-day period. Oxidant activity was measured as tissue malondialdehyde and oxidized glutathione (GSSG). Antioxidant activity was measured as tissue-reduced glutathione (GSH) and catalase activity. Rats were maintained hydrated with subcutaneous crystalloid. Animals were killed at 4, 12, and 24 hours and 5 days. RESULTS: Acute peritonitis was evident at 12 and 24 hours but was resolving at 5 days. Peritoneal fluid cultures were negative after 24 hours. A 50% mortality rate was noted between 20 and 30 hours, with no deaths after 30 hours. We noted a significant increase in lung GSSG and malondialdehyde at 4 hours that persisted for the 5 days, as did histologic evidence of a progressing severe lung inflammation. No increased conversion of lung xanthine dehydrogenase to xanthine oxidase was noted. Lung GSH and catalase activity were maintained at control despite negligible food intake. In contrast, liver GSSG was increased significantly only at the 4-hour period, corresponding with a transient conversion of xanthine dehydrogenase to xanthine oxidase from 10% to 31%. Tissue malondialdehyde did not increase despite the initial oxidant stress. However, tissue GSH and catalase values decreased by more than 50% after 24 hours and remained decreased at 5 days. CONCLUSIONS: We conclude that early lung and liver oxidant stress is initiated by acute peritonitis. Lung oxidant changes persist and lung dysfunction progresses, even though antioxidant activity is maintained and acute peritonitis is resolving. Liver lipid peroxidation did not develop despite oxidant release, probably because of a large antioxidant reserve. However, a severe and sustained decrease in liver antioxidants results, increasing the potential damage from a subsequent oxidant insult.

Animals↗

PubMed1993

Pentoxifylline does not prevent endotoxin induced lung and liver lipid peroxidation in the adult sheep.

Our purpose was to determine the effect of pentoxifylline pretreatment on endotoxin-induced (5 microgram/kg) lung and systemic oxidant activity, measured as lipid peroxidation. We used the awake adult sheep with lung and soft tissue lymph fistulae to monitor microvascular changes as well as to monitor oxygen delivery and consumption. Oxidant activity was monitored using the level of plasma conjugated dienes, a measure of circulating lipid peroxides, and lung and liver malondialdehyde content, a measure of tissue lipid peroxidation. Sixteen sheep were given endotoxin, eight of which were pretreated with pentoxifylline (20 mg/kg bolus) followed by a 6 mg/kg/hr infusion. We found that the degree of early endotoxin-induced pulmonary hypertension and hypoxia and later increased pulmonary microvascular permeability was not attenuated with pentoxifylline. In addition, a comparable increase in circulating conjugated dienes, lung neutrophil sequestration, and a three-fold increase in lung malondialdehyde was seen in both groups. Soft tissue QL also increased to the same degree in both groups. Liver MDA increased from a control of 110 +/- 20 nM/g tissue to 165 +/- 32 nM/g with endotoxin alone and to 260 +/- 55 nM/g with pentoxifylline pretreatment, a significant increase over both control and endotoxin alone groups. Pentoxifylline, however, did improve hemodynamic stability, required significantly less fluid, and prevented the hyperdynamic state seen at 4-5 hr post endotoxin. We conclude that pentoxifylline attenuates the initial endotoxin-induced hemodynamic instability, and later hyperdynamic state. However, pentoxifylline pretreatment does not appear to prevent endotoxin-induced oxygen radical release in the unanesthetized sheep.

Animals↗