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E M Camporesi

Publications and source records attributed to E M Camporesi.

At least 19 recordsLinked to original sources
PubMed2006

Hyperbaric oxygenation ameliorates indomethacin-induced enteropathy in rats by modulating TNF-alpha and IL-1beta production.

The effect of hyperbaric oxygenation (HBO2) was investigated in a rat model of indomethacin-induced enteropathy. Enteropathy was induced by two subcutaneous injections of indomethacin (7.5 mg/kg) 24 hr apart. Six groups of rats (n=8) were treated with and without HBO2 (100% oxygen at 2.3 atm absolute) for 1 hr once or twice a day for 2 or 5 days. Disease activity index (DAI) and total ulcer length were measured. Other rats were randomized into two groups (n=16) with and without HBO2 (1 hr once a day) and four rats were killed in each group at 12, 24, 48, and 72 hr after the final injection of indomethacin. Serum and intestinal mucosal TNF-alpha, IL-1beta, myeloperoxidase (MPO), and iNOS expression was measured. HBO2 treatment significantly attenuated indomethacin -induced intestinal ulceration and improved DAI. Indomethacin increased MPO activity and iNOS expression, and these were reduced by HBO2 treatment, with a concomitant reduction in TNF-alpha and IL-1beta. Our data suggest that HBO2 treatment has a beneficial effect on indomethacin-induced enteropathy and this effect is possibly mediated by decreased production of TNF-alpha and IL-1beta.

Animals↗
PubMed2006

Hyponatremic seizures after suprapubic catheter placement in 7-year-old child.

We report a case of hyponatremic seizures in a 7-year old boy with spina bifida following cystoscopy and suprapubic catheter placement. Immediate postoperative cystogram and pelvic computed tomogram (CT) after the development of seizures demonstrated a fluid collection from the suprapubic catheter site into the anterior abdominal wall. The subsequent reabsorption of free water from the fluid collection, with the contribution of postoperative hypotonic intravenous fluid administration and possible transient inappropriate antidiuretic hormone (ADH) secretion resulted in acute dilutional hyponatremia and consequent seizures. Strategies to prevent hyponatremia in children during urological procedures, with emphasis on the importance of reserving free water as the irrigation fluid are discussed.

Abdominal Wall↗
PubMed2004

Emphysematous cystitis: rapid resolution of symptoms with hyperbaric treatment: a case report.

INTRODUCTION: Emphysematous cystitis is a rare disease that occurs most often in elderly diabetic patients characterized by gas formation in the bladder wall due to infection. The infecting organism is usually an aerobic bacterium, most commonly E. coli although anaerobic species have also been reported. We report the use of hyperbaric oxygen in a patient with emphysematous cystitis and air in the femoral vein in which the treatment rapidly resolved the symptoms and radiological abnormalities. METHODS: A 65-year-old female presented to the Emergency Department with altered mental status, weakness, dark urine, dysuria and fever. She was febrile and lethargic. Abdominal exam showed suprapubic tenderness. Urinalysis was positive for white blood cells and bacteria. A CT scan of the abdomen demonstrated extensive air in the bladder wall with an air bubble in the femoral vein. Presumptive diagnosis was urinary tract infection, emphysematous cystitis, and sepsis. A question of air embolism was raised due to the intravascular gas. The patient was treated with hyperbaric oxygen (2.85 atm abs, 90 minutes) on two separate occasions in the first 12 hours. Within 24 hours, the patient's condition rapidly improved. Repeat CT scan 48 hours after admission showed near complete resolution of the emphysematous cystitis. The patient grew Klebsiella pneumonia from her urine. CONCLUSIONS: Emphysematous cystitis is a rare condition caused by either aerobic or anaerobic bacteria and may be associated with both bladder wall and intravascular gas formation. Hyperbaric oxygen therapy has not been previously reported as a treatment modality. The rapid improvement in our patient may indicate a role for hyperbaric oxygen in addition to IV hydration and antibiotics in this disease.

Aged↗
PubMed2001

Hyperbaric O2 reduces intestinal ischemia-reperfusion-induced TNF-alpha production and lung neutrophil sequestration.

Treatment with hyperbaric O2 (HBO) ameliorates ischemia-reperfusion (I/R) injury. Since tumor necrosis factor-alpha (TNF-alpha) plays an important role in I/R injury, we hypothesized that the effect of HBO in I/R injury may be due to its ability to inhibit TNF-alpha production. In this study, one group of rats received HBO during 60 min of ischemia (HBO group, n = 9), while control rats endured the same procedure but did not receive HBO (non-HBO, n = 9). A group of sham-operated control rats (SHAM, n = 6) underwent laparotomy without occlusion of the artery and HBO treatment. Intestinal I/R led to an increase in serum TNF-alpha concentration to [mean (SEM)] 165 (32) pg/ml (P < 0.01 vs SHAM rats). HBO attenuated this increase [34 (9) pg/ml; P<0.05 vs non-HBO group]. Intestinal I/R also resulted in a marked increase in lung myeloperoxidase content [0.62 (0.04) U/g vs 0.17 (0.02) U/g of SHAM rats, P<0.01]. HBO suppressed this increase [0.40 (0.04) U/g, P<0.05 vs non-HBO rats]. HBO ameliorated the injury to the intestine and lung. The number of neutrophils sequestered in the lung was reduced in HBO rats compared to non-HBO rats [6.4 (0.9) neutrophils/per oil field and 10.9 (2) neutrophils/per oil field, respectively; P < 0.05]. These findings demonstrate that HBO inhibits TNF-alpha production during intestinal I/R, and this reduced TNF-alpha production may be attributed to the beneficial effects of HBO.

Acute Disease↗
PubMed2001

Role of nitric oxide in acidosis-induced intestinal injury in anesthetized rats.

We investigated the pathogenic mechanism(s) of small intestinal injury during acidosis in relation to circulating nitric oxide (NO) in an experimental rat model. Rats were anesthetized, paralyzed, and mechanically ventilated with room air. Hydrochloric acid (0.16 mmol bolus followed by 0.132 mmol/kg/h) was infused through the jugular vein for 5 hours. Control rats received a saline infusion. Arterial blood gases, blood pressure, and blood pH were measured every 30 minutes. The involvement of NO in this acidosis model was assessed by measuring plasma concentration of nitrite/nitrate (NOx) and by evaluating inducible NO synthase (iNOS) expression in small intestinal mucosa. Intestinal injury was assessed by measuring myeloperoxidase (MPO) activity, thiobarbituric acid reactants (TBARS), and histologic scores. HCl infusion was associated with hypotension, decreased blood pH, increased plasma concentration of NOx, augmented intestinal mucosal iNOS expression, MPO activity, TBARS, and histopathologic injury scores. Pretreatment with an iNOS inhibitor, aminoguanidine (AG, 50 mg/kg), reversed HCl-induced hypotension without a change in blood pH. HCl-induced lesions, MPO activity, TBARS, and plasma NOx production were decreased by AG. Our data show that the pathogenic mechanisms of acidosis-induced small intestinal lesions involve up-regulation of NO production by increased expression of iNOS and augmentation of superoxide radicals and MPO activity.

Acidosis↗
PubMed2001

Environmental stress on diving-induced platelet activation.

Platelet activation has been suggested to play an important role in the pathogenesis of prethrombotic states and thus may be responsible for decompression illness during compressed air (scuba) diving. To investigate the effect of physical, mental, and environmental stress on platelet activation during immersion in ice-cold water, we examined 10 male breath-hold divers (BHD), 10 elite BHD (eBHD), and 10 scuba divers during immersion in an ice-covered lake at moderate altitude. Platelet activation was examined by surface expression of activation-dependent glycoproteins CD62p, CD63, and CD42a with flow cytometry 10 min before and 1 min and again 24 h after diving. Plasma epinephrine level was also measured. In addition, the relationship between the activated platelets and the epinephrine level was evaluated. The percentage of platelet activation increased from 2.1 +/- 0.4 to 5.7 +/- 0.3, 1.8 +/- 0.3 to 12.9 +/- 0.8, and 3.7 +/- 0.9 to 31.2 +/- 0.8 in BHD, eBHD, and scuba divers, respectively. The percentage of platelet activation returned to pre-immersion levels in BHD and eBHD divers 24 h after diving, but was still higher in scuba divers. A positive relationship exists between the plasma epinephrine level and the percentage of the platelet activation. This study suggests that physical and mental stress enhance platelet activation during diving in ice-cold water.

Adult↗
PubMed2000

A comparison of the cost-effectiveness of remifentanil versus fentanyl as an adjuvant to general anesthesia for outpatient gynecologic surgery.

The unique pharmacokinetic properties of remifentanil make it a potentially useful adjuvant during general anesthesia for ambulatory surgery. Fentanyl, inexpensive and easy to administer, is the most common opioid used for this purpose. As an adjuvant to general anesthesia for outpatient gynecologic surgery, we questioned if remifentanil was cost-effective as an alternative to fentanyl. Thirty-four patients undergoing gynecologic laparoscopy or hysteroscopy were prospectively and randomly assigned to a standard practice (n = 18) or a study (n = 16) group. Standard practice patients received fentanyl (3 microg/kg) before induction; study patients received remifentanil by continuous infusion (0.5 microg x kg. min(-1) at induction, then 0.2 microg x kg x min(-1)). Sevoflurane was titrated to a Bispectral index value of 40-55. We investigated recovery profiles, patient and health care professional satisfaction, and drug costs. The incidence of rescue antiemetic treatment (2 of 16 vs. 8 of 18; P = 0.013) and the nausea visual analog scale scores during second stage recovery (0.2 vs. 0.6; P = 0.044) were more frequent in the study group. However, the incidence of intraoperative adverse events and other postoperative sequelae, recovery times, pain and nausea visual analog scale scores, opioid analgesic dosage requirements in the postanesthetic care unit, and satisfaction survey responses were similar between groups. Perioperative drug costs per patient were $17.72 more in the remifentanil (vs. fentanyl) group.

Adjuvants, Anesthesia↗
PubMed1999

Segmental pulmonary vascular responses to changes in pH in rat lungs: role of nitric oxide.

BACKGROUND: Respiratory or renal failure is associated with changes in blood pH. Changes in pH may have profound effects on vascular tone and reactivity. Site of action of acidosis in the pulmonary vasculature and the role of nitric oxide production remain unclear. METHODS: We utilized isolated rat lung preparation perfused with autologous blood (Hct = 20%, flow rate = 33 ml/min), and investigated the effect of acidosis and alkalosis (induced by ventilation with high and low inspired CO2) on vascular resistance and the role of nitric oxide during resting and elevated tone conditions. Changes in resistance were described in terms of small and large arteries and veins, using the vascular occlusion technique. RESULTS: Acidosis (Pco2 = 66.7 +/- 0.7 mmHg, pH = 7.17 +/- 0.01, Po2 = 255 +/- 3 mmHg) caused vasoconstriction under resting and increased vascular tone conditions (U46619-induced). The changes in resistance occurred primarily in the small arteries. In contrast, alkalosis (Pco2 = 20.1 +/- 0.3 mmHg, pH = 7.61 +/- 0.01, Po2 = 244 +/- 3 mmHg) caused vasodilation only at elevated tone conditions. Nitro-L-arginine (LNA), an inhibitor of nitric oxide synthase, increased vascular resistance slightly but did not modulate the responses to pH, suggesting that such responses are not nitric oxide dependent. During KCl-induced contraction, the effects of pH were abolished. CONCLUSIONS: We conclude that in rat lung, acidosis causes an increase in pulmonary vascular resistance at normal and elevated tone conditions. Furthermore, the response is limited primarily to the small arteries, and is not mediated by nitric oxide. Alkalosis tends to cause the opposite effects. The effects of acidosis and alkalosis were abolished when vascular tone was elevated with a low dose of KCl, suggesting that vascular response to pH may involve changes in membrane potential.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1999

The synergistic effect of sympathectomy and hyperbaric oxygen exposure on transcutaneous PO2 in healthy volunteers.

UNLABELLED: The benefit of hyperbaric oxygen (HBO2) exposure is dependent on the oxygen delivery. Such benefit may be limited by the fact that hyperoxia causes vasoconstriction and decreases blood flow. The aim of this study was to determine whether regional sympathectomy attenuates this vasoconstriction response and thus improves oxygen delivery. In a double-blinded manner, healthy volunteers were subjected to HBO2 in a monoplace chamber on two occasions separated by at least 1 wk. Transcutaneous oxygen (tcPO2) and carbon dioxide (tcPCO2) on the forearm were monitored continuously, and blood flow in the axillary artery was measured using angiodynography before and after exposure to HBO2. During one visit, each volunteer received a sympathetic block to the upper extremity by an injection of lidocaine into the brachial plexus at the axilla. During a second visit, the volunteer received a placebo injection of isotonic sodium chloride solution into the brachial plexus of the same side. Skin temperature was recorded on the back of the hand. All subjects exhibited a small but significant increase in skin temperature (2.5%) and in upper limb blood flow (23%) (P < 0.05%) after sympathectomy, but not after isotonic sodium chloride solution injection. Sympathectomy increased tcPO2 marginally while in room air. However, during HBO2, tcPO2 was substantially and significantly higher (409.8+/-98.8 mm Hg) after sympathectomy compared with that after isotonic sodium chloride solution injection (171.3+/-38.1 mm Hg). tcPCO2 did not change significantly after sympathectomy or during HBO2. Thus, sympathectomy presumably improved oxygen delivery by preventing vasoconstriction during hyperoxia. The results suggest that sympathectomy may be a useful adjunct to HBO2 therapy in patients in whom vascular resistance is increased because of sympathetic tone or hyperoxia. IMPLICATIONS: Sympathetic nerve block of the extremities markedly enhances tissue oxygen delivery during hyperbaric oxygen treatment. Sympathectomy may be a beneficial adjunct treatment to hyperbaric oxygen in peripheral vascular insufficiency.

Adult↗
PubMed1999

Inducible nitric oxide synthase in the lung and exhaled nitric oxide after hyperoxia.

The effect of hyperoxia on nitric oxide (NO) production in intact animals is unknown. We described the effects of hyperoxia on inducible nitric oxide synthase (iNOS) expression and NO production in the lungs of rats exposed to high concentrations of oxygen. Animals were placed in sealed Plexiglas chambers and were exposed to either 85% oxygen (hyperoxic group) or 21% oxygen (negative control group). Animals were anesthetized after 24 and 72 h of exposure and were ventilated via a tracheotomy. We measured NO production in exhaled air (E(NO)) by chemiluminescence. The lungs were then harvested and processed for detection of iNOS by immunohistochemistry and Western blotting analysis. The same experiments were repeated in animals exposed to hyperoxia for 72 h after they were infused with L-arginine. We used rats that were injected intraperitoneally with Escherichia coli lipopolysaccharide to induce septic shock as a positive control group. Hyperoxia and septic shock induced expression of iNOS in the lung. However, E(NO) was elevated only in septic shock rats but was normal in the hyperoxic group. Exogenous infusion of L-arginine after hyperoxia did not increase E(NO). To exclude the possibility that in the hyperoxic group NO was scavenged by oxygen radicals to form peroxynitrite, lungs were studied by immunohistochemistry for the detection of nitrotyrosine. Nitrotyrosine was found in septic shock animals but not in the hyperoxic group, further suggesting that NO is not synthesized in rats exposed to hyperoxia. We conclude that hyperoxia induces iNOS expression in the lung without an increase in NO concentration in the exhaled air.

Animals↗
PubMed1999

Acidosis stimulates nitric oxide production and lung damage in rats.

Systemic hypotension during sepsis is thought to be due to nitric oxide (NO) overproduction, but it may also be due to acidosis. We evaluated in healthy rats the consequences of acid infusion on NO and blood pressure. Sprague-Dawley rats were anesthetized, and ventilated with room air. The animals were randomized into four groups. Group 1 (C, n = 10) received only normal saline at rates comparable to the other groups. Group 2 (A1, n = 10) received hydrochloric acid at 0.162 mmol in the first 15 to 30 min, followed by a continuous infusion of 0.058 mmol/h for 5 h. Group 3 (AG+A1, n = 6) was pretreated with aminoguanidine (AG, 50 mg/kg), and HCl was infused as above. Group 4 (A2, n = 7) received HCl at twice the rate used in A1. Nitric oxide concentration in the exhaled gas (ENO), blood gases, and mean arterial pressure were measured every 30 min. Acid infusion in A1 caused the pH to fall gradually from 7.43 +/- 0. 01 to 7.13 +/- 0.05. This moderate decrease in pH was associated with a marked increase in ENO (1.6 +/- 0.3 to 114.2 +/- 22.3 ppb), an increase in plasma nitrite/nitrate (17.3 +/- 3.7 to 35.2 +/- 4.3 microM), and a significant decrease in blood pressure (110.5 +/- 6.3 to 63.3 +/- 15.0 mm Hg). Furthermore, acidosis caused lung inflammation, as suggested by the increase in lung myeloperoxidase activity (282.2 +/- 24.7 to 679.3 +/- 57.3 U/min/g) and lung injury score (1.7 +/- 0.2 to 3.5 +/- 0.6). Acidosis after AG pretreatment was associated with a similar change in pH, but the increase in ENO, nitrite/nitrate, and systemic hypotension were prevented. Furthermore, lung injury was attenuated by AG, as suggested by a lower myeloperoxidase activity, though lung injury score was not altered. In this model, moderate acidosis causes increases in NO, hypotension, and lung inflammation. Lung inflammation and injury are due in part to acidosis and NO production. This is the first report to show a direct effect of chronic acidosis on NO production and lung injury. These results have profound implications on the role of acidosis on NO production and lung injury during sepsis.

Acidosis↗
PubMed1999

Hyperbaric oxygen therapy: from the nineteenth to the twenty-first century.

Hyperbaric oxygen technology now occupies a legitimate place in modern medical practice, and the number of clinically active hyperbaric facilities has grown. We estimate that more than 200 monoplace (single-patient) chambers and over two dozen multiplace facilities are presently active in the United States. Nevertheless, the majority of patients suffering from syndromes amenable to HBO therapy are treated in hospitals devoid of such modalities. This situation stems in part from the significant cost of appropriate facilities, the relative scarcity of trained personnel, and the difficulties in obtaining appropriate compensation in an era of rapidly changing reimbursement paradigms. Frequently, patients undergoing HBO therapy require mechanical ventilation, vasoactive drug infusions, sophisticated monitoring, and accurate fluid and electrolyte therapy during treatment. The demonstrated efficacy of HBO as an important part of the treatment of certain acute disease processes, however, justifies the facilities and skilled personnel necessary for the care of critically ill patients in a hyperbaric environment.

History, 19th Century↗
PubMed1998

Treatment of septic shock in rats with nitric oxide synthase inhibitors and inhaled nitric oxide.

OBJECTIVE: To evaluate the effect of treatment with a combination of nitric oxide synthase inhibitors and inhaled nitric oxide on systemic hypotension during sepsis. DESIGN: Prospective, randomized, controlled study on anesthetized animals. SETTING: A cardiopulmonary research laboratory. SUBJECTS: Forty-seven male adult Sprague-Dawley rats. INTERVENTIONS: Animals were anesthetized, mechanically ventilated with room air, and randomized into six groups: a) the control group (C, n=6) received normal saline infusion; b) the endotoxin-treated group received 100 mg/kg i.v. of Escherichia coli lipopolysaccharide (LPS, n=9); c) the third group received LPS, and 1 hr later the animals were treated with 100 mg/kg i.v. Nw-nitro-L-arginine (LNA, n=9); d) the fourth group received LPS, and after 1 hr, the animals were treated with 100 mg/kg i.v. aminoguanidine (AG, n=9); e) the fifth group received LPS and 1 hr later was treated with LNA plus 1 ppm inhaled nitric oxide (LNA+NO, n=7); f) the sixth group received LPS and 1 hr later was treated with aminoguanidine plus inhaled NO (AG+NO, n=7). Inhaled NO was administered continuously until the end of the experiment. MEASUREMENTS AND MAIN RESULTS: Systemic mean blood pressure (MAP) was monitored through a catheter in the carotid artery. Mean exhaled NO (ENO) was measured before LPS (T0) and every 30 mins thereafter for 5 hrs. Arterial blood gases and pH were measured every 30 mins for the first 2 hrs and then every hour. No attempt was made to regulate the animal body temperature. All the rats became equally hypothermic (28.9+/-1.2 degrees C [SEM]) at the end of the experiment. In the control group, blood pressure and pH remained stable for the duration of the experiment, however, ENO increased gradually from 1.3+/-0.7 to 17.6+/-3.1 ppb after 5 hrs (p< .05). In the LPS treated rats, MAP decreased in the first 30 mins and then remained stable for 5 hrs. The decrease in MAP was associated with a gradual increase in ENO, which was significant after 180 mins (58.9+/-16.6 ppb) and reached 95.3+/-27.5 ppb after 5 hrs (p< .05). LNA and AG prevented the increase in ENO after LPS to the level in the control group. AG caused a partial reversal of systemic hypotension, which lasted for the duration of the experiment. LNA reversed systemic hypotension almost completely but only transiently for 1 hr, and caused severe metabolic acidosis in all animals. The co-administration of NO with AG had no added benefits on MAP and pH. In contrast, NO inhalation increased the duration of the reversal in MAP after LNA, alleviated the degree of acidosis, and decreased the mortality rate (from 55% to 29%). CONCLUSIONS: In this animal model, LPS-induced hypotension was alleviated slightly and durably after AG, but only transiently after LNA. Furthermore, co-administration of NO with AG had no added benefits but alleviated the severity of metabolic acidosis and mortality after LNA. We conclude that nitric oxide synthase (NOS) inhibitors, given as a single large bolus in the early phase of sepsis, can exhibit some beneficial effects. Administration of inhaled NO with NOS inhibitors provided more benefits in some conditions and therefore may be a useful therapeutic combination in sepsis. NO production in sepsis does not seem to be a primary cause of systemic hypotension. Other factors are likely to have a major role.

Administration, Inhalation↗
PubMed1998

Chronic osteomyelitis of the tibia: treatment with hyperbaric oxygen and autogenous microsurgical muscle transplantation.

To establish the success rate of combined therapy for tibial osteomyelitis, we reviewed all cases of this infection treated with surgery, antibiotics, and hyperbaric oxygen (HBO) between 1974 and 1991 at Duke University Medical Center. The median delay from diagnosis of osteomyelitis to initiation of HBO was 12.5 months (range, 1 month to 684 months). Of 34 patients in whom follow-up data were complete, 27 (79%) were male and 7 (21%) female, with a mean age of 37.9 years (range, 20 years to 77 years). Patients received an average of 8.3 surgical procedures (range, 2 to 19) and 35 HBO treatments (range, 6 to 99). Twenty patients (59%) received free vascularized muscle flaps as part of therapy. Actuarial analysis was used to examine the effect of free vascularized flap procedures. Of 26 patients with 24 months of follow-up after treatment, 21 (81%) remained drainage free. At 60 months and 84 months after treatment, 12 of 15 (80%) and 5 of 8 (63%), respectively, were drainage free. After more than 84 months, patients who had received muscle flaps were more likely to be drainage free than patients who had received only debridement, and this difference approached statistical significance.

Adult↗
PubMed1997

Increased nitric oxide in exhaled gas is an early marker of hypovolemic states.

Acute hemorrhage is associated with a variety of physiologic and metabolic alterations, including vascular hyporeactivity and endothelial cell dysfunction. The lung is a major target organ during hemorrhagic shock. The effect of acute hemorrhage on NO production in the lung is not well described. In the present study we examined the effect of acute hemorrhage on exhaled NO (NOe), and studied how changes in blood volume and flow affect NOe. Anesthetized and mechanically ventilated rabbits were used. The effect of acute hemorrhage by slow exsanguination on NOe was examined using chemiluminescence. Because hemorrhagic shock is associated with decreased pulmonary blood flow, we established an isolated lung preparation perfused with autologous blood (Hct = 17.4%) and studied the effect of pulmonary flow rate on NOe independent of metabolic changes. In order to separate the effect of flow from the effect of changes in blood volume, we examined the effect of flow in isolated lungs perfused with a blood-free albumin solution (PAS). In the isolated lung, ventilation was similar to that used in the intact animal, and temperature, pH, pCO2, and PO2 were kept normal. Prior to exsanguination, baseline NOe in the intact animal was 24 +/- 3 ppb. At 5, 10, 15, and 20 min after initiating the hemorrhage, NOe rose to 31 +/- 3, 51 +/- 7, 94 +/- 10, and 154 +/- 16 ppb, respectively (P < 0.05). During baseline conditions in the blood-perfused isolated lungs (200 ml/min), NOe was 35 +/- 3 ppb. When flow was decreased to 70 and 0 ml/min, NOe increased to 37 +/- 3 and 56 +/- 6 ppb, respectively (P < 0.001). During baseline conditions in the PAS-perfused lungs (70 ml/min), NOe was 94 +/- 13 ppb and was unaffected by changes in flow. The perfusion pressure in the isolated lungs was in the normal range. Reduction in blood flow rate in the isolated lung was associated with less than twofold increase in NOe. This was attributed to reduction in red blood cell volume and not due to changes in blood flow rate. Reduction in flow in the intact animal during hemorrhage generated more than threefold increase in NOe, suggesting that neurohumoral mediators, in addition to changes in flow, play an important role in determining. NOe in the intact condition. NOe began to rise immediately after exsanguination began, and therefore may be a useful early marker of acute hemorrhagic shock and hypovolemia. This information may be useful in the intensive care setting.

Acute Disease↗
PubMed1997

Segmental pulmonary vascular responses to ATP in rat lungs: role of nitric oxide.

ATP exhibits vascular pressor and depressor responses in a dose- and tone-dependent manner. The vascular site of ATP-induced contraction or dilation has not previously been characterized. Using the vascular occlusion technique, we investigated the effects of ATP in isolated rat lungs perfused with autologous blood (hematocrit = 20%) and described its action during resting and elevated tone in terms of changes in resistances of the small and large arteries and veins. During resting tone, ATP (10(-5) M) caused contraction primarily in the small arteries and, to some extent, in the small veins, suggesting that P2x purinoceptors are present in these small vessels. During hypoxia, ATP caused dilation primarily in the small arteries, suggesting that P2y purinoceptors are predominant in small arteries. During U-46619-induced contraction, which occurred evenly throughout the four segments, ATP caused dilation in the large arteries and veins but not in the small arteries and veins. After treatment with N omega-nitro-L-arginine to inhibit nitric oxide synthesis, ATP-induced contraction was potentiated, and its dilatory effects during hypoxia were attenuated. The action of ATP was independent of prostanoids, because its constrictor and dilatory responses were not affected significantly by indomethacin. In conclusion, the results indicate that the effects of ATP on the pulmonary vasculature are primarily due to P2x and P2y purinoceptors in the small arteries. Contribution of these purinoceptors in other vessels to changes in total vascular resistance in rat lung was minor.

Adenosine Triphosphate↗
PubMed1997

Determinants of nitric oxide in exhaled gas in the isolated rabbit lung.

Nitric oxide concentrations in the exhaled gas (NOe) increases during various inflammatory conditions in humans and animals. Little is known about the sources and factors that influence NOe. NOe at end expiration was measured by chemiluminescence in an isolated, blood-perfused rabbit lung. The average end-expiratory concentration over 10 breaths was used. The effect of positive end-expiratory pressure (PEEP), flow rate, pH, hypoxia, venous pressure, and flow pulsatility on NOe were determined. At constant blood flow, increasing PEEP from 1 to 5 cm H2O elicited a reproducible increase in NOe from 49 +/- 7 to 53 +/- 8 parts per billion (ppb) (p < 0.05). When blood pH was increased from 7.40 to 7.74 by breathing low CO2 gas, NOe rose from 45 +/- 7 to 55 +/- 7 ppb (p < 0.001). Hypoxia caused a dose-dependent decrease in NOe from 37 +/- 3 during baseline to 23 +/- 2 during ventilation with 0% O2 (p < 0.01). Venous pressure elevation from 0 to 5 and 10 mm Hg decreased NOe from 32 +/- 5, to 26 +/- 5 and 24 +/- 5 ppb, respectively (p < 0.05). Switching from steady to pulsatile flow (same man flow) resulted in a small, albeit significant reduction in NOe; 30 +/- 4 to 28 +/- 4 ppb (p < 0.05). Changes in flow rate between 200 and 20 ml/min were associated with small changes in NOe; however, when flow was stopped, NOe rose substantially to 56 +/- 6 ppb (p < 0.05). The changes in NOe were rapid (1 to 2 min) and reversible. The results suggest that NOe is influenced by ventilatory and hemodynamic variables, pH, and hypoxia. We suggest that caution must be taken when interpreting changes in exhaled NO in humans or experimental animals. Changes in total and regional blood flow, capillary blood volume, ventilation, hypoxia, and pH should not be overlooked.

Animals↗