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Biomedical subjects

C Marshall

Publications and source records attributed to C Marshall.

At least 109 records · Page 6Linked to original sources
PubMed1987

High-dose almitrine bismesylate inhibits hypoxic pulmonary vasoconstriction in closed-chest dogs.

The effect of almitrine bismesylate on the hypoxic pulmonary vasoconstrictor (HPV) response was studied in seven closed-chest dogs anesthetized with pentobarbital and paralyzed with pancuronium. The right lung was ventilated continuously with 100% O2, while the left lung was ventilated with either 100% O2 ("hyperoxia") or with an hypoxic gas mixture ("hypoxia": end-tidal PO2 = 50.1 +/- 0.1 mmHg). Cardiac output (CO) was altered from a "normal" value of 3.10 +/- 0.18 l . min-1 to a "high" value of 3.92 +/- 0.16 l . min-1 by opening arteriovenous fistulae which allowed measurements of two points along a pressure-flow line. These four phases of left lung hypoxia or hyperoxia with normal and high cardiac output were repeated in the presence and absence of almitrine. Almitrine bismesylate was administered as a constant infusion of 14.3 micrograms . kg-1 . min-1 for a mean plasma concentration of 219.5 +/- 26.4 ng . ml-1. Relative blood flow to each lung was measured with a differential CO2 excretion (VCO2) method corrected for the Haldane effect. With both lungs hyperoxic, the percent left lung blood flow (%QL-VCO2) was 44 +/- 1%. When the left lung was exposed to hypoxia, the %QL-VCO2 decreased significantly to 22 +/- 1%. However, with the administration of almitrine, the %QL-VCO2 during left lung hypoxia increased significantly to 36 +/- 2%. The arterial oxygen tension decreased significantly between hyperoxia (PaO2 = 633 +/- 6 mmHg) and hypoxia (271 +/- 31 mmHg). With the addition of almitrine, there was no change during hyperoxia; however, during hypoxia, the PaO2 decreased significantly to 124 +/- 15 mmHg. Cardiac output did not influence these findings. The pulmonary vascular conductance (G) is the slope of the pressure-flow line.(ABSTRACT TRUNCATED AT 250 WORDS)

Almitrine↗
PubMed1987

Hyperplastic polyps of the colon and rectum. An immunohistochemical study with monoclonal antibodies against blood groups antigens (sialosyl-Lea, Leb, Lex, Ley, A, B, H).

We studied 40 hyperplastic polyps (HP) immunohistochemically with monoclonal antibodies against 8 different blood group antigens (BGA) comparing their reactivity with normal control colon and colorectal adenocarcinomas. The 8 BGA studied were: Sialosyl-Lea, Lea, Leb, Lex, Ley, A,B, and H. sialosyl-Lea, Lea, Lex, and Ley can be though of as differentiation antigens. The former 2 BGA are expressed on mature (differentiated) epithelium while the latter 2 BGA are expressed by undifferentiated epithelium of the crypt base. A, B, H and Leb are not expressed in the normal distal colon, however, they are extensively expressed on distal colorectal cancers and adenomas and can be considered oncofetal BGA. HP expressed Lea, Lex, Ley in the same compartment of the crypt as normal colon and extensively expressed Sialosyl-Lea throughout the entire length of the crypt. This latter finding indicated maturation at a lower point in the crypt than in normals. All HP failed to express B and H BGA, while 6 of 40 expressed Leb and 5 of 40 HP expressed A BGA. Of the 6 HP expressing Leb BGA, 3 were from patients with synchronous or metachronous cancers and 2 from patients with mixed hyperplastic polyp-adenomas (HP/AD). Two of the HP expressing A BGA were from patients with HP/AD. The expression and distribution of these BGA in HP, especially the extensive expression of sialosyl-Lea correlates with the known cell kinetics of HP. While nonneoplastic in nature, HP may occasionally express true oncofetal BGA. Similarly, the HP component of HP/AD may also express true oncofetal BGA. These data suggest that the lesions classified morphologically as HP may be antigenically heterogenous.

ABO Blood-Group System↗
PubMed1986

Influence of isoflurane on hypoxic pulmonary vasoconstriction in dogs.

The authors studied the influence of locally administered isoflurane anesthesia on the pulmonary vascular response to regional alveolar hypoxia (hypoxic pulmonary vasoconstriction [HPV]) over a range of cardiac outputs (COs) in seven mechanically ventilated, closed-chest dogs. The right lung was ventilated with 100% O2 throughout the study. The left lung was ventilated with either 100% O2 (normoxia) or an hypoxic gas mixture (hypoxia). Different alveolar concentrations of isoflurane (0, 1, and 2.5 MAC) were administered to the left lung in a randomized sequence. The CO was altered by opening and closing surgically produced arteriovenous fistulae, at all isoflurane concentrations, and by hemorrhage at 0 MAC isoflurane. The magnitude of the HPV response was measured by differential CO2 elimination in the absence of isoflurane and by venous admixtures in all phases. During normoxia, the left lung effective flow (QL%) measured from differential CO2 excretion was 39.9 +/- 1.2% of the total blood flow and decreased to 18.8 +/- 2.6% when ventilated with the hypoxic gas mixture. Venous admixture (QVA/QT%) was significantly correlated with QL% during hypoxic ventilation in the absence of isoflurane. QVA/QT% was 22.3 +/- 2.7% during hypoxia with normal CO, and it increased significantly to 27.7 +/- 1.1% when the CO was increased 43%. It was not significantly altered (23.6 +/- 3.6%) when the CO was decreased by 54%. Isoflurane 2.5 MAC significantly increased QVA/QT% during hypoxic ventilation of the left lung to 33.9 +/- 2.6% with low CO and 35.4 +/- 1.7% with normal CO. Isoflurane 1 MAC increased QVA/QT% to 27.2 +/- 2.7% with normal CO and 28.1 +/- 2.6% with high CO.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

The activating effect of sleep EEGs in epileptic patients with epileptic activity in their waking EEGs.

A sleep EEG was recorded in 44 patients whose waking EEG showed epileptic activity. The time in seconds in which one epileptic discharge occurred was determined. Considering the waking and sleep EEGs together one epileptic discharge occurred every 7.8 seconds. Focal epileptic activity was recorded nearly twice as frequently (1 paroxysm every 4.6 sec.), as generalized activity (1 paroxysm every 9.8 sec.) or generalized activity with lateral emphasis (1 paroxysm every 8.8 sec.). Considering the sleep and waking EEGs separately it was found that on average more epileptic activity occurred in sleep than in the waking EEG (6.4 vs. 10.8 sec.). There was no difference between generalized (8.9 vs. 13.5 sec.), generalized activity with lateral emphasis (7.7 vs. 12.9 sec.) and focal activity (3.9 vs. 7.6 sec.). Comparing, however, the frequency of epileptic activity in each individual patient during wakefulness and sleep it was seen that during sleep more activity was found in only 56.8% of the patients. If a difference of 3 seconds is considered to be due to chance, then more epileptic activity was found in 34.1% of the patients during sleep and in 24.5% during wakefulness. Thus, the sleep EEG by no means always activates epileptic activity.

Adolescent↗
PubMed1985

Hypoxic pulmonary vasoconstriction is not potentiated by repeated intermittent hypoxia in closed chest dogs.

Hypoxic pulmonary vasoconstrictor (HPV) responses were measured with repeated intermittent hypoxic challenges in eight non-traumatized closed chest dogs anesthetized with pentobarbital. The right lung was ventilated continuously with 100% O2 while the left lung was either ventilated with 100% O2 (control) or ventilated with a gas mixture containing 3-4% O2 (hypoxia). Mean per cent left lung blood flow for all four normoxic periods was 43.1 +/- 1.5% (mean +/- SE) of the total blood flow by the SF6 excretion method and 40.8 +/- 1.1% by the differential CO2 excretion method, corrected for the Haldane effect. With hypoxic ventilation, flow diversion from the hypoxic lung was maximal with the first exposure and did not change subsequently with a total of four alternating exposures to normoxia and hypoxia. Flow diversion during hypoxia was approximately 50.5 +/- 2.4% by the SF6 method and 50.3 +/- 3.5% by the VCO2 method. This result contrasts with the increasing flow diversion response with intermittant hypoxic exposure that has been reported in animals exposed first to thoracotomy and surgical dissection. It is concluded that in the absence of surgical trauma the initial response to hypoxia is maximal and is not potentiated by repeated hypoxic stimulation.

Anesthesia, Intravenous↗
PubMed1985

Hypoxic pulmonary vasoconstriction in isolated rat lungs perfused with perfluorocarbon emulsion.

Eight rat lungs were perfused in an in vitro circuit with a blood-PS solution and then with a perfluorocarbon emulsion (perfluorotributylamine, FC-43). With perfusion flow constant, the hypoxic pulmonary vasoconstrictor (HPV) response was measured as changes in pulmonary artery pressure when F1,O2 was changed to 0.1, 0.06, 0.04, 0.03, 0.02 and zero with FI,CO2 of 0.05. The hypoxic response to an FI,O2 of 0.03, with the blood-PSS perfusate, was an increase from baseline pressure of 93.5 +/- 18% and, with the perfluorocarbon perfusate was 67.5 +/- 18%; these values were not significantly different (P greater than 0.2). A stimulus-response relationship was obtained with the FC-43 perfusate by plotting the response as a percentage of the maximum response (R%max) against the logarithm of the alveolar oxygen tension. The equation for the linear portion of the response was R%max = 257.9-140.2 X log (10) PA,O2 and r = 0.78. The PA,O2 corresponding to half of the maximum response (ED50) was 30.4 mmHg. The present study demonstrated that HPV is maintained in isolated rat lungs perfused with an FC-43 emulsion. The stimulus-response relationship as well as the ED50 with the FC-43 is similar to earlier results with blood perfusate. Lung oedema was not found after perfusion with the FC-43 emulsion.

Animals↗
PubMed1984

Computed tomography of the sacroiliac joints: comparison with complex-motion tomography.

Forty-seven patients with sacroiliac joint abnormalities were examined with computed tomography and conventional complex-motion tomography. Twenty-nine patients had spondyloarthritis. Of the 29, complex-motion tomography detected bone erosions in 16 patients, whereas computed tomography revealed erosions in nine. Computed tomography was more sensitive in detection of joint narrowing, joint widening, osteosclerosis, and intraarticular bony ankylosis. In the remaining 13 patients, computed tomography was the modality of choice in detection of paraarticular soft tissue pathology, such as abscess or tumor, and in detection of the lesions involving the sacral canal and neural foramina.

Adult↗
PubMed1984

Effects of halothane, enflurane, and isoflurane on hypoxic pulmonary vasoconstriction in rat lungs in vitro.

Rat lungs were ventilated and perfused at a constant rate in vitro. The maximal hypoxic pulmonary vasoconstrictor (HPV) response was recorded by measuring the pulmonary artery pressure change when the inspired oxygen concentration was changed from 21% to 3% (with 5.5% carbon dioxide) in the absence of anesthetic vapor. In different experimental groups, the effects of halothane, enflurane, and isoflurane on HPV were examined. In random order the anesthetics were added to the inspired gas in concentrations of 0.25, 0.5, 1, 1.5, and 2 or 2.5 MAC units. The HPV pressor response to 3% oxygen in the presence of anesthetic agent was expressed as a per cent of the pressure response observed in the absence of anesthetic (R%MAX). All three agents depressed HPV in a dose-related manner. The concentrations in MAC units at which 50% depression of HPV (ED50) occurred was 0.47, 0.60, and 0.56 for halothane, isoflurane, and enflurane, respectively, and neither the ED50 values nor the slopes of these dose response curves were significantly different. It was concluded that these halogenated general anesthetics inhibit HPV with essentially the same potency.

Animals↗
PubMed1984

Time course and responses of sustained hypoxic pulmonary vasoconstriction in the dog.

The stability of the pulmonary blood pressure and flow response to alveolar hypoxia (hypoxic pulmonary vasoconstriction or HPV) was studied in six pentobarbital anesthetized, mechanically ventilated open-chested dogs. Aortic and left pulmonary artery blood flows; systemic and pulmonary arterial, central venous, left atrial, and airway pressures; hemoglobin; arterial and mixed venous blood gases were measured. The right lung was ventilated continuously with 100% oxygen, while the left lung was ventilated alternately with 100% O2 ( prehypoxia control phase), an hypoxic gas mixture containing 4% O2, 3% CO2, balance N2 for 4 h, or 100% O2 (post-hypoxia control phase). Hypoxic ventilation of the left lung resulted in an immediate and sustained decrease in left lung blood flow (QL%) from 39.0 +/- 1.8% (mean +/- SE) to 9.9 +/- 3.6% at 15 min of hypoxic ventilation. QL% remained decreased and did not vary significantly during the 4 h of hypoxia. Venous admixture correspondingly was increased and PaO2 decreased by hypoxic ventilation and did not vary significantly during the 4 h of hypoxia. All variables returned to control levels upon reestablishing ventilation with 100% O2. While the maximal reduction in QL% with left lung hypoxic ventilation was identical to that observed during atelectasis previously in our laboratory, the time course of the response was different. The response to hypoxia was maximal by 15 min, however, QL% decreased more slowly during atelectasis, where the maximal reduction was observed by 60 min. The present study therefore demonstrated that hypoxic ventilation of the left lung yielded an immediate and sustained decrease in left lung blood flow for 4 h. The stability of the HPV response probably was accounted for by the lack of such confounding factors as respiratory alkalosis, severe systemic hypoxemia, and increased cardiac output.

Analysis of Variance↗
PubMed1984

The effect of long-term controlled mechanical ventilation with positive end-expiratory pressure on renal function in dogs.

The effects of 46 h of mechanical ventilation and PEEP on urinary output, sodium excretion, and renal and cardiovascular function were examined. Dogs sedated with sodium pentobarbital were ventilated using one of three modes: spontaneous ventilation (SV), controlled mechanical ventilation (CMV), or CMV with 10 cmH2O positive end-expiratory pressure (CMV with PEEP). Intravenous fluids were given at a constant rate throughout the study and measurements of renal and cardiovascular function were made over four periods. Dogs whose lungs were ventilated with PEEP displayed more than two times the amount retention seen in the other groups as assessed by mean weight gain. This was due to an initial depression of urine flow, sodium excretion, and free water clearance. Urinary flow rate approximated the rate of fluid infusion by 20 h in SV dogs and by 27 h during CMV, while the maximum during CMV with PEEP occurred at 46 h. There were no significant differences in glomerular filtration rate, renal corticomedullary blood flow distribution, or renal blood flow between groups. During the 46 h, cardiac index increased (SV, +16%; CMV, +19%; CMV with PEEP, +64%), while systemic vascular resistance (SV, -28%; CMV, -30%; CMV with PEEP, -57%), renal vascular resistance (SV, -12%; CMV, -20%; CMV with PEEP, -23%), and mean arterial pressure (SV, -16%; CMV, -15%; CMV with PEEP, -15%) decreased in all groups. This study has demonstrated that when a constant sodium and water load was provided, the SV and CMV groups were rapidly able to adjust the urinary excretion to meet input, while the return of renal function toward normal in the CMV with PEEP group was delayed until almost 46 h from the start of ventilation.

Animals↗
PubMed1984

Metabolic and respiratory hydrogen ion effects on hypoxic pulmonary vasoconstriction.

Hypoxic pulmonary vasoconstriction (HPV) was studied in the ventilated-perfused rat lung in vitro. Respiratory acidosis and alkalosis were obtained by ventilating with 2, 7, or 10% CO2 (21% O2-balance N2). Metabolic acidosis and alkalosis were produced by the addition of 0.9 N NaHCO3 or 1 N lactic acid to the perfusate at constant PCO2. At each pH the pressor responses to 2 and 4% O2 were compared with the maximum pressor response (R%max) obtained with zero O2 and 5% CO2 at a normal pH (approximately 7.35). HPV was maximal when the [H+] was between 38 and 50 nM and was attenuated by changes of pH in either direction. Both respiratory and metabolic pH changes had similar effects. The combined linear regression equations were as follows: with 2% O2 the response to acidosis was R%max = 101.37 - 0.52 [H+] and to alkalosis was R%max = 2.03 [H+] - 3.85; with 4% O2 the response to acidosis was R%max = 56.88 - 0.3 [H+] and to alkalosis was R%max = 1.16 [H+] - 4.95. These effects were not due to changes of ionized calcium.

Animals↗
PubMed1984

Ethylene oxide allergy in a dialysis center: prevalence in hemodialysis and peritoneal dialysis populations.

Chronic hemodialysis (HD) and peritoneal dialysis (PD) patients in one dialysis center were examined for (EO)-related sensitization. Five of 56 (8.9%) HD patients and 0 of 30 PD patients skin tested with a conjugate of human serum albumin (HSA) and EO had positive skin prick tests. The sera of 13 of 107 (12.1%) HD patients including sera from 5 patients with negative skin tests were positive in an EO-HSA radioallergosorbent test (RAST). Sensitized patients in this population did not experience allergic-type reactions during hemodialysis. There were no positive EO-HSA RAST results which could be ascribed to PD. Non-specific cutaneous responsiveness of the renal failure patients was compared with that of normal adult subjects by the use of skin prick tests with codeine phosphate and histamine phosphate. A significantly reduced responsiveness is present in chronic renal failure patients which would be expected to lower the sensitivity of the diagnostic skin test by comparison with the RAST.

Adult↗
PubMed1984

A method for perfusing and ventilating rat lungs in vitro.

A method is described for perfusing and ventilating rat lungs in vitro that was developed for pharmacological studies of the pulmonary circulation. A blood-physiological salt solution-albumin (Blood-PSS-Alb) mixture is equilibrated with selected gas tensions in an oxygenator circuit composed of a pump, a reservoir and a Kolobow membrane lung. A fraction of this perfusate is diverted to the pulmonary artery of a rat lung, ventilated and suspended in a temperature-controlled chamber. Perfusate emerging from the left atrium is returned to the circuit reservoir. This technique allows independent regulation of the perfusate and alveolar gas tension and the temperature, carbon dioxide tension and pH of the system is controlled. The model has been utilized for studies of hypoxic pulmonary vasoconstriction (HPV) and consistent and reproducible responses observed for four hours. Practical details for the preparation, cleaning and successful operation of this system are described herein.

Animals↗
PubMed1983

Characterization of the stimulus-response curve for hypoxic pulmonary vasoconstriction.

Lungs from seven healthy female, sea level rats were perfused and ventilated in vitro. Hypoxic pulmonary vasoconstriction was stimulated by changing the inspired gas from 21% oxygen to 6, 4, 3 or 0% oxygen (all gases contained 5% carbon dioxide and balance nitrogen). A sigmoid stimulus-response curve was derived by probit analysis with a 50% of maximum response (ED50) at an oxygen tension of 3.49 +/- 0.17 kPa. It is suggested that such characterizations of the response to hypoxia may allow a more precise comparison of the effects of species, age, sex and drugs on hypoxic pulmonary vasoconstriction.

Animals↗
PubMed1983

Pulmonary blood pressure and flow during atelectasis in the dog.

The purpose of the study was to measure the time course, direction, and magnitude of the hypoxic pulmonary vasoconstriction (HPV) response to atelectasis. Six dogs were anesthetized with pentobarbital. With the chest open, each lung was ventilated separately. Pulmonary blood flow was measured with electromagnetic flow probes. Pulmonary arterial, left atrial, and systemic arterial pressures were measured via indwelling catheters. The right lung was ventilated continuously with 100% O2, while the left lung was either ventilated with 100% O2 (control phase), unventilated (4 hours of atelectasis), or ventilated with a gas mixture containing 4% O2, 3% CO2, and 93% N2 (hypoxia phase). Left lung atelectasis resulted in a reduction of the per cent lung blood flow from 43 +/- 4% (mean +/- SE) to 25 +/- 7% at 15 min and to 12 +/- 1% at 60 min which persisted for the remaining four-hour period. The per cent left lung blood flow was significantly lower (8 +/- 1%) and the PaO2 significantly higher (356 +/- 38 mmHg) during the maximal response to atelectasis as compared to 15 min of hypoxic ventilation (23 +/- 5%; 211 +/- 21 mmHg). With atelectasis or hypoxic ventilation, pulmonary perfusion pressure was increased significantly from the control value of 7.9 +/- 0.8 mmHg to approximately 11 mmHg. The present study demonstrated that in the open chest model without systemic hypoxemia, the response to acute atelectasis is a regional increase in pulmonary vascular resistance which develops quickly (15 min) and is maximal by 60 min and is maintained thereafter. As a result, there is a sustained diversion of blood flow away from the atelectatic lung and a generalized increase of pulmonary perfusion pressure.

Animals↗
PubMed1983

Influence of mixed venous oxygen tension (PVO2) on blood flow to atelectatic lung.

The influence of mixed venous oxygen tension (PVO2) on blood flow to the atelectatic left lung was studied at normal and reduced cardiac outputs (CO) using extracorporeal veno-venous bypass in six pentobarbital anesthetized, mechanically ventilated dogs. Aortic and left pulmonary artery flows; airway, left atrial, central venous, pulmonary, and systemic arterial pressures; hemoglobin, arterial, and mixed venous blood gases were measured. The blood flow reduction observed in atelectasis was altered by the PVO2. Approximately 50% of blood flow was diverted away from atelectatic lung when PVO2 was low (24 +/- 2 mmHg) or normal (46 +/- 2 mmHg) (mean left lung blood flow [QL%] was 23.2 +/- 4.6% with low PVO2 and 19.0 +/- 3.4%, with normal PVO2). When PVO2 was increased to greater than 100 mmHg, diversion of blood flow away from atelectatic lung did not occur and QL% was nearly the flow expected for normoxic ventilated left lung (mean QL% = 40.4 +/- 5.9%). Shunt (QS/QT%) was significantly greater when PVO2 was high than when it was normal or low (mean QS/QT% = 51.7 +/- 5.6%, 31.0 +/- 3.1%, 26.0 +/- 3.4% with high, normal, and low PVO2, respectively). Mean PaO2 was significantly greater when PVO2 was high than when PVO2 was normal or low, despite the increase in QL% and QS/QT% (PaO2 = 327 +/- 25 mmHg, 220 +/- 32 mmHg, 115 +/- 21 mmHg with high, normal, and low PVO2, respectively). A 40% reduction in cardiac output significantly decreased transmural pulmonary artery pressure but did not affect PaO2, QS/QT%, or QL%.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Site and sensitivity for stimulation of hypoxic pulmonary vasoconstriction.

Rat lungs were perfused in an in vitro circuit with separate control of alveolar and pulmonary arterial O2 tension. With perfusion flow constant, the hypoxic pulmonary vasoconstrictor (HPV) response was measured as changes of perfusion pressure. HPV was a function of both alveolar O2 tension (PvO2) and was described by a double sigmoid response surface. Where RA-v is this pressure response expressed as a percent of the maximum, the linearized form of the response surface is given by log [RA-v/(100-RA-v)] = 3.93 - 1.029 (log PvO2) - 1.623 (log PAO2). From this relationship it was concluded that 1) HPV is determined by PAO2 and PvO2; 2) the fundamental stimulus-response relationship is a sigmoid with a 50% response when both PAO2 and PvO2 are 30.3 Torr; 3) PAO2 has a greater effect than PvO2 due in part to the geometry of the vascular wall but principally due to O2 exchange between alveolar gas and blood in small pulmonary arteries; 4) there is not a localized sensor for HPV (the response is accounted for by each smooth muscle cell in the pulmonary arterial wall responding to the O2 tension in its vicinity); and 5) the characteristics of the response suggest that the cell sensor resembles a cytochrome.

Animals↗