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Biomedical subjects

I S Paterson

Publications and source records attributed to I S Paterson.

35 records · Page 2Linked to original sources
PubMed1989

Reperfusion pulmonary edema.

Reperfusion following lower-torso ischemia in humans leads to respiratory failure manifest by pulmonary hypertension, hypoxemia, and noncardiogenic pulmonary edema. The mechanism of injury has been studied in the sheep lung lymph preparation, where it has been demonstrated that the reperfusion resulting in pulmonary edema is due to an increase in microvascular permeability of the lung to protein. This respiratory failure caused by reperfusion appears to be an inflammatory reaction associated with intravascular release of the chemoattractants leukotriene B4 and thromboxane. Histological studies of the lung in experimental animals revealed significant accumulation of neutrophils but not platelets in alveolar capillaries. We conclude that thromboxane generated and released from the ischemic tissue is responsible for the transient pulmonary hypertension. Second, it is likely that the chemoattractants are responsible for leukosequestration, and, third, neutrophils, oxygen-derived free radicals, and thromboxane moderate the altered lung permeability.

Animals↗
PubMed1989

The endothelial cell cytoskeleton modulates extravascular polymorphonuclear leukocyte accumulations in vivo.

Actin microfilaments, key elements in the endothelial cell (EC) cytoskeleton, have been noted in in vitro studies to play a modulating role in the diapedesis of polymorphonuclear leukocytes (PMN). The role of the cytoskeleton in PMN diapedesis in vivo was the subject of this study. Small skin abrasions were produced in rabbits. Cytoskeletal manipulation was accomplished by local application of phalloidin which promotes microfilament assembly or cytochalasin B which causes their disassembly, prior to addition of a chemotaxin. When the initial treatment to the abrasion site was saline, the secondary addition of more saline resulted in PMN accumulations, expressed as PMN/mm3 of 36 +/- 19, while 10(-4) M cytochalasin B led to 91 +/- 32 (P less than 0.05). Secondary addition of chemotaxins or histamine also led to significant PMN accumulations of 169 +/- 54 with 10(-8) M leukotriene (LT) B4, 318 +/- 85 with zymosan-activated plasma (ZAP), and 158 +/- 48 with 10(-4) M histamine. When the initial treatment was 10(-8) M phalloidin, PMN accumulations were reduced to 31 +/- 22 with cytochalasin B (P less than 0.05 relative to saline as initial treatment); 63 +/- 43 with LTB4 (P less than 0.05); 137 +/- 48 with ZAP (P less than 0.05); and 51 +/- 35 with histamine (P less than 0.05). In contrast, initial blister treatment with cytochalasin B rather than saline increased PMN accumulations in response to LTB4, 291 +/- 71 (P less than 0.05), and histamine, 270 +/- 56 (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Regional variation in surface properties of Norway spruce and scots pine needles in relation to forest decline.

Measurements of leaf wettability (contact angle), amounts of epicuticular wax and of surface dust are reported for Scots pine (Pinus sylvestris L.) and Norway spruce (Picea abies (L) Karst) trees growing at 12 sites in Europe from SW Germany to NE Scotland. At each site, three year classes (current year, 1 and 2-year-old) of needles were sampled from the mid-crown of up to 12 trees. Trees were selected at random from two strata, those showing visible decline symptoms (i.e. loss of needles or discoloration) and those apparently healthy. Needles for analysis were taken from apparently healthy (green) shoots in both cases. There were no significant differences between 'declining' and 'healthy' trees within sites, suggesting that leaf surface properties reflect environmental exposure rather than plant response. There were significant differences between sites, particularly for Norway spruce, which may be related to environmental factors including air pollution. Contact angles were consistently smaller at low-altitude sites in Britain and The Netherlands than at high-altitude sites in Germany where forests show decline symptoms. Leaf wettability decreased (contact angles increased) with wax amount and increased with dust amount. Leaf surface properties integrate environmental influences over long periods, and may be useful in identifying sites 'at risk' of developing decline symptoms, but causal relationships cannot be deduced without further direct experimentation.

Journal Article↗
PubMed1989

The rapid induction by interleukin-2 of pulmonary microvascular permeability.

The clinical use of interleukin-2 (IL-2) is limited by severe cardiopulmonary dysfunction. This study examines the mechanism of respiratory failure related to IL-2, using sheep with chronic lung lymph fistulae. Awake animals were infused with an intravenous (I.V.) bolus of IL-2 10(5) U/kg (n = 5) or its excipient (EXC) control (n = 3), every 8 hours for 4 to 5 days. Cardiopulmonary function was monitored daily for at least one 8-hour period. Within 2 hours after each IL-2 administration, mean pulmonary arterial pressure (MPAP) rose. On Day 1, the mean rise was from 13 to 26 mmHg (p less than 0.05), and on Day 5, to 29 mmHg (p less than 0.05). MPAP returned to baseline levels after 2-3 hours. Pulmonary arterial wedge pressure was unchanged from 4 mmHg. There were transient falls in arterial oxygen tension, from 88 to 77 mmHg on Day 1 and to 73 mmHg (p less than 0.05) on Day 5. Lung lymph flow (QL) rose from 2.4 to 6.8 ml/30 minutes (p less than 0.05) on Day 1, and from 4.7 to 10.2 ml/30 minutes (p less than 0.05) on Day 5, whereas the lymph/plasma protein ratio increased on Day 1 from 0.69 to 0.83 (p less than 0.05) and from 0.63 to 0.71 (p less than 0.05) on Day 5. This documents an increase in pulmonary microvascular permeability. Thromboxane (Tx)B2 levels increased transiently after each IL-2 injection in plasma from 195 to 340 pg/ml (p less than 0.05) and in lung lymph from 222 to 772 pg/ml (p less than 0.05) on Day 1, and to similar levels on Day 5. There was a progressive rise in cardiac output from 5.7 to 8.6 1/minute (p less than 0.05) during the 5 days of infusion. Systemic blood pressure did not change. Temperature rose from 39.1 to 41.2 C (p less than 0.05), and shaking chills were common. There was a progressive fall in leukocyte count, from 8.4 to 3.2 X 10(3)/mm3 (p less than 0.05) by Day 5, reflecting a 77% fall in lymphocytes. Lung lymph lymphocyte counts rose, and lymphocyte clearance increased.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Vasodilating prostaglandins attenuate ischemic renal injury only if thromboxane is inhibited.

Ischemia-induced renal injury is prevented by inhibition of thromboxane (Tx) synthesis. This protection was believed to be secondary to a high prostaglandin (PG)/TxA2 ratio. This study tests whether increasing the PG/Tx ratio by administration of vasodilating PGs protects the reperfused ischemic kidney. Anesthetized rats underwent right nephrectomy and 45 minutes of left renal pedicle clamping. Beginning 10 minutes before clamp release, animals were treated intravenously with the following: saline placebo (n = 10); the cyclooxygenase inhibitor ibuprofen (Ibu), 12.5 mg/Kg in a bolus (n = 8); a stable analogue of prostacyclin (PGI2), 500 ng/kg/minute for 2 hours (n = 9); PGE1, 400 ng/kg/minute for 2 hours (n = 8); the combination Ibu and PGI2 (n = 8) or PGE1 (n = 8). In saline treated ischemic controls, 5 minutes after reperfusion plasma, thromboxane (TxB2) and 6-keto-PGF1 levels were 2537 and 317 pg/ml, respectively--higher than the TxB2 and 6-keto-PGF1 levels of 750 and 80 pg/ml, respectively, in nephrectomized but nonischemic sham controls (n = 7) (p less than 0.05). In ischemic control animals at 24 hours, creatinine levels were 4.6 mg/dl, relative to 0.9 ml/dl in sham animals (p less than 0.05); the weight of the left (L) ischemic kidney relative to the right (R) normal kidney was 118%, compared with 99% in sham animals (p less than 0.05); and renal histology of ischemic control animals at 24 hours showed acute tubular necrosis (ATN) relative to normal findings in sham animals. Pretreatment with Ibu led to: TxB2 and 6-keto-PGF1 levels of 116 and 40 pg/ml, lower than those of sham animals (p less than 0.05); creatinine levels of 4.6 mg/dl, L/R renal weight of 119%; and ATN similar to that of ischemic controls. Treatment with a PGI2 analogue or PGE1 was not protective and led to increases in TxB2, 6-keto-PGF1, creatinine, L/R renal weight, and ATN similar to that of ischemic controls. The combination of Ibu and either PGI2 or PGE1 led to: reduced levels of TxB2 and 6-keto-PGF1 (p less than 0.05); attenuated increases in creatinine to 2.2 and 2.3 mg/dl, respectively (p less than 0.05); and limited ATN (p less than 0.05). These data indicate that the vasodilating PG protect the ischemic reperfused kidney only when Tx is inhibited.

6-Ketoprostaglandin F1 alpha↗
PubMed1989

Noncardiogenic pulmonary edema after abdominal aortic aneurysm surgery.

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

Aged↗
PubMed1989

Leukotrienes but not complement mediate limb ischemia-induced lung injury.

Reperfusion after limb ischemia leads to sequestration of polymorphonuclear leukocytes (PMN) in the lungs and to leukocyte- (WBC) and thromboxane- (Tx) dependent respiratory dysfunction. This study examines the intermediary role of the chemoattractants leukotriene (LT)B4 and complement (C) fragments. Anesthetized sheep with chronic lung lymph fistulae underwent 2 hours of tourniquet ischemia of both hind limbs. In untreated controls (n = 7), 1 minute after tourniquet release, mean pulmonary artery pressure (MPAP) rose from 13 to 38 mmHg (p less than 0.05) and returned to baseline within 30 minutes. Pulmonary artery wedge pressure was unchanged from 3.6 mmHg. There were increases in plasma LTB4 levels from 2.46 to 9.34 ng/ml (p less than 0.01), plasma TxB2 levels from 211 to 735 pg/ml (p less than 0.05), and lung lymph TxB2 from 400 to 1005 pg/ml (p less than 0.05). C3 levels were 96% of baseline values. Thirty minutes after reperfusion, lung lymph flow (QL) increased from 4.3 to 8.3 ml/30 minutes (p less than 0.05), lymph/plasma protein ratio was unchanged from 0.6, and the lymph protein clearance increased from 2.6 to 4.6 ml/30 minutes (p less than 0.05), data consistent with increased microvascular permeability. WBC count fell within the first hour from 6853 to 3793/mm3 (p less than 0.01). Lung histology showed leukosequestration, 62 PMN/10 high-power fields (HPF) and proteinaceous exudates. In contrast to this untreated ischemic group, animals treated with the lypoxygenase inhibitor diethylcarbamazine (n = 5) demonstrated a blunted reperfusion-induced rise in MPAP to 17 mmHg (p less than 0.05). There were no increases in LTB4, TxB2, QL or lymph protein clearance (p less than 0.05). WBC count was unchanged and lung leukosequestration was reduced to 40 PMN/10 HPF (p less than 0.05). Decomplementation with cobra venom factor (n = 4) resulted in plasma C3 levels, 10% of baseline, but tourniquet release still led to pulmonary hypertension, elevated LTB4, TxB2 levels, and a decline in WBC count similar to that of untreated ischemic control animals. Histology showed 46 PMN/10 HPF sequestered in the lungs. Further, bilateral hind limb ischemia in either genetically sufficient (n = 10) or deficient (n = 10) C5 mice led to significant lung leukosequestration of 108 and 106 PMN/10 HPF, respectively, compared with 42 and 47 PMN/10 HPF in sham C5(+) and C5 (-) mice (n = 20) (p less than 0.01). These results suggest that the lung leukosequestration and increased microvascular permeability after lower torso ischemia are mediated by the chemotactic agent LTB4, but not by the complement system.

Animals↗
PubMed1989

Postischemic renal injury is mediated by neutrophils and leukotrienes.

Neutrophils have been implicated as central mediators in myocardial and skeletal muscle ischemia-reperfusion injury. This study tests whether these cellular elements and the chemoattractant leukotriene (LTB4) play a role in postischemic renal failure. Anesthetized rats underwent 45 min of left renal pedicle clamping. Five minutes after reperfusion, LTB4 levels were elevated to 1.42 ng/ml (P less than 0.05); thromboxane (Tx)B2 was 2,840 pg/ml, higher than 503 pg/ml in sham controls (P less than 0.05); renal artery blood flow was 67% of preclamping values at 1 min of reperfusion compared with 111% in sham (P less than 0.05). At 24 h, creatinine levels were 4.6 mg/dl (P less than 0.05). At 24 h, creatinine levels were 4.6 mg/dl (P less than 0.05); histology showed acute tubular necrosis (ATN). Neutrophil depletion by rabbit antiserum (n = 8) led during reperfusion to reduced LTB4 and TxB2 levels, 1.04 ng/ml and 1.043 pg/ml (P less than 0.05); increased renal blood flow of 174% (P less than 0.05); reduced creatinine levels of 1.8 mg/dl (P less than 0.05); and limited ATN. Pretreatment with diethycarbamazine prevented the increases in LTB4 and TxB2 (P less than 0.05), increased renal blood flow (P less than 0.05), minimized creatinine increase to 1.7 mg/dl (P less than 0.05), and reduced ATN. These data indicate that neutrophils and LTB4 play a role in ischemia-induced Tx synthesis and mediate postischemic renal injury.

6-Ketoprostaglandin F1 alpha↗
PubMed1989

Thromboxane A2 mediates increased pulmonary microvascular permeability following limb ischemia.

Lower torso ischemia and reperfusion lead to respiratory dysfunction characterized by pulmonary hypertension and increased lung microvascular permeability. This is associated with lung leukosequestration and thromboxane (TX) generation. This study tests the role of elevated TX levels following muscle ischemia in mediating remote lung injury. Anesthetized sheep prepared with chronic lung lymph fistulae underwent 2 hours of bilateral hind limb tourniquet ischemia. In untreated controls (n = 7), 1 minute after reperfusion there was a transient increase in plasma immunoreactive (i)-TXB2 levels from 211 to 735 pg/ml (p less than 0.05), and at 30 minutes, lung lymph i-TXB2 levels rose from 400 to 1,005 pg/ml (p less than 0.05). At 1 minute, the mean pulmonary arterial pressure (MPAP) increased from 13 to 38 mm Hg (p less than 0.05) and pulmonary microvascular pressure (Pmv) from 7 to 18 mm Hg (p less than 0.05). Lung lymph flow (QL) rose from 4.3 to 8.3 ml/30 min (p less than 0.05), the lymph/plasma (L/P) protein ratio was unchanged from 0.6, and the lymph protein clearance increased from 2.6 to 4.6 ml/30 min (p less than 0.05). Two hours after reperfusion, neutrophils were observed sequestered in lung capillaries and proteinaceous exudates were found in alveoli in contrast to sham-operated animals (n = 3). To maximize lung vascular surface area and achieve a pressure independent L/P protein ratio a left atrial balloon was inflated during one group of ischemia-reperfusion experiments (n = 5). This resulted in a baseline rise in MPAP to 20 mm Hg (p less than 0.05); a 4.3-fold increase in QL (p less than 0.05), a decrease in the L/P ratio from 0.70 to 0.28 (p less than 0.05) and a protein reflection coefficient (sigma d) of 0.72. During reperfusion the L/P ratio rose to 0.49 (p less than 0.05) and the sigma d decreased to 0.51 (p less than 0.05), documenting an increase in lung microvascular permeability. In contrast to untreated ischemic controls, inhibition of TX synthetase with OKY 046 (n = 6) reduced plasma i-TXB2 levels to 85 pg/ml (p less than 0.05) but also increased i-6-keto-PGF1 alpha levels to 78 pg/ml relative to 15 pg/ml in untreated controls (p less than 0.05). OKY 046 prevented the increase in MPAP, Pmv, QL, and lymph protein clearance (p less than 0.05). Lung histology was normal in distinction to the leukosequestration in untreated ischemic controls.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1989

Pulmonary edema after aneurysm surgery is modified by mannitol.

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

Aged↗
PubMed1989

Thromboxane mediates the ischemia-induced neutrophil oxidative burst.

Indirect evidence exists that the reperfusion of ischemic tissue activates white blood cells. Thus local and systemic reperfusion injuries are prevented by making animals leukopenic or by inhibiting white blood cell lung entrapment by blocking thromboxane A2 generation. This study tests directly whether ischemia and reperfusion activates neutrophils, as measured by their oxidative burst, and whether thromboxane mediates this event. Anesthetized rats underwent 4 hours of bilateral hind limb tourniquet ischemia followed by 60 minutes of reperfusion. Plasma thromboxane B2 levels increased to 2750 pg/ml at 5 minutes of reperfusion, higher than the sham control (n = 36) value of 370 pg/ml (p less than 0.01). In untreated ischemic animals (n = 30) the intracellular H2O2 production of circulating neutrophils, as assayed flow cytometrically by dichlorofluorescein oxidation, increased from a preischemic value of 133 to a peak of 251 femtomoles dichlorofluorescein/neutrophil at 5 minutes of reperfusion (p less than 0.01). Treatment of neutrophils with phorbol myristate acetate (PMA) 10(-7) mol/L led to a 91% increase in neutrophil H2O2 production before ischemia, and 5 minutes after reperfusion there was an enhanced response to PMA of 222% (p less than 0.01). Pretreatment of animals with the thromboxane-synthetase inhibitor OKY 046 (n = 36) prevented ischemia-induced thromboxane generation, neutrophil H2O2 production (p less than 0.05), as well as the enhanced response to PMA stimulation (p less than 0.05). Treatment with the thromboxane-receptor antagonist SQ 29,548 (n = 36) did not affect the increase in plasma thromboxane levels after ischemia but was as effective as OKY 046 in preventing the ischemia-induced increase in neutrophil H2O2 production and the enhanced response to PMA stimulation. These data indicate that lower-torso ischemia leads to neutrophil activation, manifest by H2O2 production, an event mediated by thromboxane.

Animals↗
PubMed1989

Oxygen free radicals mediate ischemia-induced lung injury.

Lower torso ischemia leads during reperfusion to leukocyte (white blood cell)-dependent lung injury. This study tests the intermediary role of oxygen free radicals (OFRs) in mediating this event. Chronically instrumented anesthetized sheep underwent 2 hours of bilateral hindlimb ischemia. In untreated control animals (n = 7), 1 minute after tourniquet release, mean pulmonary artery pressure rose from 13 to 38 mm Hg (p less than 0.05), whereas pulmonary artery wedge pressure was unchanged from 4 mm Hg. The pulmonary hypertension was temporally related to an increase in plasma thromboxane (Tx) B2 levels from 211 to 735 pg/ml (p less than 0.05). At 30 minutes of reperfusion lung-lymph TxB2 levels rose from 400 to 1005 pg/ml (p less than 0.05). This coincided with an increase in lung-lymph flow from 4.3 to 8.3 ml/30 min (p less than 0.05), which remained elevated for 2 hours, an unchanged lymph/plasma protein ratio, and a rise in lymph protein clearance from 2.6 to 4.6 ml/30 min (p less than 0.05). These changes are consistent with increased lung microvascular permeability. White blood cell count fell during the first hour of reperfusion from 6853 to 3793/mm3 (p less than 0.05), and lung histologic findings showed marked leukosequestration relative to sham animals (n = 3). Pretreatment with the OFR scavengers, superoxide dismutase and catalase both conjugated to polyethylene glycol (n = 6) blunted the rise in mean pulmonary artery pressure to 19 mm Hg (P less than 0.05) and prevented the increase in plasma and lymph TxB2 lymph flow, and lymph protein clearance (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Allopurinol↗
PubMed1988

Effects of air filtration at small SO2 and NO2 concentrations on the yield of barley.

Two cultivars of Igri and Gerbel winter barley Horteum vulgare L. were grown in open-top chambers in filtered and unfiltered air at a site with approximately 10 nl litre(-1) SO2 and 12 nl litre(-1) NO2 (seasonal mean). The experiment ran for three consecutive seasons 1982-1983, 1983-1984, 1984-1985, and significant effects of filtration were observed for each crop. In years 1982-1983 and 1984-1985, the crops in unfiltered air yielded larger grain dry matter, 9% in 1982-1983, and 8% in 1984-1985. For both crops, the differences were statistically significant at the 5% level. Differences were also observed for the remaining above-ground dry matter, and these were consistent in direction in each year but statistically significant only in 1984-1985. In both growing seasons (1982-1983 and 1984-1985), there were no major pest infestations and no long-term water stress or photochemical ozone episodes. In the remaining experiment (1983-1984) similar air concentrations of SO2 and NO2 produced effects of the opposite sign to those observed in 1982-1983 and 1984-1985. Significant reductions in grain yield (13%) were obtained in unfiltered air. The only major environmental difference for the 1983-1984 crop was a notable dry period in May and June 1984 with marked water stress in the crop, requiring irrigation. These results suggest that the relationship between yield and pollutant concentration may be confounded by additional stresses, many of which are a common component of the growing season for major crops.

Journal Article↗
PubMed1988

Limb ischemia-induced increase in permeability is mediated by leukocytes and leukotrienes.

This study tests the role of white blood cells (WBC) and leukotrienes in mediating the increased microvascular permeability following ischemia and reperfusion. Anesthetized dogs (n = 23) underwent 2 hours of hind limb ischemia induced by tourniquet inflation to 300 mmHg. In untreated animals (n = 7), tourniquet release led after 5 minutes to a rise in plasma thromboxane (Tx) B2 levels from 360 to 1702 pg/ml (p less than 0.05); after 2 hours, lymph TxB2 concentration had risen from 412 to 1598 pg/ml (p less than 0.05). There were decreases in circulating WBC from 11,766 to 6550/mm3 and platelets from 230 to 155 x 10(3)/mm3. During reperfusion, popliteal lymph flow (QL) increased from 0.07 to 0.24 ml/hour (p less than 0.05), while the lymph/plasma (L/P) protein ratio was unchanged from 0.39, changes consistent with increased microvascular permeability. WBC depletion (n = 7) to 302/mm3 by hydroxyurea or nitrogen mustard attentuated (p less than 0.05) the reperfusion induced rise in plasma TxB2 from 91 to 248 pg/ml and prevented the increase in lymph TxB2 concentration. Within 5 minutes of tourniquet release WBC counts further decreased to 191/mm3 (p less than 0.05) and platelets declined from 175 to 93 x 10(3)/mm3 (p less than 0.05). QL increased from 0.07 to 0.12 ml/hour (p less than 0.05), lower than untreated animals (p less than 0.05), and the L/P protein ratio declined from 0.49 to 0.37 (p less than 0.05), dilutional changes consistent with increased filtration pressure but not permeability to protein. Pretreatment with the lipoxygenase inhibitor diethylcarbamazine (DEC) (n = 8) prevented the reperfusion-induced increase in plasma and lymph TxB2 levels (p less than 0.05) and the fall in WBC counts (p less than 0.05), while platelet counts declined from 381 to 210 x 10(3)/mm3 (p less than 0.05). QL rose from 0.09 to 0.23 ml/hour (p less than 0.05) during reperfusion, and the L/P protein ratio of 0.3 remained unchanged, a value lower than in untreated dogs (p less than 0.05). In two animals of each group, vascular recruitment was induced by tourniquet inflation to 50 mmHg. This led to a high QL of 0.25 ml/hour and a low L/P ratio of 0.18. In untreated animals during reperfusion, QL further increased to 1.3 ml/hour, and L/P ratio rose to 0.44, documenting increased vascular permeability. In contrast, reperfusion in leukopenic or diethylcarbamazine (DEC)-treated dogs with vascular recruitment, was not associated with increases in QL or the L/P protein ratio.(ABSTRACT TRUNCATED AT 400 WORDS)

6-Ketoprostaglandin F1 alpha↗
PubMed1988

Lower torso ischemia-induced lung injury is leukocyte dependent.

Lower torso ischemia leads on reperfusion to sequestration of polymorphonuclear leukocytes (PMN) in the lungs and increased permeability. This study tests the role of circulating leukocytes (WBC) in mediating this lung injury. Anesthetized sheep prepared with chronic lung lymph fistulae underwent 2 hours of bilateral hind limb tourniquet ischemia. In untreated controls (n = 7), 1 minute after reperfusion there were transient increases in mean pulmonary arterial pressure (MPAP) from 13 to 38 mmHg (p less than 0.05) and pulmonary microvascular pressure (Pmv) from 7 to 18 mmHg (p less than 0.05), changes temporally related to a rise in plasma thromboxane (Tx) B2 levels from 211 to 735 pg/ml (p less than 0.05). Lung lymph TxB2 levels rose from 400 to 1005 pg/ml at 30 minutes (p less than 0.05), and remained elevated longer than plasma levels. Lung lymph flow (QL) rose from 4.3 to 8.3 ml/30 minutes (p less than 0.05) after 30 minutes of reperfusion and remained elevated for 2 hours. The lymph/plasma (L/P) protein ratio was unchanged from 0.6, while the lymph protein clearance increased from 2.6 to 4.6 ml/30 minutes (p less than 0.05), suggesting increased microvascular permeability. WBC counts decreased within the first hour of reperfusion from 6853 to 3796/mm3 (p less than 0.05), and lung histology after 2 hours showed proteinaceous exudates and leukosequestration of 62 PMN/10 high-powered fields (HPF), higher than the 22 PMN/10 HPF (p less than 0.05) in sham animals (n = 3). Recruitment of the pulmonary vasculature by left atrial balloon inflation (n = 3) resulted in a rise in MPAP to 20 mmHg. After 3 hours of balloon inflation, QL stabilized at 9.8 ml/15 minutes, and a pressure-independent L/P protein ratio of 0.3 was achieved. During reperfusion, QL increased further to 11.2 ml/15 minutes, the L/P ratio rose to 0.56 and the calculated osmotic reflection coefficient decreased from 0.70 to 0.44, documenting an increase in lung microvascular permeability. In contrast to these untreated ischemic controls, sheep (n = 7) rendered leukopenic with hydroxyurea or nitrogen mustard and having a total WBC count of 760/mm3 and PMN count of 150/mm3 did not manifest reperfusion-induced increases in MPAP, Pmv, QL, lymph protein clearance, or lung lymph. TxB2 level (p less than 0.05). Plasma TxB2 levels rose slightly at 30 minutes from 199 to 288 pg/ml (p less than 0.05). Lung histology was normal. These data indicate that WBC mediate the ischemia-induced increase in pulmonary microvascular permeability.

Animals↗