This study was carried out to determine leukocyte phospholipase A2 (PLA2) activity and plasma lysophosphatidylcholine (LPC) levels in normal subjects and in patients with asthma and rhinitis and to examine their relationship to airway sensitivity to histamine. Leukocyte PLA2 activity and plasma LPC levels were highly correlated (rs = 0.90), and were found significantly raised in both the disease groups, more so in the asthmatics. Both PLA2 activity and LPC levels showed overall negative correlations with the log dose of histamine producing a 35% fall in specific airway conductance (PD35 histamine) when the patients and the normal subjects were examined together (rs = -0.77 and rs = -0.83, respectively). The patients with leukocyte PLA2 activity more than 1.8 U (nmol 14C-AA released/mg protein/10 min at 30 degrees C) or plasma LPC levels more than 8.7% of total phospholipids (mostly asthmatics) showed high airway sensitivity to histamine (PD35 histamine less than or equal to 1 mg/ml). On the other hand, the PD35 histamine values of patients with leukocyte PLA2 activity equal to or less than 1.96 U or plasma LPC levels equal to or less than 8.7% overlapped with those of normal subjects in the range of 1.2 to 10 mg/ml. Lowering of plasma LPC levels, which probably reflect tracheobronchial LPC content as shown in guinea pigs, seems to be an essential step in the return of airway reactivity toward normal.

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Superovulatory response and embryo production efficacy were investigated in adult (age 2-4 years, average body weight: 27-43 kg) cycling Jakhrana goats (n = 15) under semi-arid environmental conditions of India by administering different superovulatory regimens. Goats were reared under semi-intensive system of management in established farm conditions. To synchronize oestrus, a luteolytic dose of carboprost tromethamine (Upjohn, UK) was administered intramuscularly to all does at the dose rate of 5 microg per kg body weight in a double dose schedule with an interval of 11 days. For superovulation, 750 IU of PMSG (Folligon, Intervet, Boxmeer, Holland) per goat was administered intramuscularly 24 h before administering a second dose of luteolytic agent in five does (treatment 1). FSH (Sigma, St. Louis, MO, USA) 12.50 IU per goat was administered intramuscularly in a decreasing daily dose schedule (2.50, 2.50; 1.875, 1.875; 1.25, 1.25; 0.625, 0.625) at 12 h intervals over four days, initiated 48 h before administering second dose of carboprost tromethamine in 5 does (treatment 2). FSH (Super-Ov, Ausa Intern, USA) was administered at a uniform dose rate of 8.33 units per goat intramuscularly at 24 h intervals over three consecutive days (total dose was 25 units), initiated 48 h before administering a second dose of carboprost tromethamine in 5 does (treatment 3). To synchronize ovulation in responders, human chorionic gonadotrophin (hCG, Chorulon, Intervet) was injected intramuscularly at a dose rate of 500 IU in each goat on the day of oestrus appearance. Goats were laparotomized 72-82 h following the onset of synchronized oestrus and their genitalia were flushed using a standard collection procedure. Variability (p > 0.05) in superovulatory response (number of established corpora lutea) was observed: FSH (Sigma), 11.8 +/- 2.9; FSH (Super-Ov), 11.6 +/- 4.5; PMSG (Intervet), 8.4 +/- 2.3. A similar pattern was reflected in mean embryo and transferable embryo recovery, respectively (p > 0.05): FSH (Sigma), 8.0 +/- 1.8, 5.2 +/- 1.7; FSH (Super-Ov), 6.6 +/- 2.4, 5.4 +/- 2.4; PMSG, 5.8 +/- 1.9, 3.8 +/- 2.2. In PMSG-treated does, comparatively more unfertilized ova or retarded embryos were recovered than in FSH-treated does. The superiority of FSH preparations over PMSG was reflected in terms of total and transferable embryo production (p > 0.05). On average, five transferable embryos (excellent and good quality) were recovered per doe treated with FSH of either source. The mean ova/embryo recovery was satisfactory (55-68%). Results indicated that Jakhrana goats can be superovulated for embryo production using FSH of either source to augment productivity.

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The aim of this study was to investigate the basis of disturbances in sodium transport in asthma and in airway hyperresponsiveness without symptoms of asthma (asymptomatic AHR). We measured the intracellular sodium (Na(i)); activity of Na(+)/K(+)-ATPase in unstimulated cells (resting activity) and in cell homogenate under optimal conditions (maximal activity); and sodium influx, in mixed leukocytes of 15 normal subjects, 12 subjects with asymptomatic AHR, and 26 asthmatics with or without active symptoms. Resting Na(+)/K(+)-ATPase activity was the same as sodium influx, consistent with homeostasis. Compared with normal subjects, those with asymptomatic AHR or asthma with controlled symptoms had a twofold increase in sodium influx and Na(i). Symptomatic asthmatics also had a twofold increase in sodium influx but a fourfold elevation of Na(i). Maximal Na(+)/K(+)-ATPase activity was reduced by half in symptomatic asthmatics compared with normal subjects. The reduction of maximal Na(+)/K(+)-ATPase activity was associated with a significant decrease in ATP turnover per Na(+)/K(+)-ATPase molecule but not number of Na(+)/K(+)-ATPase molecules per cell. In summary, airway hyperresponsiveness with or without asthma is associated with increased sodium influx and Na in leukocytes. Resting activity of Na(+)/K(+)-ATPase is also increased as a compensatory response to the increased sodium influx, but it is achieved at the expense of higher Na(i). Symptomatic asthma is additionally associated with reduction in maximal activity of Na(+)/K(+)-ATPase, resulting in reduced capacity to handle the increase in sodium influx and consequent severe elevations in Na(i).