ABSTRACT:Alternative methods of selection to increase litter size in mice have been practiced for 21 generations followed by six generations of relaxed selection. Three replicates were used with four selection criteria: index of components (IX: I = 1.21 x total ovulation rate + 9.05 x ova success), uterine capacity (UT), litter size (LS), and an unselected control (LC). In IX, ovulation rate and ova success were measured by number of corpora lutea and number of pups bornlnumber of corpora lutea, respectively. In UT, uterine capacity was measured and defined as number of pups born to unilaterally ovariectomized (right ovary excised) females. Selection in LS was based on number born to unaltered dams. In all cases, number born was fully formed, live or dead pups. Pups from 16 randomly chosen LC dams and from the top 16 dams in IX, UT, and LS were selected to produce the next generation in each criterion-replicate line.

Cardio-pulmonary function was measured in male broilers reared on diets formulated to contain 1.5% arginine (NORMAL group) or 2.5% arginine (ARGININE group). A snare placed around the right pulmonary artery permitted acute shunting of the entire cardiac output (CO) through the left pulmonary artery, resulting in sustained increases in blood flow (BF) through the left lung in both groups. The unilateral increase in BF was accompanied by sustained increases in pulmonary arterial pressure (PAP) and pulmonary vascular resistance (PVR) in the NORMAL group. However, following initial transient increases in PAP and PVR in the ARGININE group, subsequent pulmonary vasodilation gradually reduced PVR, and thus PAP, in spite of the ongoing elevation of BF through the left lung. The capacity of the pulmonary vasculature in the ARGININE group to accommodate an increased BF at a normal PAP accounts for the previously reported lower incidence of pulmonary hypertension syndrome (PHS, ascites) in cold-stressed broilers fed supplemental dietary arginine. Hypoxemia and respiratory acidosis ensued rapidly in both groups after tightening the pulmonary artery snare, in spite of a compensatory increase in the respiratory rate. The gradual return of PVR and PAP to presnare levels in the ARGININE group did not eliminate the concurrent ventilation-perfusion mismatch caused by the increased rate of BF through the left lung. Tightening the pulmonary artery snare caused mean systemic arterial pressure (MAP) to drop from control levels of approximately 98 mm Hg to sustained hypotensive levels of approximately 65 mm Hg in both groups. This systemic hypotension was caused by decreases in CO and total peripheral resistance (TPR). The reduction in CO were caused by reduction in stroke volume (SV) rather than heart rate (HR), suggesting that acutely tightening the pulmonary artery snare increased PVR sufficiently to impede left ventricular filling. Accordingly, the maximum increment in PAP attainable by the right ventricle during acute increases in PVR apparently was inadequate to propel the entire CO through the pulmonary vasculature, setting the stage for the congestive right-sided pooling of blood routinely associated with PHS in broilers.

Two experiments were conducted to test the hypothesis that a primary increase in pulmonary vascular resistance can initiate a pathophysiological progression leading to pulmonary hypertension syndrome (PHS, ascites). Pulmonary vascular resistance was increased by surgically clamping the left pulmonary artery when male broiler chicks were 15 to 19 d of age, resulting in a 90% incidence of PHS in Experiment 1, and a 68% incidence of PHS in Experiment 2. The incidence of PHS was 8% for control or sham-operated broilers in Experiment 1, whereas in Experiment 2 no (0%) PHS occurred in sham-operated broilers or in individuals with a pulmonary artery that only was partially occluded. Broilers with a fully occluded left pulmonary artery developed pulmonary hypertension, as demonstrated by increased right:total ventricular weight ratios (right ventricular hypertrophy) and by increased electrocardiogram lead II R-S wave amplitudes (generalized ventricular dilation and hypertrophy). Forcing the entire cardiac output through the right lung resulted in a lower percentage saturation of hemoglobin with oxygen and an elevated hematocrit, reflecting generalized systemic hypoxemia. Pulmonary hypertension and hypoxemia also were specifically characteristic of all birds that developed ascites, regardless of treatment group. These observations demonstrate for the first time that PHS (ascites) can be directly induced by a primary increase in pulmonary vascular resistance. The observed changes in percentage saturation of hemoglobin with oxygen suggest that the lungs of broilers may be unable to efficiently oxygenate the blood when forced to receive an increased cardiac output at an elevated pulmonary arterial pressure.

The incidence of pulmonary hypertension syndrome (PHS; ascites) was evaluated in two experiments using broiler breeder male by-product chicks exposed after 3 wk of age to cool environmental temperatures (10 to 15 C). In Experiment 1, 3- to 6-wk-old birds were fed a grower diet to which 0 (Control), .25, .5, or 1% supplemental L-arginine HCl had been added. During Weeks 7 to 8, all groups in Experiment 1 were fed a finisher diet containing no supplemental arginine. In Experiment 2, the Control group received no supplemental arginine, a second group was fed a grower diet supplemented with 1% L-arginine HCl (Weeks 3 to 6), and a third group was fed grower and finisher diets supplemented with 1% L-arginine HCl (Weeks 3 to 8). Cumulative PHS mortality was significantly reduced by 1% L-arginine HCl on Days 34 to 46 in Experiment 1. When data from all birds fed grower or finisher diets supplemented with 1% L-arginine HCl were pooled in Experiment 2, cumulative PHS mortality was marginally lower (P = .065) than for the Control group. Supplemental L-arginine HCl had no effect on final body weights, weight gain, or feed conversion in either experiment. Neither body weight on Day 1 or 21 nor net weight gain from Days 1 to 21 determined susceptibility to PHS during the subsequent grower and finisher intervals in either experiment.(ABSTRACT TRUNCATED AT 250 WORDS)

The incidence of pulmonary hypertension syndrome (PHS; ascites) was evaluated in two experiments using broiler breeder male by-product chicks exposed after 3 wk of age to cool environmental temperatures (10 to 15 C). In Experiment 1, 3- to 6-wk-old birds were fed a grower diet to which 0 (Control), .001, .005, .010, or .015% furosemide had been added. All groups in Experiment 1 were fed a finisher ration containing no furosemide during Weeks 7 to 8. In Experiment 2, the Control group received no furosemide, a second group received .015% furosemide during the grower phase only (Weeks 3 to 6), and the third group received .015% furosemide during the grower and finisher phases (Weeks 3 to 8). Cumulative PHS mortality was significantly reduced by furosemide in both experiments. Compared with Controls, birds fed .015% furosemide did not have lower (P = .077) final body weights in Experiment 1 but did have significantly lower final body weights in Experiment 2. Lower levels of furosemide significantly reduced PHS mortality without reducing body weights. Furosemide did not improve feed conversion in either experiment. Neither body weight on Day 1 or 21 nor net Day 1 to 21 weight gain were predictive of susceptibility to PHS during the subsequent grower and finisher intervals in either experiment. On Day 55 of Experiment 2, large healthy birds fed .015% furosemide had significantly lower right:total ventricular weight ratios than control birds, indicating that furosemide reduced right ventricular hypertrophy, presumably by reducing pulmonary arterial pressure.