| Id |
Subject |
Object |
Predicate |
Lexical cue |
| T1 |
0-87 |
Sentence |
denotes |
Pathogenesis of lethal shock after intravenous staphylococcal enterotoxin B in monkeys. |
| T2 |
88-206 |
Sentence |
denotes |
The pathogenesis of shock in the rhesus monkey given intravenous staphylococcal enterotoxin B (SEB) is not understood. |
| T3 |
207-362 |
Sentence |
denotes |
Several cardiovascular changes produced by a highly purified preparation of SEB were studied after administration of doses ranging from 50 to 1,000 mug/kg. |
| T4 |
363-440 |
Sentence |
denotes |
Irreversible arterial hypotension was found consistently at the higher doses. |
| T5 |
441-526 |
Sentence |
denotes |
Arterial blood pressure and cardiac output declined substantially as shock developed. |
| T6 |
527-652 |
Sentence |
denotes |
Total peripheral vascular resistance did not rise at any time, but showed a significant fall during the late stages of shock. |
| T7 |
653-720 |
Sentence |
denotes |
Portal and central venous pressures remained essentially unchanged. |
| T8 |
721-920 |
Sentence |
denotes |
Venous O(2) content and pO(2) declined gradually throughout the period of toxemia, but arterial O(2) content remained constant until just prior to death, when a slight fall was noted in some monkeys. |
| T9 |
921-1124 |
Sentence |
denotes |
These changes were consistent with a pooling of blood in the peripheral vascular beds and seemed to resemble cardiovascular responses reported to occur in monkeys during shock due to bacterial endotoxin. |
| T10 |
1125-1293 |
Sentence |
denotes |
Epinephrine, administered in the late stages of shock, caused arterial pressure to increase almost immediately and cardiac output to return to normal about 1 min later. |
| T11 |
1294-1493 |
Sentence |
denotes |
Although life could occasionally be prolonged for several hours by continuous or intermittent epinephrine infusions, this therapy never succeeded in reversing the lethal effects of high doses of SEB. |
| T1 |
0-87 |
Sentence |
denotes |
Pathogenesis of lethal shock after intravenous staphylococcal enterotoxin B in monkeys. |
| T2 |
88-206 |
Sentence |
denotes |
The pathogenesis of shock in the rhesus monkey given intravenous staphylococcal enterotoxin B (SEB) is not understood. |
| T3 |
207-362 |
Sentence |
denotes |
Several cardiovascular changes produced by a highly purified preparation of SEB were studied after administration of doses ranging from 50 to 1,000 mug/kg. |
| T4 |
363-440 |
Sentence |
denotes |
Irreversible arterial hypotension was found consistently at the higher doses. |
| T5 |
441-526 |
Sentence |
denotes |
Arterial blood pressure and cardiac output declined substantially as shock developed. |
| T6 |
527-652 |
Sentence |
denotes |
Total peripheral vascular resistance did not rise at any time, but showed a significant fall during the late stages of shock. |
| T7 |
653-720 |
Sentence |
denotes |
Portal and central venous pressures remained essentially unchanged. |
| T8 |
721-920 |
Sentence |
denotes |
Venous O(2) content and pO(2) declined gradually throughout the period of toxemia, but arterial O(2) content remained constant until just prior to death, when a slight fall was noted in some monkeys. |
| T9 |
921-1124 |
Sentence |
denotes |
These changes were consistent with a pooling of blood in the peripheral vascular beds and seemed to resemble cardiovascular responses reported to occur in monkeys during shock due to bacterial endotoxin. |
| T10 |
1125-1293 |
Sentence |
denotes |
Epinephrine, administered in the late stages of shock, caused arterial pressure to increase almost immediately and cardiac output to return to normal about 1 min later. |
| T11 |
1294-1493 |
Sentence |
denotes |
Although life could occasionally be prolonged for several hours by continuous or intermittent epinephrine infusions, this therapy never succeeded in reversing the lethal effects of high doses of SEB. |