1992
DOI: 10.1007/978-1-4615-3428-0_64
|View full text |Cite
|
Sign up to set email alerts
|

Regional Cardiac Hemodynamics and Oxygenation during Isovolemic Hemodilution in Anesthetized Pigs

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
1
1

Citation Types

0
6
0

Year Published

1992
1992
2017
2017

Publication Types

Select...
3
1
1

Relationship

0
5

Authors

Journals

citations
Cited by 6 publications
(6 citation statements)
references
References 5 publications
0
6
0
Order By: Relevance
“…2). Nevertheless, data from studies of exercise-induced increases in MVO 2 in swine [which display little change in coronary venous PO 2 (270)] and hemodilution-induced anemia (normal arterial PO 2 with progressive increases in coronary venous PO 2 [934, 935)] clearly demonstrate that reductions in tissue oxygen tension are not required for robust coronary vasodilation (Fig. 13B).…”
Section: Metabolic Control Of Coronary Blood Flowmentioning
confidence: 99%
See 2 more Smart Citations
“…2). Nevertheless, data from studies of exercise-induced increases in MVO 2 in swine [which display little change in coronary venous PO 2 (270)] and hemodilution-induced anemia (normal arterial PO 2 with progressive increases in coronary venous PO 2 [934, 935)] clearly demonstrate that reductions in tissue oxygen tension are not required for robust coronary vasodilation (Fig. 13B).…”
Section: Metabolic Control Of Coronary Blood Flowmentioning
confidence: 99%
“…Assuming that values of coronary venous PO 2 reflect levels of myocardial tissue PO 2 (469, 919), these findings collectively support that mechanisms to invoke metabolic coronary vasodilation are progressively activated as myocardial tissue PO 2 falls below a critical threshold value. The physiologic relevance of this relationship is also supported by the essential observations that pronounced reductions in coronary microvascular resistance are also observed in response to reductions in perfusion pressure (84, 201, 252254, 333, 690, 853), arterial PO 2 [i.e., hypoxemia; (2,22,89,205,262,376,458,608,645,670,671,708,767, 849, 917, 940, 958)], arterial oxygen content [i.e., anemia; (59, 102, 120, 204, 206210, 323, 372, 377, 482, 486, 509, 691, 905, 934, 935, 947, 957, 976)], and overt myocardial ischemia (2729,33,36,97,110,189,246,497,498,730732) (see Fig. 2).…”
Section: Metabolic Control Of Coronary Blood Flowmentioning
confidence: 99%
See 1 more Smart Citation
“…Myocardial O 2 extraction at rest is already about 50% (5). The ability to increase coronary blood flow depends upon the coronary vasodilator reserve, which may achieve a maximal increase of 400–600% (5, 6). When Hct is lowered below a threshold at which coronary blood flow cannot be adequately increased, which is when coronary vasodilatory reserve is exhausted, myocardial ischemia occurs at that critical Hct‐value (Hct crit ) (7).…”
mentioning
confidence: 99%
“…Although surprising, our finding that MABP progressively fell when Hct dropped below 24% is consistent with observations in other animal species and humans. In humans (11,40,64) and animals (2,48,63), MABP rarely falls until Hct drops below 20 -25%. Because MABP is normally a regulated variable, it would be expected that the normal homeostatic response would result in an increase in peripheral resistance and/or CO to maintain MABP, the driving force for organ blood flow.…”
Section: Resultsmentioning
confidence: 99%