Rj. Byrick et al., Inhaled nitric oxide does not alter pulmonary or cardiac effects of fat embolism in dogs after cemented arthroplasty, CAN J ANAES, 46(6), 1999, pp. 605-612
Citations number
21
Categorie Soggetti
Aneshtesia & Intensive Care","Medical Research Diagnosis & Treatment
Journal title
CANADIAN JOURNAL OF ANAESTHESIA-JOURNAL CANADIEN D ANESTHESIE
Purpose: We examined the effect of inhaled nitric oxide (NO) on the acute p
ulmonary hypertension and right ventricular (RV) dilation after fat embolis
m.
Methods: A bilateral cemented arthroplasty (BCA), created fat embolism in 2
0 dogs. In Part A, 12 dogs were randomized to an NO group (n=6, inhaled NO
40 ppm before BCA and throughout-the study) ora control group (n=6). In Par
t B, a third group of dogs (n=8) were given NO 20-40 ppm 2-3 min after BCA
when pulmonary artery pressure (PAP) increased. Transesophageal echocardiog
raphy (TEE) and invasive hemodynamic monitoring evaluated the hemodynamic r
esponse to BCA. Postmortem, quantitative morphometry was used to estimate t
he number of fat emboli and diameter of lung vessel occluded by fat.
Results: Part A: The increase in PAP ir the NO group (16 +/- 1 to 34 +/- 9
mmHg) within three minutes of BCA was not different from that in the contro
l group (14 +/- 4 to 35 +/- 9 mmHg). Within three minutes of BCA, TEE demon
strated RV dilation in all groups (P < 0.05) but there was no difference in
the change in RV area in the NO and control groups. When NO was given afte
r BCA, no difference in PAP or RV dilation was noted from that in the contr
ol group. There were no differences, at post mortem, between the groups in
the diameter of lung vessel occluded by fat
Conclusion: Whether given before the embolic insult or two to three minutes
after the onset of pulmonary hypertension, inhaled NO did not attenuate th
e acute pulmonary hypertension or RV dilation after cemented arthroplasty.