The temperature of pine smoke inhaled did not exceed 40°C. As shown in Table 1, the volume of Oa in the smoke decreased (p <0.001) and CO increased significantly with a simultaneous elevation of arterial HbCO (p <0.001). Three of 22 sheep insufflated with the pine smoke died at the end of smoke inhalation. One died at 1 h and five died from 13 to 23 h; the others survived and were killed at 2 h (n = 3), 6 h (n = 3) and 24 h (n = 7) postinjury, respectively.

FIGURE 3. The changes of respiratory rates and arterial blood gases following smoke inhalation (n=6). *p<0.05; **p<0.01, for differences from baseline values.

Clinically, wheezing and rales appeared at 2 h, and respiratory distress with tracheobronchorrhea and sooty sputum was found after 6 h. Coughing with foamy fluid and pieces of pseudomembrane casts was very common after 12 h postinjury. In some cases, the animals respiration was improved and the sheep survived after having coughed up segments of casts, but in other cases, the sheep did not survive, although they coughed up some casts.

FIGURE 4. The changes of pulmonary compliance (Cdyn), alveolar- arterial oxygen gradient (P[A-a]OT) and pulmonary shunt (QS/QT) (n = 6). *p<0.05; **p<0.01, for differences from baseline values.

Table 1—Changes in Concentrations of 02 and CO in Fine Smoke and Arterial HbCO during Smokq Inhalation (n=6)

Smoke Inhalation (min)

Mean

Air

±SD

Breath

2

4

6

average

Oa (Vol %)

20.8

15.7*

17.2*

16.1*

16.3*

±0.8

±2.6

±1.5

±1.4

±0.8

CO (Vol %)

0.0

3.3*

2.2*

2.1*

2.5*

±0.9

±0.9

±0.7

±0.7

HbCO (%)

9.2

59.4*

73.9*

77.7*

±1.1

±20.1

±14.2

±10.2

In all injured sheep, Hb and HbMet did not have obvious changes (p >0.05, Table 2 and Table 3), but HbCO increased significantly with a peak at the end of smoke inhalation and a decline to baseline at 6 h postinjury (Fig 2). The Hb02 decreased significantly at the end of smoke inhalation, returned to a higher level at 6 h (p <0.05), and then progressively decreased (p <0.05~0.01, Fig 2). Dramatic changes were noted in the HbCO and Hb02 exposed sheep who died at the end of smoke inhalation. (Table 4).

FIGURE 5. Photographs of tracheobronchial pseudomembrane casts after smoke inhalation injury. A: The cast in situ completely obstructs the tracheobronchial lumen of the sheep No: 8634 died at 16 h postinjury. B: The cast peeled off from sheep No 8610 killed at 24 h after smoke inhalation shows that the cast existed in segmental bronchi.

Table 2—Hb, HbMet and SaOt in Sheep Killed 24 h after Smoke Inhalation Injury (n = 6)

Postinjury (h)

Mean ± SD

Baseline

1/6

1/2

1

2 4

6

12

24

Hb(g/L) HbMet (%) Sa02 (%)

90± 11 1.2±0.8 97±2

96± 17 1.5±0.8 90±8

96± 18 0.7±0.7 87 ±9

99 ±25 0.7 ±0.5 90 ±7

96± 11 106 ±19 0.9 ±0.5 0.9±0.5 90±6 91 ±7

92 ±17 0.9 ±0.6 93±5

92 ±16 0.9±0.6 91 ±7

93± 18 0.6±0.4 87 ±11

As shown in Figure 3 and Table 5, following smoke inhalation, respiratory rates went up over 35 times/ min in all injured sheep at as early as 1 h postinjury. The Pa02 decreased significantly within 2 h, returned to a higher level at 6 h, and then declined progressively, dropping to the lowest level of 7.1 kPa at 24 h postinjury (Fig 3). The PaC02 also decreased (p <0.05) within 6 h and then increased significantly, and both P(A-a)02 and Qs/Qt increased significantly, but Cdyn had decreased dramatically (p<0.05-0.001) (Fig 4). Table 6 shows that the variables of acid-base balance had no significant change except HCO3 and TC02 in the sheep killed at 24 h exhibiting a decrease at 2 h postinjury (p <0.05).

FIGURE 6. An electron micrograph taken from a sheep killed at 2 h after smoke inhalation shows epithelial necrosis with edematous fluid and red blood cells in alveolar space which occasionally appeared at 2 h but existed in almost all the sections from the sheep killed after 6 h postinjury. Alv, alveolar space; Ep, type I alveolar epithelium; En, pulmonary capillary endothelium; N, endothelial nucleus (original magnification, x 4,830)

Table 3—Hb, HbCO; HbOt, HbMet and SaOt in Sheep who Died 13 to 23 h after Smoke Inhalation (n = 5)

Postinjury (h)

Mean ± SD

Baseline

End[1]

1/6

1/2

1

2

4

6

12

HbCO (%) HbOt(%) HbMet (%) Hb(g/L) Sa02 (%)

9± 1 88± 1 1.4±0.2 120 ±25 96± 1

78$ ± 10 22* ±9

50$ ±8 46$ ±7 1.8± 1.4 118 ±30 91 ±6

40$ ±9 54f±10 1.2±0.2 112 ±36 87 ±8

31$ ±9 62$ ±9 0.9±0.1 125 ±42 88± 1

24$ ±6 69$ ±8 1.2±0.2 110 ±23 90±5

20$ ±7 77 ±7 1.2±0.3 123 ±34 92 ±4

9±2 81 ±1 1.0±0.2 96 ±41 92 ±4

9±3 71$ ±6 2.4±2.0 97 ±35 85±6

In GE, tracheobronchial mucosa congestion and exudation were found in the sheep that died at the end of smoke inhalation. Thin tracheobronchial pseu- domembranes formed in all sheep killed at 2 h and thickened at 6 h with cast formation in one case resulting in partial tracheobronchial obstruction. Sheep that died or were killed after 12 h all revealed casts obstructing their lumens partially or completely (Fig 5). Foamy efflux in all sections of the lungs, segmental atelectasis, expansion of the lung mass and compensatory emphysema along its margin were also found. Microscopically, pulmonary perivascular edematous cuffs were found as early as 2 h, as well as swelling, necrosis and sloughing of epithelia and ac­cumulation of fluid rich in protein in the alveolar space (Fig 6). Polymorphonuclear neutrophil (PMN) infiltra­tion was found in all sheep killed after 2 h, and partial or/and complete airway lumen blockages, by fibrinous exudation, blood cells and epithelial debris were found in not only the bronchi, but also bronchioli of almost all sheep who died or were killed after 12 h. Pulmonary microatelectasis was not infrequently found after the injury.

FIGURE 7. Schema of the sequence of events following smoke inhalation injury. NOz, nitrogen dioxide; S02, sulfur dioxide; HCL, hydrogen chloride; HA, histamine.

Table 4—Arterial Blood Gases and HbCO, HbOt and SaOt in Sheep who Died at the End of Smoke Inhalation (n=3)

Mean

Pa02

Sa02

PaCO£

ньо2

HbCO

±SD

(kPa)

(%)

(kPa)

(%)

(%)

Baseline

12.1.7

97 ± 1

5.6±0.3

90±4

10±3

Ending

2.7 ±0.9*

92 ±10

6.2 ±0.8

6 ±2$

95 ± 1$

Table 5—Arterial Blood Gases and Pulmonary Compliance (Cdyn) of Sheep Who Died 13 to 23 h after Smoke inhalation (n = 5)

Postinjury (h)

Mean±SD

Baseline

1/6

1/2

1

2

4

6

12

PaO, (kPa)

12.0±1.2

7.2$±2.1

6.5$ ±1.9

7.2$ ±2.0

7.3t±2.8

9.1±2.8

8.3t±2.8

6.7$ ±1.9

PaC02 (kPa)

5.9±0.7

5.6±0.8

5.5±1.1

5.3± 1.1

4.9t±0.9

4.9t±0.8

4.8t ± 1.1

4.8t ±0.9

P(A-a)Oa (kPa)

1.0±0.9

5.9$ ±2.3

6.4$ ±2.9

5.2f±2.8

5.7$ ±2.9

6.8$ ±2.1

Qs/QT («)

0.8 ±0.6

4.4f ±2.8

5.0| ±2.5

4.4f ±2.0

4.7f ±2.9

6.2f ±3.2

Cdyn

(170.098 kPa)

.18 ±.02

.08f ± .03

.08t±.04

.07f ± .03

.lit ±.04

.05$ ± .03

Resp rates

(times/min)

24±3

31 ±8

36±5

40 ±7

41 ±13

39 ±10

45±8

Table 6—Variables of Acid-base Balance in Sheep Killed at 24 h following Smoke Inhalation (n = 6)

Postinjury (h)

Mean ± SD

Baseline

1

2

4

6

12

24

pH

7.43 ±.05

7.43 ±

.05

7.39 ±

.12

7.42 ±.08

7.42± .08

7.44 ±.06

7.38 ±.10

HCOl (mmol/L)

25.3±2.6

21.4±

5.9

17.8* ±

7.9

22.9±5.5

22.5 ±4.9

25.6±4.0

25.3±5.7

TC02 (mmol/L)

27.4±3.6

26.0 ±

2.6

21.5* ±

5.1

24.5±5.3

24.2 ±5.1

27.3 ±4.0

27.3±5.7

SB (mmol/L)

27.5 ±2.9

26.2 ±

2.7

22.7 ±

5.1

25.2±4.6

25.3±4.4

25.9±4.3

26.4 ±4.0

BEecf (mmol/L)

2.4±4.3

1.8 ±

3.4

— 4.3±

6.7

— 0.8±6.4

-0.9 ± 6.2

2.4±4.7

1.6±4.0

BEb (mmol/L)

3.3±3.8

1.9 ±

3.4

— 2.6±

6.4

0.6±5.8

0.8±5.8

3.5±4.2

2.4±5.1