EFFECT

OF HYPERTHERMIA

ON DEVELOPMENT PULMONARY WITH

AND HYPOTHERMIA

AND COURSE

EDEMA

OF ACUTE

IN A N I M A L S

ANESTHETIZED

ETHER N. G. T rinyak

UDC 616.24-005.98-092 : [615.832-059 : 617-089.578.141

I u t r a p e r i t o n e a l injection of 6% ammonium chloride solution (40 m g / 1 0 0 g body weight) into r a t s led to the development of acute p u l m o n a r y edema and death of the animal. H y p e r t h e r m i a of the r a t s (rectal t e m p e r a t u r e 39-41 ~ intensified, while e t h e r a n e s t h e s i a and hypothermia (rectal 9 20-23 ~) p r e vented development of p u l m o n a r y e d e m a .

Although considerable attention has been paid to the study of p u l m o n a r y e d e m a [1-5], m a n y a s p e c t s of this highly important problem have not yet been finally solved. We have studied the effect of high and low t e m p e r a t u r e s in animals anesthetized with e t h e r on the development of toxic p u l m o n a r y edema. EXPERIMENTAL

METHOD

AND

RESULTS

Pulmonary edem~ was produced by intruperitoneal injection of 6~ a m m o n i u m chloride solution in a dose of 40 r a g / 1 0 0 g body weight. TABLE 1, Effect of E t h e r A n e s t h e s i a of Development of P u l m o n a r y Edema during H)~)er- and Hypothermia ~

.....

Experimental

,~.1~o |~ r

Pulmonary coefficient

~ N o r m a l e x t e r n a l environment 46 Hyperthermia 60 Hypothermia 60* Light e t h e r anesthesia 24 E t h e r a n e s t h e s i a for lh 24 H y p e r t h e r m i a aguiasl baokgro,and of e t h e r ane sthe s 24 Hypothermiaa~inst background of e t h e r anesthesia 24t

Animals surviving ( s a c r i riced)

Animals dying

36-38] 39-41! 23-201

46 60

91.30 =~0.048 1.99 -~ 1.012

Duration of I ~ ]Pulm~176176 survival (in o =., coefficien Survival rain) 20.5 ~- 0.852 12.3 :~ 1.048

).81~0.008

45

] I

36-38

I

36-38 i

18

1.03 :~ 0.025

40.5 :~ 2.8

6 ]

0.72

2h 30 rain I h 30 rain

|

2

1.20

26

22 10.76 ~0.01

2h

!

! i

39.8-41

i

15

1.003 4- 0.028 58.06 ~ 3.5

9 I

I

I

23-19

2

0.71

12

0.89

I

0,75 ~:0,03

2h 2h

a'-'----~mals * 15 which, r e m a i n e d f o r obser~ation were iadistinguighable f r o m kealthy ruts a f t e r 5 ' 6 h. t 10 a n i m a l s remaining for observation w e r e indistinguishabl~ f r o m healthy rats a f t e r 24 h, F a c u l t y of S u r g e r y and Patholo~r pi~ystoi.ogy, C h e r n o v t s y Medical Instigate (Presented by A c a d e m i c i a n V. V. Parin). T r a n s l a t e d f r o m Byulleten' EksperimentaVn01 Biologii i Meditstny, Vol, 669 ~o. 7~ pp. 40-41, July, 1968. Original a r t i c l e submitted F e b r u a r y 24, 1967.

748

E x p e r i m e n t s were p e r f o r m e d on 262 albino rats in which the body t e m p e r a t u r e was m e a s u r e d by an e l e c t r o t h e r m o m e t e r . The degree of p u l m o n a r y e d e m a was d e t e r m i n e d by m i c r o s c o p i c investig-ation of the lungs and calcutatioa of the p u l m o n a r y coefficient (PC). The e x p e r i m e n t a l results a r e given in Table 1. The development of p u l m o n a r y edema under n o r m a l external environmental conditions (experiments of s e r i e s I) was st udied in 46 r a t s . Injection of a m m o n i u m chloride into intact rats led to the development of p u l m o n a r y edema and to death of all the a n i m a l s . In the 60 r a t s in s e r i e s II p u l m o n a r y edema was produced a f t e r h y p e r t h e r m i a had been produced in the a n i m a l s in an incubator at 40-50 ~ for 15 min. H ) ~ e r t h e r m i a intensified the p u l m o n a r y edema in all the a n i m i d s . In 60 a n i m a l s p u l m o n a r y edemas was p r o d u c e d in a state of h y p o t h e r m i a (cooling of the body in an external t e m p e r a t u r e of --17 ~ with a r e c t a l t e m p e r a t u r e of 20-23 ~ (series liD. Cooling prevented the development of p u l m o n a r y edema in all the animals. In s e r i e s IV, p u l m o n a r y edema was produced in a state of light e t h e r a n e s t h e s i a . P u l m o n a r y edema developed in 18 of the 24 a n i m a l s . In s e r i e s V p u l m o n a r y e d e m a was produced in a state of deep e t h e r a n e s t h e s i a , m a i n tained for 1 h. P u l m o n a r y e d e m a developed in only two of the 24 a n i m a l s a f t e r waking. In s e r i e s VI, a n i m a l s deeply anesthetized with e t h e r were placed f o r 15 min in an incubator at 40-50% a f t e r which p u l m o n a r y edema was produced. Of the 24 a n i m a l s , 15 died, but p u l m o n a r y e d e m a could not be found in a n y of them m i c r o s c o p i c a l l y , and the i n c r e a s e in p u l m o n a r y coefficient was evidently a s s o c i a t e d with s e v e r e congestion of the lung tissue with blood. In s e r i e s VII p u l m o n a r y e d e m a was produced a f t e r deep e t h e r a n e s t h e s i a had fallen to 23-19 ~ Hypothermia against a background of e t h e r a n e s t h e s i a prevented the development of e d e m a in 22 of the 24 a n i m a l s . Hence, hypothermia against a backg-round of light e t h e r a n e s t h e s i a and deep e t h e r a n e s t h e s i a lasting 1 h prevented the development of p u l m o n a r y e d e m a . H y p e r t h e r m i a , both when acting alone and in c o n j u n c tion with e t h e r a n e s t h e s i a , had a a unfavorable effect on the development of the acute p u l m o n a r y e d e m a . LITERATURE I. 2. 3. 4. 5.

CITED

Yu. I. Vikhlyaev, N. L L o s e r , and I. M. Shapiro, B)~ll, ~ksp. Biol. i Med., No. 6, 42 (1956). Yu. S. Ezhov, Vestn. Akad. Med. Nauk SSR, No. 8, 29 (1962). G . S . Kan, The Nervous System and Acute P u l m o n a r y E d e m a [in Russian], Leningrad (1953). Ya. A, L a z a r i s and I. A. Serebrovska~-a, P u l m o n a r y E d e m a [in Russian], Moscow (1962). A . S . Lonshchakova, P a t . Fiziol., No. 3, 49 (1958).

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