Trauma induced increases in plasma vasopressin and angiotensin II.

Previous investigators have shown that hypotension will cause an increase in plasma levels of both vasopressin and angiotensin II. Significant increases in peripheral resistance after thermal trauma suggested that a similar increase in plasma vasopressin and angiotensin II levels might occur under this condition. This possibility has been studied in the pentobarbital anesthetized dog. Peripheral resistance was calculated from measured cardiac output and mean arterial blood pressure. Vasopressin and angiotensin II levels were measured by radio-immunoassay. The results of this study showed that vasopressin plasma levels increase 4 to 6 fold 15 minutes after thermal trauma and remained elevated (3 to 4 fold) for at least 6 hours. Angiotensin II increased in a linear manner from 15 minutes to 6 hours post trauma. At 6 hours post trauma angiotensin II plasma levels were 4 times pretrauma levels. For the first 4 hours post trauma there was a positive correlation between the sum of vasopressin and angiotensin II plasma levels and the increase in peripheral resistance. These results suggest that the trauma induced increase in peripheral resistance is due to increases in plasma vasopressin and angiotensin II.

Cerebrospinal fluid from morphine-dependent rats precipitates opiate abstinence syndrome.

Cerebrospinal fluid (CSF) was withdrawn from opiate-dependent rats following six hours of abstinence. It was infused into the third ventricle of opiate-dependent rats, precipitating immediate abstinence signs. The effect was similar to that of infusing the opiate antagonist naloxone, suggesting that opiate-dependent organisms may secrete an endogenous opiate antagonist substance. CSF withdrawn from non-dependent rats failed to precipitate an abstinence syndrome in morphine-dependent recipients. Conversely, CSF withdrawn from opiate-dependent rats following six hours of abstinence failed to precipitate an abstinence syndrome in non-dependent recipients. The active factor in the CSF is probably a peptide since it is filterable through a 10,000 MW filter and its activity is destroyed by three different proteolytic enzymes.

Handicap-related problems in mothers of children with physical impairments.

An inventory was developed for the measurement of handicap-related problems experienced by mothers of children with chronic physical conditions and an initial evaluation of its psychometric properties was completed in a sample of 119 mothers of children with physical or sensory impairments. Principal component analysis of the Handicap-related Problems for Parents Inventory (HPPI) yielded three subscales, which accounted for 54% of the total variance. The HPPI demonstrated excellent internal consistency for each scale and total score. It also generally had good test-retest reliability over 6-, 12-, and 18-month periods. There was minimal covariation between HPPI scores and demographic status. Concurrent validity was demonstrated by significant correlations between appropriate HPPI scales and measures of daily stress and the child's physical condition or disability status. Support for its construct validity was obtained when expected convergent and discriminant relationships were confirmed between HPPI scales and measures of maternal adaptation, maternal social support, and child behavior problems. Among other results, HPPI scores predicted maternal adaptation 18 months later. The potential uses of the HPPI in research and intervention with mothers of children with chronic physical conditions were discussed.

Effects of thermal trauma on cardiac force of contraction.

Previous studies have reported that administration of potent peripheral vasodilating drugs will significantly increase thermal trauma-induced depression of cardiac output. This finding suggests that most of the depression in cardiac output after thermal trauma is due to an increase in peripheral resistance and a decrease in venous return rather than a direct depression of myocardial contractile force. Studies have been carried out using a strain gauge arch sewn on the left ventricle to measure myocardial force of contraction in the mongrel dog anaesthetized with sodium pentobarbital and receiving a 15 per cent total body surface area full skin thickness flame burn. The results of this study showed a significant decrease in cardiac output immediately after burn, which persisted for 7 h. Myocardial force of contraction, measured in grams, fell immediately after burn and returned to pre-burn values by 3 h post-burn. In one series of animals, verapamil, a calcium-channel-blocking substance, was administered. In these animals cardiac output returned to pre-burn levels following the administration of the drug, but myocardial force of contraction remained significantly lower than pre-burn value for the duration of the experiment. Correlation coefficients comparing cardiac output and myocardial force of contraction showed no significant relationship between values in either untreated or verapamil-treated animals.

The relationship between post-burn increases in peripheral resistance and vasopressin.

Using the dog anaesthetized with sodium pentobarbital receiving a 15 per cent total body surface full skin thickness flame burn as an experimental model, it was observed that administration of the vasopressin, V-1 receptor, blocking agent d(CH2)5Tyr(Me)AVP (SK&F100273) prior to burn could significantly reduce the increase in peripheral resistance which occurs in untreated burned animals. At 30 min post-burn peripheral resistance was 60.2 +/- 7.8 units in treated animals and 117.1 +/- 16.8 units in untreated animals. At 60 min post-burn these values were 71.3 +/- 7.2 units and 117.0 +/- 13.5 units, respectively. Changes in cardiac output were significantly less in treated than untreated experimental animals. The mean arterial blood pressures were not significantly different. Plasma levels of vasopressin were measured by radio-immunoassay prior to burn and at 30-min intervals for 6 h following burn. At the time of taking blood samples for vasopressin levels, mean arterial blood pressure and cardiac output were measured and peripheral resistance was calculated. The results of this study showed that immediately post-burn vasopressin plasma levels increased from 6.2 +/- 2.2 pg/ml to 27.3 +/- 9.5 pg/ml and peripheral resistance increased from 62.3 +/- 6.3 units to 128.0 +/- 20.3 units. During the remaining 6 h of the experimental study both vasopressin plasma levels and peripheral resistance remained elevated. These results show that following thermal injury there is a significant release of vasopressin and suggest that the increase in peripheral resistance observed could be due in part to the vasoconstrictor action of the released vasopressin.

Effects of blockade of vasopressin V-1 receptors on post-burn myocardial depression.

It has been suggested that post-burn myocardial depression may be due to coronary constriction which results in myocardial ischaemia. It has been demonstrated that the levels of vasopressin, a potent natural constrictor of blood vessels, increase four- to six-fold immediately after thermal trauma. Therefore, this substance could be responsible for post-burn coronary constriction and myocardial depression. This was tested using the dog anaesthetized with sodium pentobarbital receiving a 15 per cent total body surface area full thickness flame burn as the experimental model. Cardiac output was measured by the thermal dilution technique. Arterial blood pressure was sensed by a Stathem P-23 transducer. Cardiac force of contraction was measured by a Walton-Brody strain gauge arch sewn on the left ventricle. The results of this study showed a significant decrease in cardiac output, increase in peripheral resistance and decrease in myocardial force of contraction immediately after thermal trauma in untreated animals. The decrease in cardiac output and increase in peripheral resistance remained for the duration of the experimental observations (3 h). The decrease in force of contraction returned to pre-burn levels 1 h post-burn. Pretreatment of the experimental animals with d(CH2)5 Tyr(Me)AVP (SK&F 100273), a vasopressin V-1 receptor blocking agent, prevented the initial decrease in cardiac output, increase in peripheral resistance and decrease in the force of contraction. A correlation plot of peripheral resistance vs. cardiac force of contraction showed a positive correlation between these two variables in the pretreated animals.(ABSTRACT TRUNCATED AT 250 WORDS)