Increase In Intratracheal Pressure Research Articles

Gas Chromatographic Mass Analysis and Further Pharmacological Actions of Cymbopogon proximus Essential Oil

The present study reports Gas chromatographic mass analysis (GC-MS) as well as important biological activities of Cymbopogon proximus essential oil. The chemical composition of the essential oil of Cymbopogon proximus was investigated by GC-MS. Furthermore, the effects of Cymbopogon proximus essential oil on the cardiac parasympathetic ganglia in rats, the intra-tracheal pressure in guinea-pigs and on carrageenan-induced inflammation in the rats paw, were studied. The GC-MS study led to the identification of 22 components with Piperitone representing (73.81%), Elemol (9.32%), alpha-Eudesmol (5.21%) and alpha-Terpineol (3.01%) of the oils composition. The percentage protective effect of the oil on the vagus-induced bradycardia in rats was 90.1±3.1%, which represents a significant protection. As for the effect of Cymbopogon oil on bronchoconstrictors-induced increase in intra-tracheal pressure in guinea-pigs, the oil antagonized the actions of 5-HT and histamine by 80±3.7 and 93±8.3%, respectively. Pharmacological investigations using Cymbopogon oil revealed its inherent ability to possess a bronchodilator activity mediated via blockade of both histamine and serotonin receptors. It possessed a significant ganglionic blocking action and a limited anti-inflammatory activity that seemed to involve blockade of histamine and serotonin receptors in the rats' paws.

Abordagem laparoscópica do câncer de endométrio

Objetivo: apresentar uma nova abordagem laparoscopica para tratamento do câncer de endometrio. Metodos: de fevereiro de 1996 a fevereiro de 1998, doze pacientes com câncer de endometrio, diagnosticadas por histeroscopia e biopsia, foram submetidas a linfadenectomia pelvica associada a histerectomia e salpingooforectomia por laparoscopia. A media de idade das pacientes foi de 58,1 anos; o numero medio de gestacoes foi 2,3 e o indice de massa corporea medio foi de 28,6. Resultados: o tempo anestesico medio foi de 4,8 horas. O tempo medio de internacao foi de 3,3 dias. O numero total de linfonodos retirados foi de 176, sendo 104 (59,1%) do lado direito e 72 (40,9%) do lado esquerdo. Nao foram encontrados linfonodos comprometidos. O numero medio de linfonodos retirados por paciente foi de 18,5. Foram observadas duas complicacoes: em um caso houve necessidade de abandonar o procedimento por aumento da pressao endotraqueal e uma das pacientes evoluiu com formacao de granuloma em cupula vaginal. Conclusoes: nesta avaliacao preliminar dos resultados de histerectomia total com anexectomia bilateral e lifadenectomia laparoscopica para o tratamento do câncer de endometrio, obtivemos resultados satisfatorios quanto ao estadiamento da neoplasia ao numero de linfonodos retirados e quanto as complicacoes cirurgicas observadas.

Regional Deposition of Inhaled Evans Blue Dye in Mechanically Ventilated Rabbits with Air or Helium Oxygen Mixture

An animal model has been used and further developed to examine and evaluate differences in regional deposition patterns of an Evans Blue dye (EB) tracer aerosol. This was done by using different carrier gas composition of either He-O2 (80% helium, 20% oxygen) or air (79% nitrogen, 21% oxygen) in histamine-provoked and nonprovoked rabbits. The ratio of peripheral deposition to total deposition (central + peripheral), in relation to percentage increase in intratracheal pressure (ITPΔ%), was used as an evaluation tool. The animals were tracheostomized, cannulated, and ventilated in a volume-controlled mode until they were stable. Saline or histamine was then administrated for 2 min before the tracer aerosol EB was given. The percentage increase in intratracheal pressure before and after provocation was calculated (7TPA%) and was, on average, 51 ± 20% for air and 51 ± 20% for He-O2. EB was extracted from lung tissues and measured with a spectrophotometer. The absorbance in different lung regions was used as a measure of the distribution of aerosol. Bronchial provocation gave a central deposition 0.55 ± 0.11 (mean ± SD, ratio = peripheral deposition/central + peripheral deposition) compared to 0.80 ± 0.09 in the control group. He-O2-ventilated rabbits showed significantly higher peripheral deposition ratio (0.67 ± 0.12) compared with air-ventilated rabbits (0.55 ± 0.11). The latter finding may be due to the difference in the degree of turbulent flow. There were significant correlations between intratracheal peak pressure and peripheral deposition, r = -.60 and r = -.71 for air and He-O2, respectively. This study demonstrates the possibility of using a rabbit model and different carrier gases for evaluation of effects of bronchial provocation.

BRONCHOPULMONARY EFFECTS OF 8-EPI-PGF2AIN ANAESTHETISED GUINEA PIGS

The compound 8-epi-prostaglandin F2α(8-epi-PGF2α), a F2-isoprostane formed mainly via a non-cyclooxygenase pathway, has been shown to constrict both human and guinea pig airway smooth musclein vitro. We investigated whether this compound has any activity on bronchial resistance and plasma exudation in tracheal tissue of anaesthetised guinea pigs. 8-Epi-PGF2α(12.5, 25 and 50 μg kg−1i.v.) elicited a dose-dependent increase in intratracheal pressure. Diphenhydramine (2 mg kg−1i.v.), indomethacin (1 mg kg−1i.v.) andNG-nitro-L-arginine methyl ester (L-NAME, 10 mg kg−1i.v.) did not affect the 8-epi-PGF2α(25 μg kg−1i.v.)-induced bronchoconstriction. On the contrary, while atropine (0.5 mg kg−1i.v.) injected 10 min prior to 8-epi-PGF2α(25 μg kg−1i.v.) significantly reduced to 55% (P<0.05) the increase in intratracheal pressure induced by the isoprostane, the selective thromboxane A2receptor antagonist, ICI-192,605 (0.5 mg kg−1i.v.) abolished it (95%,P<0.001). Furthermore, 8-epi-PGF2α(50, 100 and 200 μg kg−1i.v.) increased plasma leakage, measured according to the Evans Blue dye technique, in tracheal tissue. This effect was particularly evident when 8-epi-PGF2αwas injected at the dose of 200 μg kg−1i.v. (105% increase;P<0.01) and it was markedly reduced by ICI-192,605 (0.5 mg kg−1i.v.) (36%;P<0.01) but not by diphenhydramine (2 mg kg−1i.v.). In isolated perfused lungs, 8-epi-PGF2α(2.5 μg ml−1min−1perfused for 2 min) increased the thromboxane A2formation which was significantly reduced by ICI-192,605 (16 μg ml−1min−1perfused for 5 min) and abolished by indomethacin (1 μg ml−1min−1perfused for 15 min). These data indicate that 8-epi-PGF2αinduces bronchoconstriction in guinea pigin vivoand that this effect, which seems to be related to activation of thromboxane A2receptor, is associated to an augment of vascular permeability with plasma leakage in airway smooth muscle.

Vagal stimulation augments pulmonary anaphylaxis in the guinea pig lung.

The effect of bilateral vagal stimulation on aerosolized antigen-induced responses was examined in the sensitized, perfused guinea pig lung. Vagal stimulation in the sensitized, perfused lung resulted in bronchoconstriction (peak response 160 +/- 18% above baseline) that was unaffected by either atropine (1 microM), a muscarinic receptor antagonist, or CP 96,345 (1 microM), a NK-1 receptor antagonist, but was transiently augmented in the presence of physostigmine (1 microM), a cholinesterase inhibitor, through an atropine-sensitive mechanism. However, SR 48968 (1 microM), a NK-2 receptor antagonist, and SR 48968 + CP 96,345 reduced by approximately 50 and 90%, respectively, vagally mediated increases in intratracheal pressure in the perfused lung. Simultaneous challenge with vagal stimulation and aerosolized antigen in the sensitized perfused lung resulted in a significant (p < 0.01) increase in intratracheal pressure (Pi), pulmonary arterial pressure (Ppa), and lung weight (LW) compared with either vagal stimulation or aerosolized antigen alone. Increases in Pi, Ppa, and LW in response to vagal stimulation + aerosolized antigen were associated with elevated venous effluent concentrations of thromboxane A2 (TXA2), prostacyclin, leukotriene C4, and histamine. Vagally mediated potentiation of aerosolized antigen-induced increases in Pi, Ppa, and LW was unaffected by atropine or CP 96,345 but was inhibited by the NK-2 receptor antagonist, SR 48968. These data suggest that vagally mediated (predominantly NK-2) potentiation of aerosolized antigen-induced increases in Pi, Ppa, and LW is characterized by elevated venous effluent concentrations of eicosanoids and histamine.

Redistribution of air within the lungs may potentiate “fright” bradycardia in submerged crocodiles ( Crocodylus porosus)

1. 1. Voluntary undisturbed dives by Crocodylus porosus were short in duration (3.08 ± 1.87 min, mean ± SD) and accompanied by a small but significant bradycardia (14.3 ± 5.9% drop). 2. 2. When crocodiles were disturbed underwater there was a rapid onset of “fright” bradycardia, to 65 ± 6.0% of surface heart rates and dive durations were prolonged to 19.6 ± 1.8 min. 3. 3. The development of “fright” bradycardia was not accompanied by any increase in intratracheal pressure or expulsion of lung gas. However, sustained contraction of the abdomen and expansion of the thorax revealed a redistribution of air anteriorly within the lungs. 4. 4. We propose that the redistribution of air within the lungs may generate an afferent signal which potentiates the initiation of a severe, dive-prolonging bradycardia.

Cigarette smoke‐induced changes in guinea‐pig airway responsiveness to histamine and citric acid

The effect of 50 min cigarette smoke exposure on airway responsiveness to the bronchoconstrictor and tussive effects of histamine and citric acid has been examined in guinea-pigs. Intravenous histamine increased intratracheal pressure (ITP) in anaesthetized guinea-pigs and the dose-response curve was significantly (P less than 0.05) steeper in cigarette smoke- than in air-exposed animals. ED50 values were 11.4 nmol kg-1 (7.4-16.8, 95% confidence interval) and 42.5 nmol kg-1 (28.8-61.4, 95% confidence interval), respectively (P less than 0.05) in smoke- and air-exposed guinea-pigs indicating an enhanced reactivity. However, the sensitivity to intravenous histamine was not changed by the cigarette smoke exposure, and the maximum increase in intratracheal pressure was the same as in control animals (air: 247 +/- 21%, n = 4; smoke: 223 +/- 18%, n = 7). The cigarette smoke-induced hyperresponsiveness to intravenous histamine was not altered by pretreatment with nebulized lidocaine (0.20 M), ipratropium bromide (0.30 mM) or cromoglycate (0.06 M), suggesting that a neural reflex is unlikely to be involved in the development of hyperresponsiveness. Conscious, smoke-exposed guinea-pigs had a significantly (P less than 0.001) reduced responsiveness to citric acid (0.40 M) and cigarette smoke. Both cough and bronchoconstriction were suppressed for about 1 h, but unchanged 24 h after exposure. The hyporesponsiveness to citric acid was inhibited by atropine (1.4 mumol kg-1 i.p.) and may therefore, at least in part, be due to increased airway secretions. The present data demonstrate that inhalation of cigarette smoke may alter guinea-pig airway responsiveness to tussive and bronchoconstrictor stimuli.(ABSTRACT TRUNCATED AT 250 WORDS)

Hydrogen peroxide-induced epithelial damage increases terbutaline transport in guinea-pig tracheal wall: Implications for drug delivery

An isolated vagus nerve-tracheal tube preparation from guinea-pig was treated intraluminally with hydrogen peroxide (H 2O 2) at various concentrations. Exposure to, 100 mmol/L H 2O 2 for 20 min was chosen for further experiments since it appeared to cause selective damage to the epithelium. Thus the subepithelial layers of the tracheal wall appeared intact as judged by light microscopic examination. The response to nerve stimulation (increase in intratracheal pressure) was attenuated by only about 20%. Terbutaline administered into the tracheal lumen caused a concentration-dependent inhibition of the response to nerve stimulation. In tracheal preparations pretreated with 100 mmol/L H 2O 2 there was a 20-fold decrease in the EC 50 for terbutaline. The EC 50 for terbutaline added to the external medium was not changed by the H 2O 2 pretreatment. The efflux of 3H-terbutaline from the tracheal lumen into the external medium was three times higher in H 2O 2-treated than in control preparations. It is concluded that in the H 2O 2-damaged epithelium the absorption of terbutaline is enhanced resulting in a better availability of the drug in the smooth muscle layer after intraluminal administration.

Phospholipase A2-induced Pulmonary and Hemodynamic Responses in the Guinea Pig: Effects of Enzyme Inhibitors and Mediator Antagonists

The effect of phospholipase A2 (Naja naja) PLA2) on mean arterial blood pressure and intratracheal pressure was examined in anesthetized guinea pigs. Intracheally administered PLA2 (1 to 10 U) produced acute, dose-dependent increases in mean arterial blood pressure and intracheal pressure. However, Intravenously administered PLA2 (doses as large as 1,000 U) did not alter monitored variables. Acute PLA2-induced morphologic alterations were characterized by airway constriction, airway/alveolar cell damage, and pulmonary sequestration of both leukocytes and platelets. PLA2-induced increases in both mean arterial blood pressure and intratracheal pressure were attenuated to varying degrees by pretreating intravenously with indomethacin (10 mg/kg), a cyclooxygenase inhibitor, and WEB 2086 (0.1 mg/kg), a platelet-activating factor antagonist. Both ICI 198,615 (1 mg/kg), a leukotriene D4, receptor antagonist given intravenously, and dexamethasone (50 mg/kg), a steroidal anti-inflammatory agent given intraperitoneally as a 2-day pretreatment, reduced PLA2-induced increases in intratracheal pressure. Pyrilamine (2 mg/kg), a histamine1-receptor antagonist given intravenously, did not modify PLA2-induced pathophysiologic responses. Guinea pigs exposed to aerosolized PLA2 (100 U/ml) exhibited evidence of increased bronchoalveolar lavage macrophage, leukocyte, and lymphocyte accumulation at 24 h post-PLA2. These studies suggest that in vivo PLA2-induced pathophysiologic changes in the guinea pig involve alterations in resident airway cell populations as well as sequestration and infiltration of inflammatory cells. Both eicosanoids and platelet-activating factor appear to contribute to these PLA2-induced pathophysiologic effects.

Pathophysiologic Changes Induced by Phospholipase A2in the Isolated, Perfused Guinea Pig Lung

Pathophysiologic changes induced by phospholipase A2 (PLA2), a lipolytic enzyme implicated in a variety of pulmonary diseases, were examined in the isolated, perfused guinea pig lung. Thirty microliters of vehicle (saline) or 30 units of PLA2 suspended in saline was given as a bolus injection into either the trachea or pulmonary artery, and the lungs were examined by combined light and transmission electron microscopy at 1, 10, and 30 min following administration. Pulmonary morphologic and physiologic changes were observed only in animals that received PLA2 via the trachea. Initially, morphologic evidence of airway constriction was accompanied by a significant increase in intratracheal pressure. No morphologic change was observed in alveolar parenchymal cell populations at this time. Later there was marked swelling of airway epithelial cells accompanied by pronounced blebbing of the apical cytoplasm with a subsequent decrease in airway lumen size. Interalveolar septa were multifocally thickened by edema and alveolar spaces contained sparse fibrogranular material 10 min after intratracheal PLA2. Significant increases in lung weight were observed at this time. Morphologic features of vasoconstriction, characterized by undulating and convoluted endothelium with prominent cytoplasmic processes resulting in decreased luminal size were observed in small caliber vessels and occurred in conjunction with significant increases in pulmonary arterial pressure. There was pronounced injury to type I alveolar epithelium, including marked cell swelling and fragmentation, accompanied by lesser injury in type II alveolar epithelium. This study demonstrates that the airway epithelium was the initial cell population having morphologic change following intratracheal PLA2, and that the airway epithelium and type I alveolar epithelium were the cell populations most severely affected following intratracheal PLA2. Results further suggest that normal circulating levels of blood-formed elements are not essential for the development of PLA2-induced morphologic change in the isolated, perfused guinea pig lung.

Pulmonary responses to phospholipase A2 in the perfused guinea pig lung.

We examined the effect of phospholipase A2 (PLA2; Naja naja) challenge on pulmonary hemodynamics, airway constriction, and fluid filtration in isolated Ringer-perfused guinea pig lungs. Intratracheal PLA2 (10-100 U) produced dose-dependent increases in pulmonary arterial pressure, intratracheal pressure, and lung weight, although intravenous PLA2 administration had no effect on monitored variables. Morphological features indicative of airway constriction and pulmonary edema were observed by light microscopy. PLA2-induced increases in intratracheal pressure and/or lung weight were attenuated to varying degrees by pretreatment with indomethacin (1 microM, a cyclooxygenase inhibitor), ICI-198,615 (1 microM, a leukotriene D4 receptor antagonist), and WEB 2086 (1 microM, a platelet-activating factor antagonist). PLA2-induced increases in pulmonary arterial pressure and intratracheal pressure were also reduced in lungs removed from animals pretreated with dexamethasone (50 mg/kg ip for 2 days; a steroidal antiinflammatory agent). Pyrilamine (1 microM, a histamine1-receptor antagonist) and Takeda AA861 (1 microM, a delta 5-lipoxygenase inhibitor) did not produce significant inhibitory effects on PLA2-induced pathophysiological changes. Intratracheal instillation of high-dose platelet-activating factor (50 micrograms) or lysophosphatidylcholine (100 micrograms) produced gradual increases in intratracheal pressure and lung weight, but these changes were not as large as those induced by PLA2. Thus these studies suggest that resident cell populations associated with airways may play an important role in PLA2-induced pathophysiological changes in the perfused guinea pig lung. These PLA2-induced effects are most likely partially mediated by generation of eicosanoids and platelet-activating factor.

Peak intratracheal pressure during controlled ventilation in infants and children. A computer study of the Servo 900C ventilator.

The mathematical relationship between peak ventilator breathing system pressure displayed on the digital meter of the Siemens SV900C ventilator, and peak intratracheal pressure measured at the distal end of the tracheal tube, was defined and incorporated into a computer program. The mean difference between peak airway pressure calculated by the computer and directly measured peak intratracheal pressure was 0.02 kPa (SD 0.10) in 18 infants and children. The mean difference between ventilator breathing system pressure and intratracheal pressure in the same group was 0.82 kPa (SD 0.91). Bench tests established that the decrease in peak pressure displayed by the ventilator (from 1.36 to 0.38 kPa) while inspiratory time was increased from 20 to 80% of the respiratory period, concealed an increase (from 0.2 to 0.38 kPa) in intratracheal pressure which occurs during this process; and that the large increase in pressure displayed by the ventilator (from 0.3 to 6 kPa) while respiratory frequency was increased from 20 to 120 breaths/minute, concealed a small increase in peak intratracheal pressure (0.2-0.3 kPa) which occurs during this process. These changes were accurately predicted by the computer program. The increase in intratracheal pressure associated with prolonged inspiratory times explains the high incidence of barotrauma which has recently been associated with this procedure in infants.

Attenuation of antigen-induced bronchospasm by fenoterol in the guinea-pig.

When guinea-pigs sensitized to ovalbumin were challenged with ovalbumin, the histamine concentrations in lung tissue decreased, whereas those in tracheal and heart tissues increased during the 15 min following challenge. Fenoterol (2.5 mg/kg, i.p.), administered 30 min prior to challenge, attenuated both the decrease and the increase in lung and tracheal histamine concentrations, respectively. The challenge-induced increase in heart histamine was also prevented. In the anaesthetized guinea-pig, a marked increase in intratracheal pressure (ITP) occurred on challenge. This was of longer latency than the increase in ITP induced by histamine and was consistent with a release process. Treatment of challenged guinea-pigs with fenoterol (2.5 mg/kg, i.v.) markedly reduced the increased ITP. However, when fenoterol was administered prior to challenge, the increase in ITP was abolished. These results indicate that there is an apparent relationship between the inhibition of histamine release in vivo by fenoterol pretreatment and the greater inhibitory effect of fenoterol on antigen-induced increases in ITP when administered prophylactically.

Effect of dazoxiben, a specific inhibitor of thromboxane synthetase, on acute pulmonary responses to E. coli endotoxin in anaesthetized cats.

1 The effects of acute pretreatment with the thromboxane synthetase inhibitor dazoxiben 5 mg/kg intravenously (UK 37248-01) were examined on the acute pulmonary responses of pentobarbitone-anaesthetized cats to E. coli endotoxin 2 mg/kg intravenously. 2 E. coli endotoxin in control, untreated, cats resulted in a marked pulmonary hypertension, an increase in intra-tracheal pressure (at a constant pulmonary inflation volume), an increase in both pulmonary arterial and aortic concentrations of thromboxane B2 (TXB2) and a reduction in systematic arterial PO2. 3 Dazoxiben prevented, or markedly reduced, the endotoxin-induced pulmonary release of TXB2, the decrease in systematic arterial PO2 and the pulmonary arterial hypertension, but did not modify the increase in intratracheal pressure. 4 These results may suggest that TXA2 is responsible for the endotoxin-induced pulmonary arterial hypertension but that some other arachidonic acid derivative (prostaglandin F2 alpha) is responsible for the reduced lung compliance that follows the acute administration of E. coli endotoxin.

Antigen-induced bronchial anaphylaxis in actively sensitized SD rats. Effects of immunization and provocation doses of antigen and of pretreatment with DSCG, theophylline, terbutaline and a new anti-allergic xanthine derivative, D4026.

Bronchial anaphylactic reactions, estimated as increase in intratracheal pressure, were precipitated by intravenous injections of antigen into actively sensitized SD rats. The degree of bronchial reactivity was found to depend on both the challenge dose and the immunization dose of antigen; therefore the course of the capacity to respond was recorded as a function of these variables. The degree of the bronchial anaphylactic response could be reduced by pretreatment with disodium cromoglycate, terbutaline or a new anti-allergic xanthine derivative, D 4026, in some groups of animals. The efficacy of each agent was found to depend on the dose of antigen used for sensitization and for provocation of the bronchial reaction rather than on the strength of the response. Taken together, the data suggest that more than one type of homocytotropic antibody mediates bronchial anaphylactic reactivity in the SD rat.

The bronchodilator activity of 20-isopropylidene prostaglandin E 2 (CS-412)

The bronchodilator activity of 20-isopropylidene prostaglandin E 2 (CS-412) was studied in vivo . In the conscious guinea pig, aerosols of CS-412, prostaglandin E 2 (PGE 2), or salbutamol afforded similar protection against histamine-induced convulsions. In the anesthetized guinea pig, where increase in intratracheal pressure was taken as an index of bronchoconstriction, CS-412, PGE 2, and salbutamol were equipotent in inhibiting the bronchoconstriction induced by histamine. CS-412, PGE 2 and salbutamol were equally effective in reducing the serotonin-induced increase in pulmonary resistance in the anesthetized cat. CS-412 was different from PGE 2 in bronchoconstrictor activity in anesthetized cats with normal bronchotonus. PGE 2 caused bronchoconstriction in the cats. CS-412 showed 30 times less constrictor activity than PGE 2. It was concluded that CS-412 is an effective bronchodilator without unfavorable side effects.

Inhibition of baroreceptor and chemoreceptor reflexes on heart rate by afferents from the lungs.

1. Brief stimuli were delivered to the carotid baroreceptors or chemoreceptors in dogs anaesthetized with chloralose and paralysed with D-turbocurarine. Baroreceptor stimulation was achieved by forceful retrograde injection of 2-5 ml or air-equilibrated saline into the external carotid artery after first clamping the common carotid artery. Chemoreceptor stimulation was achieved by rapid retrograde injections of 0.2-0.5 ml of warmed CO2-equilibrated saline into the external carotid artery. Observations were made during periods of temporary cessation of artificial ventilation. 2. When the volume of the lungs was not changing, prompt decreases in heart rate were evoked by chemoreceptor or baroreceptor stimuli except when these were delivered during the inspiratory phase of breathing (as judged from the records of phrenic nerve activity). 3. No changes in heart rate were evoked when these stimuli were timed to occur during expansion of the lungs in response to a rapid increase in intratracheal pressure (6-10 mmHg in 1-2 sec). Decreases in heart rate were evoked when the stimuli occurred during slower inflations of the lungs. 4. Both stimuli regained their effectiveness on heart rate with time after inflations of the lung when the lungs were held inflated. Both stimuli evoked large decreases in heart rate when delivered during deflations of the lung. 5. The effects of lung inflation on the effectiveness of both cardiodepressor reflexes were abolished by surgical denervation of the lungs.

Cricoid Fracture With Tracheal Avulsion

CRICOID FRACTURE with complete avulsion of the trachea is usually fatal. In closed, nonpenetrating injuries, it is difficult to imagine large numbers of survivors. Observations regarding the problems associated with the management of such a case are herein presented. As the trachea is an elastic structure, it should not be subject to great stress from purely stretch injuries. Tracheal ruptures have been reported from a blow on the chest during a period of glottic closure, such ruptures being the result of marked increase in intratracheal pressure, probably occurring with the trachea under stretch due to extension of the head.¹Such a force may also produce recurrent laryngeal nerve injury. Cricoid fractures are usually incurred in a head extended position due to direct force of considerable magnitude. Tracheal retraction occurs with avulsion due to the elasticity of the intercartilaginous ligaments.² Such an injury allows no time for extended diagnostic

ARTERIAL AND VENOUS BLOOD PRESSURE RESPONSES DURING A REDUCTION IN BLOOD VOLUME AND HYPOXIA AND HYPERCAPNIA IN INFANTS DURING THE FIRST TWO DAYS OF LIFE

In 46 normal full-term infants (0.5-36.5 hours of age) the mean systolic pressure in the lower aorta, catheterized through the umbilical artery, was 70 S.D. ± 8 mm Hg and the mean diastolic pressure 44 S.D. ± 7 mm Hg. The mean venous pressure in the thoracic inferior vena cava, catheterized through the umbilical vein and ductus venosus was 1.4 S.D. ± 2 cm H2O. Higher pressures were recorded in the portal sinus. The mean arterial O2 tension in the lower aorta was 84 S.D. ± 13 mm Hg and the mean CO2 tension 37 S.D. ± 7 mm Hg. The mean rectal temperature was 36.2 S.D. ± 0.7°C. Arterial pressure tracings recorded during, and in the recovery period following, a 10% reduction in blood volume suggest that vasomoter baroreceptor responses to a reduction in pulse pressure are not very active during the first 2 days of life. Cardiac responses are more active. In contrast to the adult, passive tipping of the newborn infant into the head-up position caused little change in the inferior vena cava pressure or in the arterial pressure. An increase in intratracheal pressure of 7-10 cm H2O caused immediate bradycardia. Frequently the heart rate was halved but little fall in mean pressure occurred over 10 seconds. Breathing hypoxic mixtures caused hypotension and tachycardia. Hypotension was observed with no change in heart rate when the arterial CO2 was raised simultaneously. Differences in blood volume distribution, and the relative size of the circulatory beds under reflex and chemical control, possibly share with the apparent unresponsiveness of the peripheral vessels in causing the differences in responses observed between the infant and the adult.

Pressure breathing: functional circulatory changes in the dog.

Observations were made on two series of dogs breathing air at 17 and 26 mm Hg positive pressure. In one series (8 dogs) the animals had the benefit of counterpressure while the other group (10 dogs) did not. Systolic blood pressure decreased in each group while breathing against 17 mm Hg positive pressure, but to a greater extent in the group without counterpressure. While breathing against 26 mm Hg positive pressure, there was essentially no difference between the two groups. Changes in diastolic blood pressure followed a pattern similar to the changes in systolic pressure. Pulse pressure was essentially maintained. Venous pressure increased markedly during pressure breathing. This increase in the group with counterpressure more nearly approximated the simultaneous increase in intratracheal pressure. Intracranial pressure was elevated during pressure breathing. This increase was greatest and maintained in the group with counter-pressure. Heart rate increased during pressure breathing, especially in the group with counterpressure, and slightly decreased in the group without counterpressure. A period of apnea occurred at the onset of pressure breathing in the group without counterpressure while respiration rate remained essentially unchanged in the group with counterpressure. Hematocrit determinations indicated hemoconcentration during pressure breathing. Submitted on June 27, 1955