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D L Beckman

Publications and source records attributed to D L Beckman.

At least 37 records · Page 2Linked to original sources
PubMed1980

Absence of stellate ganglion influence on alveolar-duct constriction.

Previous work has shown decreased lung compliance with high wash fluid surface tensions, but normal ratios of lung weight to body weight during stellate ganglion stimulation (SGS) in cats and monkeys. In the present study, effects of SGS on diameters of alveolar ducts were determined in spontaneously breathing cats under ketamine anesthesia. Compliance and pulmonary resistance were also measured. A fluorocarbon cooled to - 100 degrees C was poured onto an exposed lung lobe after rapidly opening the chest after sham operation and during SGS. Examination of the outer 2 mm of the lungs by light microscopy revealed no alveolar-duct constriction by SGS, although compliance decreased by 15%. Pulmonary resistance was unchanged. Alveolar-duct diameters were 157 +/- 4.3 micron (mean +/- SEM) in control animals and 163 +/- 4.6 micron in SGS cats. Absence of alveolar-duct constriction suggests that peripheral airway constriction did not contribute to the decrease in compliance during SGS.

Airway Resistance↗
PubMed1979

Lung compliance and cholesterol during stellate ganglion stimulation.

The relationships between lung compliance, surface tension, and cholesterol during stimulation of the sympathetic nervous system were studied in 28 cats. Cats were anesthetized with ketamine hydrocholoride, injected with one of five sympathetic blocking agents or inhibitors and injected with isoprotenol. The left stellate ganglion was then stimulated electrically for 5 min. We found that stimulation decreased lung compliance and increased the surface tension and the cholesterol concentration in the lung wash fluid. Alpha blockers (phentolamine and phenoxybenzamine) and catecholamine inhibitors (reserpine and guanethidine) prevented these changes, but the beta blocker practolol did not. In additional experiments airway resistance, functional residual capacity and lung weights did not change during stellate stimulation. The results from the present study suggest that stellate ganglion stimulation resulted in decreased lung compliance with an increased surface tension and cholesterol in lung wash fluid.

Animals↗
PubMed1978

Rat lung hyper-reactivity to stress.

Rats have been used frequently as a model for determining the pulmonary response to various stressful situations. It has been shown in the literature that rat lungs are remarkably sensitive to factors which result in the development of gross pulmonary injury, such as stress from exposure to hyperbaric oxygen. Similarly, a high degree of pulmonary reactivity was found in rats after administration of various CNS, convulsants and also exposure to mechanical vibration. The present study was confined to a determination of the gross pulmonary response of rats exposed to mechanical CNS traumatization compared to that of 10 other laboratory species. The frequency and severity of pulmonary injury from CNS traumatization, as indicated by lung weight/body weight ratios and gross appearance, was very striking in the traumatized rats, but we found little or no change in cats, dogs, rabbits and guinea pigs, in Rhesus, squirrel, vervet, and cynomolgus monkeys or in baboons and chimpanzees. Previous studies showed that the gross pulmonary injury from this mechanical head injury in rats, as well as from hyperbaric oxygen exposure, vibration, and CNS convulsants, was ameliorated by the prior administration of various sympathetic blocking agents. The results from the present comparative study tend to suggest that rat lungs are hyper-reactive to this stress.

Animals↗
PubMed1978

Protection against high-pressure oxygen seizures by amino-oxyacetic acid.

A variety of autonomic blocking agents, general anesthetics, and anticonvulsants have been shown to offer protection from seizures caused by hyperbaric oxygen. Amino-oxyacetic acid (AOAA) has been shown to offer rats only minimal protection from such seizures. This study investigated whether AOAA protected cats and mice from hyperbaric-oxygen-induced seizures. Cats and mice were exposed to 100% oxygen at 5 ATA until seizures occurred or for a period of up to 60 min. Approximately half of the animals were pretreated with AOAA either 30 or 240 min before oxygen exposure. Results showed that the interval between exposure and grand mal seizures increased significantly in cats pretreated 30 or 240 min before exposure with 17 to 25 mg/kg AOAA; the number of cats remaining seizure-free for 60 min also increased markedly. However, mice received little protection even at doses up to 40 mg/kg. At higher doses the AOAA itself caused seizures even in the absence of hyperbaric oxygen.

Acetates↗
PubMed1976

Aspiration pneumonitis and pulmonary phospholipids.

Peptic aspiration pneumonitis (Mendelson's syndrome) results when gastric acid is aspirated into the lung, as may occur during anesthesia. In the present study, 0.1 N HCl was insufflated via the endotracheal tube into pentobarbital-anesthetized dogs in an amount sufficient to cause severe pulmonary damage. At death, the thorax was opened, the lungs grossly examined, and either weighed and desiccated for determination of wet/dry lung weight ratios, rinsed with saline for removal of alveolar surface phospholipids, or homogenized for whole lung phospholipid determination. Gross appearance and wet/dry lung weight ratios indicated severe pulmonary edema. The surface tension values of the lung wash were elevated over control values. Lysophophatidyl-choline (LPC) showed a striking increase over control values. Because LPC is a potent hemolytic agent which builds up in the lung following this pulmonary insult, and because increased hemorrhaging gradually develops following experimental acid insufflation, it is concluded that LPC is most probably causally related to the hemorrhagic pneumonia of Mendelson's syndrome.

Animals↗
PubMed1975

Pulmonary surface tension and head injury.

Previous studies have shown that exposure of monkeys to lethal experimental head injury by means of a captive-bolt mechanism results in a decreased lung compliance and a high minimum surface tension. Such changes which occurred in the absence of any increase in lung weight/body weight ratios were ameliorated by the prior administration of various sympathetic blocking agents. Exposure of monkeys and cats to stimulation of the pulmonary sympathetics via the stellate ganglion also resulted in similar compliance and surface tension changes without any increase in lung weight. The present experiments were carried out in order to determine the effect of lethal mechanical head injury in the cat on the surface tension of the alveolar lining layer and reasons for any possible changes. Previous reports have shown that the addition of very small amounts of cholesterol to lung wash fluid raised the minimum surface tension to abnormal levels. The results from the present study show that a sudden lethal blow to the occiput in cats results in an abnormally high minimum surface tension (over 20 dynes/cm) in the lung wash fluid and a nearly 200% increase in cholesterol content. There was little or no change in lung wet weight/dry weight ratios or gross lung appearance following this head injury. Thus the results from the present study strongly suggests that the previously reported decreased lung compliance and high minimum surface tension following a blow to the head may be due in part at least to the presence of increased intra-alveolar cholesterol.

Animals↗
PubMed1975

Neurogenic influence on pulmonary surface tension and cholesterol in cats.

Previous work showed that stress involving the sympathetic nervous system via mechanical head injury and hyperbaric oxygen results in a decreased lung compliance and altered alveolar surfactants. Similar changes were associated with sympathetic nerve stimulation via the stellate ganglion. In view of reports that the minimum surface tension attained by lung wash fluid is increased by very small amounts of cholesterol content of the alveoli. The results show a nearly 200% increase in intra-alveolar cholesterol as well as high minimum surface tensions following sympathetic nerve stimulation. Such changes developed in the absence of any increase in lung wet wt/dry wt ratios. The results from the present study suggest that the previously reported decreased lung compliance and increased minimum surface tension associated with sympathetic stimulation may be due at least in part to contamination of the alveolar surfactants with large amounts of cholesterol.

Animals↗
PubMed1975

Hyperbaric oxygen and pulmonary surface tension.

Previous work has shown that short-term exposure of cats to oxygen at high pressure (OHP), to the extent of overt convulsive seizures, has little or no effect on the lung appearance or lung weight but does alter the alveolar surfactants. More prolonged exposure results in hemorrhagic edema of the cat lung similar to that observed in rats after only short-term exposure. Previous work showed that sympathetic stimulation via the stellate ganglion and mechanical CNS injury results in altered surfactants attributed to increased intra-alveolar cholesterol. In the present study, cats exposed to OHP until the animals convulsed intermittently for 3 min (approximately 1 hour, 6 ATA) similarly showed altered surfactants with a high minimum surface tension and a 150% increase in intra-alveolar cholesterol. These changes also occurred in the absence of any gross lung injury. The results from the present study suggest that an important causal mechanism involved in the development of gross lung injury associated with prolonged OHP exposure is an initial increase in minimum surface tension due to increased intra-alveolar cholesterol.

Animals↗