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Biomedical subjects

P B Bennett

Publications and source records attributed to P B Bennett.

At least 109 records · Page 6Linked to original sources

Effects of aspirin and dipyridamole on platelet function, hematology, and blood chemistry of saturation divers.

Twenty-four young male divers were assigned randomly to 4 treatment groups: Group I received aspirin (325 mg) three times daily; II received dipyridamole (75 mg) three times daily; III received both drug regimens; and IV received matching placebo. Double-blind procedures were followed. Treatment began 24 h prior to a 48-h saturation dive (inclusive of 17 h decompression) at a simulated depth of 18.3 m and continued throughout and for 3 days after the dive. A post-dive reduction in circulating platelet count was observed in all groups, except the group that received aspirin only. Platelet survival was shortened in all treatment groups. Five cases of Type I decompression sickness occurred and were treated by recompression, two in the aspirin plus dipyridamole group, two in the dipyridamole group, and one in the placebo group. Blood chemistry and hematology profiles showed that divers with decompression sickness had more elevated GOT, GPT, CPK, cholesterol and triglyceride levels, and greater reductions in platelet count, Platelet Factor 4 and Thrombin Clotting Time than most other subjects. Subjects receiving either aspirin or aspirin plus dipyridamole had fewer changes in these parameters. Failure of aspirin to potentiate, or add to, dipyridamole may be due to other actions of aspirin such as inhibition of prostacyclin synthesis. Further studies of the role of antiplatelet drugs in decompression sickness are warranted.

Adult↗

Effect of helium/nitrogen/oxygen mixtures on HPNS convulsion threshold in euthermic rats.

This study compares the effects of various so-called trimix mixtures (10, 20, and 40% N2 in He-O2) on the convulsion threshold pressure (Pc) and EEG activity in 60 adult male Wistar rats with chronically implanted electrodes with those in 20 rats in He-O2 only. Restrained animals were individually compressed with trimix mixtures at 80 or 160 atm per hour to a simulated depth of 138 ATA; colonic temperature was maintained at normal levels. Pc was defined as the initial occurrence of overt sustained generalized tonic-clonic seizures, accompanied by typical "spike and wave" patterns in all EEG leads. As in man, in rats trimix increased the depth of the onset of HPNS tremors and myoclonic jerks in all six groups of rats. However, the Pc of the trimix groups was no different from the Pc of the helium-oxygen group (113 ATA), and at 40% N2, rats showed EEG seizures but no overt convulsions. These results are discussed in relation to those of other studies showing the extension of Pc in mice and monkeys attained by adding narcotics to heliox; the paper also considers the relevance of method of compression, addition of nitrogen, core temperature, and species differences, as well as the need for EEG measurements and direct observation of overt convulsions as indicators of an effective antagonism of HPNS.

Animals↗

Nitrogen-oxygen saturation therapy in serious cases of compressed-air decompression sickness.

Decompression sickness and arterial air embolism which follow exposure to raised environmental pressures of compressed air are usually adequately treated by accepted recompression procedures of relatively short durations. With serious cases, however, conventional treatment may not allow sufficient time at depth for the complete resolution of manifestations because of the need to avoid pulmonary oxygen toxicity which is associated with a prolonged period of breathing compressed air. Treatment by nitrogen-oxygen saturation at a pressure equivalent of 30 m (100 ft) sea water is proposed. Based upon the success of three refractory cases treated by this procedure, recommendation are made for the conversion of standard compressed-air chambers into an emergency saturation mode for therapy.

Adult↗

Naloxone fails to antagonize the righting response in rats anesthetized with halothane.

The righting responses of 75 Wistar rats during exposure to halothane, 0.5 per cent, 10 min after subcutaneous injection of naloxone, 10 or 20 mg/kg, or saline solution were examined. There was no difference in recoveries of the righting responses among the three groups. It is concluded that naloxone does not antagonize the loss of righting response produced by halothane anesthesia in the rat.

Anesthesia, Inhalation↗

Pulmonary oxygen toxicity in chickens and rabbits.

Chickens exposed to hyperbaric oxygen (3 to 5 ATA) or to 100% oxygen at atmospheric pressure for prolonged periods showed no pathologic pulmonary damage, although hydrogen peroxide did accumulate in their airways. Superoxide dismutase in the peripheral nucleated red blood cells and the rate of oxidation of specifically labeled glucose were increased in chickens exposed to hyperbaric oxygen for three hours. Superoxide dismutase increased in the lung lavage of the rabbits and in the peripheral nucleated red blood cells. Glucose oxidation was unchanged. The difference in superoxide dismutase is probably the result of the desquamated, damaged cells found in the rabbit lung lavage. That only rabbit bronchi are lined with oxidant-sensitive ciliated cells suggests that the absence of these ciliated cells in fowl may well be responsible for the observed resistance of these birds to oxidant damage by oxygen.

Animals↗

Effect of cerebellar ablation on the high pressure nervous syndrome in rats.

To evaluate the interaction between high pressure nervous syndrome (HPNS) seizures and cerebellar integrity, seizure threshold pressure (Pc) of normal rats was compared with that of rats sustaining cerebellar ablation two weeks prior to exposure to 136 ATA in a helium-oxygen atmosphere. All rats exhibited severe HPNS symptoms which culminated in seizures. Pc was reduced in cerebellectomized animals, and the number of seizure episodes increased twofold, but the average duration of seizure episodes was unchanged. The spike-and-wave pattern in the electroencephalogram remained a prominent feature in both groups.

Animals↗

Cerebellar and cerebral electroencephalogram during the high pressure nervous syndrome (HPNS) in rats.

Electroencephalographic activity of the frontal cortex, cerebellar vermis, and superior vestibular nucleus was recorded in awake rats during the high pressure nervous syndrome (HPNS) by means of permanently implanted electrodes. Power-spectrum analysis revealed a decline in the faster frequencies and an increase in the slow frequences as the seizure end-point was approached. Effects of compression to 4500 fsw varied from severe tremor and myoclonic jerks to status epilepticus, with seizures occurring at an average depth of 3560 fsw. In all animals, multifocal-spiking activity progressed in severity with increasing depth. The predominant seizure pattern observed was a spike and slow-wave pattern reminiscent of absence seizures. Initial evidence of generalized seizure activity was equally divided between the cerebellum and cortex. It is concluded that the cerebellum participates in HPNS seizures. Possible evolution of the syndrome by loss of Purkinje cell inhibitory influence on subcortical sites that modulate cortical excitability is discussed.

Animals↗

Effect of compression rate on HPNS convulsion threshold in the euthermic rat.

The modification of the development of the high pressure nervous syndrome (HPNS) has been demonstrated by varying the external environment (chamber temperature, compression rate) or the internal environment (core temperature, pharmacology, age). This study examined the effects of compression rate on the convulsion-threshold pressure and EEG activity in 68 adult male Wistar rats with chronically implanted electrodes. Restrained animals were individually compressed at a predetermined rate in helium-oxygen to a simulated depth of 4500 fsw (137 ATA), with colonic temperature maintained at normal levels. Six compression rates showed that convulsion-threshold pressure for euthermic rats did not significantly differ between any of the groups.

Animals↗

Inner ear decompression sickness.

With recent increases in commercial, military, and sport diving to deeper depths, inner ear injuries during such exposures have been encountered more frequently and noted during several phases of diving: during compression, at stable deep depths, with excessive noise exposure in diving, and during decompression. The pathophysiology of these injuries differs, depending upon the phase of diving in which the injuries occur. In this report, 23 cases of hearing loss, tinnitus, and/or vertigo occurring during or shortly after decompression are presented. Thirteen of these cases occurred in helium-oxygen dives involving a change to air during the latter stages of decompression. A significant correlation is present between prompt recompression treatment, relief of symptoms, and lack of residual deficits. Current knowledge indicates that the management of otologic decompression sickness should include: 1. prompt recompression to at least 99 feet deeper than the symptom onset depth; 2. recompression using the previous helium-oxygen mixture when the injuries occur during or shortly after a switch from helium-oxygen to air during the latter stages of decompression; 3. the use of parenteral diazepam for symptom relief and cyclic inhalations of oxygen enriched treatment gases; and 4. the avoidance of further diving by divers who exhibit permanent inner ear injuries after the acute symptoms have subsided.

Adult↗

Alteration of high pressure nervous syndrome in rats by alteration of colonic temperature.

The components of the high pressure nervous syndrome (HPNS) have been clearly described previously. Animal studies of HPNS, however, have been characterized by nonstandardized definitions of the various HPNS parameters, based on visual observations. Where EEG's have been used in HPNS studies, the frequent occurrence of movement-induced artifact has made much of the data difficult to interpret. Because of these limitations, efforts to clarify the influence of environmental variables on the syndrome have led to varying results, especially with respect to the influence of temperature. The technique used in this study consistently yielded artifact-free EEGs from unanesthetized, moving rats during simulated heliox dives. Typical seizure patterns in the EEG recordings were combined with clinical seizure activity to define HPNS convulsion-threshold pressure (Pc). By manipulating body temperature artificially, three groups of rats were investigated--hypothermic, euthermic, and hyperthermic animals. An inverse relationship between body temperature and HPNS convulsion-threshold pressure was demonstrated.

Animals↗

Optimal use of nitrogen to suppress the high pressure nervous syndrome.

Five subjects were compressed to 1000 ft (31 ATA) for 2 h breathing 3.2 ATA nitrogen, 0.5 ATA oxygen, and the remainder helium. The compression took 33 min with a 10-s stage at 50 ft (2.5 ATA), 1 MIN AT 320 FT (10.7 ATA), and 2 min at 700 ft (22 ATA). Hypothetically, this 1:10 ratio for nitrogen-helium partial pressures should induce neither nitrogen narcosis nor the High Pressure Nervous Syndrome (HPNS). Tests, therefore, were made during the experiment of postural tremor, spontaneous electroencephalogram, psychomotor and intellectual activities, and subjective sensations. One diver worked underwater for 40 min on a simulated engineering assembly while breathing with a closed-circuit breathing apparatus and wearing a battery-heated suit in water at 56 degrees F. Decompression was in 4 d using 0.8 ATA oxygen and helium. The performance tests indicated no narcosis and little or no signs of HPNS. No tremor or EEG changes were seen. The "wet" diver reported sensations of mild euphoria but the other four reported no difficulties. No nausea or dizziness of HPNS was reported. It is concluded that use of a ratio of 1:10::N2:He is effective in the control of narcosis and HPNS during rapid compression to 1000 ft (31 ATA).

Atmospheric Pressure↗

Calculation of the percentage of a narcotic gas to permit abolition of the high pressure nervous syndrome.

A theoretical method is derived for computation of the interactin of pressure and a weak anesthetic such as nitrogen or other narcotic gases in a two-dimensional material so as to prevent signs and symptoms of the high pressure nervous syndrome. A ratio of one part nitogen to 9 parts helium (pressure) is derived, which is in excellent agreement with previous human experiments in men at 31 ATA, with PO2 = 0.5 ATA.

Diving↗