{"title":"Distribution of cardiac output in awake rats during exposure to 5 bar.","authors":"J Risberg, G W Bergø, C Hordnes, I Tyssebotn","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Previous studies have reported increased total myocardial blood flow (TMBF) after 15 min stable pressure in a normoxic O2-N2 and O2-He at 5 bar, although cardiac output (CO), heart rate (HR), and mean arterial pressure (MAP) remained unchanged. In the present study, 2 groups of awake rats were exposed to normoxic 5 bar atmospheres; group 1 breathing a He-O2-N2 mixture and group 2 a O2-N2 mixture. Organ blood flow was determined by the microsphere method in control (C) (group 1) and after 15 (T1) and 75 min (T2) hyperbaric exposures (groups 1 and 2). MAP and HR remained at control levels in group 2 animals and increased slightly (6-10%, P less than 0.05) in group 1 rats. CO remained unchanged during the experimental period in both groups. In group 1, TMBF had increased by 13% (P less than 0.05) at T1 and continued to increase at T2 for both groups. Blood flow to the liver and spleen increased during the exposure in both groups. Renal blood flow fell by 25% from C to T2 (P less than 0.05). The arterial blood gases and pH remained at the predive control level in group 2 rats, whereas serum corticosterone concentration fell to 60% during compression (P less than 0.01), possibly due to N2 narcosis, but increased gradually toward 80% of C value during the pressure exposure. We conclude that the increase in TMBF, which is initiated by compression to a 5-bar normoxic atmosphere, persists when stable pressure is maintained.</p>","PeriodicalId":76778,"journal":{"name":"Undersea biomedical research","volume":"17 6","pages":"503-14"},"PeriodicalIF":0.0,"publicationDate":"1990-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13439025","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Treatment of experimental cerebral air embolism with lidocaine and hyperbaric oxygen.","authors":"J J McDermott, A J Dutka, D E Evans, E T Flynn","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Experiments were performed to assess the combined therapeutic effects of hyperbaric oxygen (HBO) and i.v. lidocaine on neural function after ischemia induced by cerebral air embolism in anesthetized cats. Neural function was determined by measuring the somatosensory evoked potential (SEP) amplitude. Air was infused into the carotid artery in increments of 0.08 ml to maintain the SEP amplitude at 10% or less of baseline values for 15 min. Three groups were studied. A control group (n = 9) received no further treatment after SEP suppression. An HBO group (n = 8) was treated with oxygen at 2.8 atm abs for 130 min. A third group (n = 8) received an i.v. lidocaine infusion in addition to HBO. Air infusion suppressed the SEP amplitude to the same level in all groups. The control group recovered 27.4 +/- 5.5% (mean +/- SEM) of the baseline SEP amplitude, whereas the HBO group recovered 62.0% +/- 7.2%, and the HBO plus lidocaine group recovered 75.3 +/- 5.7%. The results show that both HBO and the combination of HBO and lidocaine promote a significant recovery of the SEP amplitude compared to no treatment. However, lidocaine therapy adds no benefit to HBO therapy alone.</p>","PeriodicalId":76778,"journal":{"name":"Undersea biomedical research","volume":"17 6","pages":"525-34"},"PeriodicalIF":0.0,"publicationDate":"1990-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13439027","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
P Radermacher, B Santak, C M Muth, J Wenzel, P Hampe, L Vogt, M Hahn, K J Falke
{"title":"Nitrogen partial pressures in man after decompression from simulated scuba dives at rest and during exercise.","authors":"P Radermacher, B Santak, C M Muth, J Wenzel, P Hampe, L Vogt, M Hahn, K J Falke","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>In 5 subjects arterial and central venous nitrogen partial pressures (PN2) were measured after decompression from a chamber dive following a decompression schedule for scuba diving. The simulated dives consisted of exposure to air at 6 bar for 30 min corresponding to a depth of 50 m. Afterward the subjects were decompressed with decompression stops at 2.5, 2.2, 1.9, 1.6, and 1.3 bar with a total decompression time of 67 min. In 3 of the subjects the measurements were repeated after they had exercised (workload 75 W) during bottom time. Immediately after decompression and every 40 min until Minute 240 arterial and central venous blood samples were analyzed for PN2 using a manometric Van Slyke apparatus. Venous PN2 remained elevated until 160 min after decompression, indicating still incomplete nitrogen washout for at least 2 h after decompression had been accomplished. We did not find any difference in PN2 values after decompression from dives at rest and after exercise. Applying a computer program based on a wide range of theoretical tissue half-times nitrogen elimination proved to be consistent with Haldanian theories when using our decompression profile. Our data confirm that nitrogen elimination is prolonged after decompression from simulated dives at rest and after exercise.</p>","PeriodicalId":76778,"journal":{"name":"Undersea biomedical research","volume":"17 6","pages":"495-501"},"PeriodicalIF":0.0,"publicationDate":"1990-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13439024","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Transient osteoporosis of the hip.","authors":"J Vorosmarti","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":76778,"journal":{"name":"Undersea biomedical research","volume":"17 6","pages":"543"},"PeriodicalIF":0.0,"publicationDate":"1990-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13439029","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Measurement of static and dynamic pulmonary work during pressure breathing.","authors":"J B Morrison, N A Taylor","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Various environments alter static and flow-resistive pulmonary mechanics. Of interest to diving physiologists is the negative pressure breathing induced during upright immersions without appropriate modification of air supply pressure. This paper outlines methodologic considerations for determining static and flow-resistive pulmonary work under such exposures. Ten males performed inspiratory pressure-volume relaxation maneuvers and spontaneous breathing in air, and during upright immersion with mouth pressure air supply. The immersed lung centroid pressure (PLC) was +1.19 kPa relative to the hydrostatic pressure at the sternal notch. Immersion elevated inspiratory static work from 0.36 to 1.74 J.liter-1 (P less than 0.05). Pulmonary flow-resistive work was elevated from 0.20 to 0.75 J.liter-1 (P less than 0.05), whereas pulmonary resistance, determined at 0.5 liter.sec-1, increased from 0.18 to 0.44 kPa.liter-1.sec (P less than 0.05). No significant changes in the iso-volume compliance of the lung tissue, chest wall, or total respiratory system were observed (P greater than 0.05). Results indicate that increases in the work of breathing are due to a combination of hydrostatic pressure imbalance, increased pulmonary resistance, and reduced end-expiratory total respiratory compliance.</p>","PeriodicalId":76778,"journal":{"name":"Undersea biomedical research","volume":"17 5","pages":"453-67"},"PeriodicalIF":0.0,"publicationDate":"1990-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13370998","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Combined arterial gas embolism and decompression sickness following no-stop dives.","authors":"T S Neuman, A A Bove","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Decompression sickness (DCS) has been clinically classified as Type I (predominantly joint pain) or Type II (predominantly spinal cord lesions). We present 3 cases that are all characterized by severe (Type II) DCS with signs and symptoms of spinal cord injury occurring in conjunction with arterial gas embolism (AGE). We consider the AGE \"minor\" because only 2 of the 3 subjects initially lost consciousness, and in all cases the signs and symptoms of the AGE had essentially resolved within 1 h or by the time recompression therapy began. DCS was resistant to recompression therapy, even though treatment began promptly after the accident in 2 of the 3 cases. None of the cases had a good neurologic outcome and there has been one death. None of the divers exceeded the U.S. Navy \"no-stop\" limits for the depths at which they were diving. We have observed a previously unreported clinical syndrome characterized by severe Type II DCS subsequent to AGE following pressure-time exposures that would normally not be expected to produce DCS. We postulate that AGE may have precipitated or predisposed to this form of DCS.</p>","PeriodicalId":76778,"journal":{"name":"Undersea biomedical research","volume":"17 5","pages":"429-36"},"PeriodicalIF":0.0,"publicationDate":"1990-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13371939","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Cardiovascular changes in anesthetized rats during exposure to 30 bar.","authors":"L E Stuhr, J A Ask, I Tyssebotn","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The effect of exposure to 30 bar (PHe = 29.0 bar, PN2 = 0.8 bar, PO2 = 0.2 bar) on left ventricular pressure, cardiac contractility, heart rate (HR), and arterial pressure was studied in anesthetized rats. During compression there was a progressive increase in maximal left ventricular pressure (LVPmax), maximal velocity of LVP rise (+ dP/dtmax) and fall (- dP/dtmax), systolic pressure (APsys), and pulse pressure (delta AP). The greatest increase in contractility per bar was found between 1 and 5 bar. Immediately after 30 bar was reached, LVPmax (19%), + dP/dtmax (60%), and - dP/dtmax (22%). APsys (19%), and delta AP (43%) were significantly increased from predive values, with an additional increase detected for all these variables after 60 min at 30 bar. An increase in estimated oxygen consumption (work load) of the heart was also found during compression to and at 30 bar. No changes in HR, mean arterial pressure, and end-diastolic pressure were observed during the high-pressure exposure, indicating that the inotropic changes were not due to changes in peripheral hemodynamics.</p>","PeriodicalId":76778,"journal":{"name":"Undersea biomedical research","volume":"17 5","pages":"383-93"},"PeriodicalIF":0.0,"publicationDate":"1990-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13371937","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Effects of breathing-gas pressure on pulmonary function and work capacity during immersion.","authors":"N A Taylor, J B Morrison","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Upright immersion induces respiratory mechanical changes that may impair pulmonary function during hyperbaric exercise. To evaluate this, 10 divers performed an incremental cycling protocol while immersed upright at 1.02 and 6.05 atmospheres absolute (atm abs). Air was supplied at each of two hydrostatic pressures: mouth pressure (Pm: to stimulate a mouth-held demand regulator) and lung centroid pressure (PLC). Subjects perceived air delivery at PLC to be more comfortable at each level of exercise at both absolute pressures (P less than 0.05). At 6.05 atm abs subjects perceived narcosis to be greater for Pm than for PLC air delivery. Hypoventilation was encountered at 6.05 atm abs with PLC air delivery and was further exacerbated when air was delivered at Pm (P less than 0.05). It was concluded that hypoventilation and narcosis are reduced whereas respiratory comfort is increased when air is delivered at PLC. This change is possibly due to improved pulmonary mechanics accompanying PLC air supply pressure.</p>","PeriodicalId":76778,"journal":{"name":"Undersea biomedical research","volume":"17 5","pages":"413-28"},"PeriodicalIF":0.0,"publicationDate":"1990-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13371938","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Effect of hydration state on renal responses to head-out water immersion in conscious dogs.","authors":"J L Sondeen, S K Hong, J R Claybaugh, J A Krasney","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Renal responses to head-out water immersion (WI) (37 degrees C, WI 100 min) were studied in conscious, instrumented dogs during volume repletion (R), when all blood and urine losses were replaced with 0.9% NaCl, or without volume repletion (NR), to determine the influence of hydration state. The lithium clearance method was used to estimate the locus of the renal tubular fractional sodium excretion (FENa) responses. WI in the R condition increased urine flow (V) from 0.9 (+/- 0.1 SE) to 4.2 (+/- 0.6) ml/min and FENa from 0.7 (+/- 0.1) to 3.2 (+/- 0.8)%. Fractional proximal sodium reabsorption (FPRNa) decreased from 0.82 (+/- 0.03) to 0.69 (+/- 0.1)% and fractional distal sodium reabsorption decreased from 0.96 (+/- 0.01) to 0.88 (+/- 0.04)%. By comparison, WI in the NR condition elicited smaller increments in V and FENa, no change in FPRNa and a significant decrease of FDRNa from 0.97 (+/- 0.01) to 0.93 (+/- 0.01). Although there were quantitative differences in the renal responses in the R and NR conditions, there were similar increments in both arterial and atrial pressures as well as plasma atrial natriuretic peptide concentration; plasma arginine vasopressin was unaltered in either situation, and plasma renin activity was depressed in both conditions. Since plasma protein concentration was significantly lower during the R condition, the differing renal responses are probably related to differing levels of volume expansion in the R vs. NR condition.</p>","PeriodicalId":76778,"journal":{"name":"Undersea biomedical research","volume":"17 5","pages":"395-411"},"PeriodicalIF":0.0,"publicationDate":"1990-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13299623","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
R S Lillo, J W Morris, J M Caldwell, D M Balk, E T Flynn
{"title":"Atmosphere contamination following repainting of a human hyperbaric chamber complex.","authors":"R S Lillo, J W Morris, J M Caldwell, D M Balk, E T Flynn","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The Naval Medical Research Institute currently conducts hyperbaric research in a Man-Rated Chamber Complex (MRCC) originally installed in 1977. Significant engineering alterations to the MRCC and rusting of some of its interior sections necessitated repainting, which was completed in 1988. Great care was taken in selecting an appropriate paint (polyamide epoxy) and in ensuring correct application and curing procedures. Only very low levels of hydrocarbons were found in the MRCC atmosphere before initial pressurization after painting and curing. After pressurization, however, significant chemical contamination was found. The primary contaminants were aromatic hydrocarbons: xylenes (which were a major component of both the primer and topcoat paint) and ethyl benzene. The role that pressure played in stimulating off-gassing from the paint is not clear; the off-gassing rate was observed to be similar over a large range in chamber pressures from 1.6 to 31.0 atm abs. Scrubbing the chamber atmosphere with the chemical absorbent Purafil was effective in removing the contaminants. Contamination has been observed to slowly decline with chamber use and is expected to continue to improve with time. However, this contamination experience emphasizes the need for a high precision gas analysis program at any diving facility to ensure the safety of the breathing gas and chamber atmosphere.</p>","PeriodicalId":76778,"journal":{"name":"Undersea biomedical research","volume":"17 5","pages":"437-51"},"PeriodicalIF":0.0,"publicationDate":"1990-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13370997","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}