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J S Wasser

Publications and source records attributed to J S Wasser.

At least 19 recordsLinked to original sources
PubMed2001

Activation of heat-shock factor by stretch-activated channels in rat hearts.

BACKGROUND: Previously, we have observed that the isolated, erythrocyte-perfused rabbit heart has increased levels of heat-shock protein (HSP) 72 after a mild mechanical stress. We hypothesized that stretch-activated ion channels (SACs) mediated this increase. Methods and Results-- To test this hypothesis, we subjected isolated, perfused rat hearts to mechanical stretch. Gel mobility shift assay showed that heat-shock factor (HSF) was activated in hearts with mechanical stretch, but not in controls. Supershift experiments demonstrated that HSF1 was the transcription factor. Northern blots revealed the concomitant increase in HSP72 mRNA in stretched rat hearts. In a separate set of experiments, gadolinium, an inhibitor of SACs, was added to the perfusate. Gadolinium inhibited the activation of HSF and decreased HSP72 mRNA level. Because gadolinium can inhibit both SACs and L-type calcium channels, we perfused a group of hearts with diltiazem, a specific L-type calcium channel blocker, to eliminate the involvement of L-type calcium channels. Diltiazem failed to inhibit the activation of HSF. CONCLUSIONS: Stretch in the rat heart results in activation of HSF1 and an increase in HSP72 mRNA through SACs. This represents a novel mechanism of HSF activation and may be an important cardiac signaling pathway for hemodynamic stress.

Animals↗
PubMed2001

Activation of the heat shock response: relationship to energy metabolites. A (31)P NMR study in rat hearts.

Heat shock factor (HSF), the transcription factor for the heat shock proteins, is activated by cardiac ischemia, but the mechanism of activation is unknown. Ischemia is accompanied by changes in the energy state and acid-base conditions. We hypothesized that decreased ATP and/or intracellular pH (pH(i)) might activate HSF. To test this hypothesis, we perfused rat hearts within an NMR spectrometer. NMR data showed that after 6.5, 13, and 20 min of ischemia, ATP dropped to 62.7, 23.1, and 6.9% of the control level, and pH(i) was 6.16, 5.94, and 5.79, respectively. Reperfusion after ischemia partially restored ATP levels, and this was associated with greater activation of HSF1. HSF1 was also activated after 6.5 min of ischemia. Activation of HSF1 was less after 13 min of ischemia and barely detectable after 20 min of ischemia. In conclusion, 1) a moderate decrease in intracellular ATP correlates with activation of HSF1 in the heart; and 2) a severe depletion in ATP correlates with an attenuation in HSF1 activation, and the restoration of ATP leads to greater activation of HSF1, suggesting that a critical ATP level is required for activation of HSF1.

Adenosine Triphosphate↗
PubMed2000

Simultaneous optical and nuclear magnetic resonance spectroscopy for monitoring cardiac energetics in vivo.

There are a number of applications in which it is useful to simultaneously collect data from what are traditionally separate instrumentation modalities. In particular, in vivo physiological investigations in which data from parallel experiments must be correlated would benefit from simultaneous data collection through 1) elimination of subject variability, 2) elimination of treatment variability, and 3) a reduction in the number of animal preparations required. Here we describe the simultaneous collection of fluo-3 optical fluorescence and 31P nuclear magnetic resonance (NMR) spectra to measure intracellular calcium levels and high-energy phosphate metabolism, respectively, in vivo. This work is part of ongoing research into the profound anoxia tolerance exhibited by the hearts of certain turtle species. An NMR compatible optical fluorescence spectrometer was constructed and tested. In the 31-cm bore of a 2 T superconducting magnet, NMR and optical spectra were collected every 10-15 min from the in situ, in vivo hearts of anesthetized turtle subjects prior to and during one to three hours of anoxia. It was found that while PCr stores became significantly depleted during anoxia, beta-adenosine triphosphate (ATP) levels remained within 20% of control values, and intracellular diastolic calcium levels did not vary by more than 10%. The ability to make simultaneous phosphorus and calcium measurements on a single subject is important to understanding the exact relationship between phosphorus energy state and maintenance of calcium homeostasis.

Adenosine Triphosphate↗
PubMed2000

Expression of heat shock proteins in turtle and mammal hearts: relationship to anoxia tolerance.

Heat shock proteins (HSPs) may play a cardioprotective role during hypoxia or ischemia. We hypothesized that cardiac tissue from hypoxia-tolerant animals might have high levels of specific HSPs. We measured myocardial HSP60 and HSP72/73 in painted and softshell turtles during normoxia and anoxia (12 h) and after recovery (12 or 24 h). We also measured myocardial HSPs in normoxic rats and rabbits. During normoxia, hearts from the most highly anoxia-tolerant species, the painted turtle, expressed the highest levels of HSP60 (22.6+/-2.0 mg/g total protein) followed by softshells (11.5+/-0.8 mg/g), rabbits (6.8+/-0.9 mg/g), and rats (4.5+/-0.5 mg/g). HSP72/73 levels, however, were not significantly different. HSP60 levels in hearts from both painted and softshell turtles did not deviate significantly from control values after either 12 h of anoxia or 12 or 24 h of recovery. The pattern of changes observed in HSP72/73 was quite different in the two turtle species. In painted turtles anoxia induced a significant increase in myocardial HSP72/73 (from 2.8+/-0.1 mg/g normoxic to 3.9+/-0.2 mg/g anoxic, P<0.05). By 12 h of recovery, HSP72/73 had returned to control levels (2.7+/-0.1 mg/g) and remained there through 24 h (2.6+/-0.2 mg/g). In softshell turtles, HSP72/73 decreased significantly after 12 h of anoxia (from 2.4+/-0.4 mg/g normoxic to 1.3+/-0.2 mg/g anoxic, P<0.05). HSP72/73 levels were still slightly below control after 12 h of recovery (2.1+/-0.1 mg/g) and then rose to significantly above control after 24 h of recovery (4.1+/-0.7 mg/g, P<0.05). We also conclude that anoxia-tolerant and anoxia-sensitive turtles exhibit different patterns of myocardial HSP changes during anoxia and recovery. Whether these changes correlate with their relative degrees of anoxia tolerance remains to be determined.

Air↗
PubMed2000

Brain high energy phosphate responses to alcohol exposure in neonatal rats: an in vivo 31P-NMR study.

BACKGROUND: The mechanisms that mediate fetal brain injury which results from maternal alcohol consumption are not well understood. Although fetal hypoxia is a popularly proposed mechanism, it has been difficult to assess brain oxygenation in vivo. We measured intracellular high energy phosphate concentrations and estimated intracellular pH (pHi) in brains of unanesthetized neonatal rat pups by using in vivo 31P-NMR spectroscopy. We reasoned that decreases in brain oxygenation sufficient to result in brain injury would also reduce high energy phosphates and pHi. METHODS: On postnatal day 4, before alcohol administration, pups were placed into a 20 mm diameter NMR probe, their heads were positioned carefully in the center of the 31P detection coil, and spectra were collected over 20 min. Animals were then fed diet with or without 4.5 g/kg of ethanol in two (in succession) of 12 daily feedings via artificial rearing methods. A second spectrum was collected at 90 min after the beginning of the second alcohol feeding, at the time that coincided with the peak blood alcohol concentration (BAC). Identical feedings were performed daily until day 9, when pre- and postfeeding spectra were again obtained. Positive control groups were fed control diet and were studied in atmospheres of 5% oxygen, 95% nitrogen or 0% oxygen, 100% nitrogen. RESULTS: Phosphocreatine (PCr), beta-adenosine triphosphate (ATP), and pHi decreased and inorganic phosphate (Pi) increased in day 4 animals subjected to 0% oxygen (20 min) compared with pretreatment and all other treatment groups. Day 9 animals did not tolerate these conditions. There were no significant changes in response to 5% oxygen on day 4, but Pi increased and beta-ATP decreased compared with pretreatment values and compared with alcohol and control groups on day 9. There were no changes in PCr, beta-ATP, or pHi in response to alcohol treatment at either age. PCr was significantly increased in the alcohol and 5% oxygen groups and apparently increased in the control group on day 9 compared with day 4, most likely due to increases in cranial muscle mass within the NMR coil. CONCLUSIONS: We conclude that acute alcohol exposure that results in peak BACs of 315 mg/dl does not alter brain high energy phosphate concentrations or pHi in neonatal rat pups, although these BACs are known to result in significant brain injury. These findings do not support hypoxia as a mechanism of alcohol-mediated brain injury during the third trimester equivalent in the rat pup model.

Adenosine Triphosphate↗
PubMed1999

Biomedical device design discovery team approach to teaching physiology to undergraduate bioengineering students.

Teaching effectiveness is enhanced by generating student enthusiasm, by using active learning techniques, and by convincing students of the value of acquiring knowledge in the area of study. We have employed a technique to teach physiology to bioengineering students that couples students' enthusiasm for their chosen field, bioengineering, with an active learning process in which students are asked to design a biomedical device to enhance, replace, or create a new cellular or organ system function. Each assignment is designed with specific constraints that serve to direct students' attention to specific areas of study and that require students to create original designs. Preventing students from using existing designs spurred student invention and enthusiasm for the projects. Students were divided into groups or "design discovery teams" as might be done in a biomedical device industry setting. Students then researched the physiological issues that would need to be addressed to produce an acceptable design. Groups met with faculty to brainstorm and to obtain approval for their general design concepts before proceeding. Students then presented their designs to the instructors in a structured, written outline form and to the class as a 10-minute oral presentation. Grades were based on the outline, oral presentation, and peer evaluations (group members anonymously rated contributions of other members of their team). We believe that this approach succeeded in generating enthusiasm for learning physiology by allowing the students to think creatively in their chosen field of study and that it has resulted in students developing a more thorough understanding of difficult physiological concepts than would have been achieved with a traditional didactic lecture approach.

Animals↗
PubMed1997

Effects of dry season dormancy on oxygen uptake, heart rate, and blood pressures in the toad, Bufo paracnemis.

The cardiodynamic consequences of dry season dormancy in ectothermic vertebrates is not well known. Our hypothesis was that dormancy would reduce cardiac activity. We therefore determined oxygen uptake and cardiovascular function in aestivating toads, Bufo paracnemis, native to São Paulo State, Brazil. Specimens were collected and kept in the laboratory under controlled temperature and light regimes. We compared oxygen uptake, heart rate, blood pressure, rate-pressure product (RPP), and blood gases in toads during aestivation (dry winter season) and their early active season (spring). Oxygen uptake of winter toads at 25 degrees C was considerably lower than that of spring toads (winter: 24.0 +/- 1.8 ml/(kgh); early spring: 44.4 +/- 5.1 ml/(kgh); mean +/- SE; same in the following). A seasonal dichotomy was also observed at 15 degrees C although the differences was less pronounced (15.8 +/- 1.8 ml/(kgh) winter; 23 +/- 2.1 ml/(kgh) early spring). Chronic arterial cannulation permitted measurements of cardiodynamic variables without any undesired change in VO2. Heart rates of winter toads were significantly lower than those of early spring animals at both experimental temperatures (25 degrees C: winter 25 +/- 1.4 beats/min.; early spring: 35.2 +/- 5.1 beats/min. 15 degrees C: winter 15, 4 +/- 1.8 beats/min.; early spring: 23.9 +/- 2.1 beats/min). Systemic, diastolic and mean arterial pressures decreased slightly but not significantly during aestivation. We conclude that: (1) Bufo paracnemis downregulates metabolic rate during the dry season and (2) heart rate is also downregulated with little change of blood pressure. While the energetics of these responses are probably beneficial for survival during aestivation, the underlying biochemical mechanisms remain obscure.

Animals↗
PubMed1997

Effects of anoxia on intracellular free Ca2+ in isolated cardiomyocytes from turtles.

One of the most important negative consequences of hypoxic stress in the mammalian myocardium is a breakdown in intracellular calcium homeostasis. This study examines the effects of anoxic stress on intracellular calcium regulation in isolated ventricular myocytes from a hypoxia tolerant vertebrate, the western painted turtle (Chrysemys picta bellii). Isolated calcium tolerant cardiomyocytes from turtle hearts were mounted on a glass cover slip that formed the bottom of a sealed, Plexiglas perfusion chamber. Free [Ca2+]i (determined by FURA2 fluorescence) in isolated turtle cardiomyocytes averaged 31.7 +/- 3.2 nM after 30 min of normoxic perfusion (20 degrees C, pHc = 7.77). This value is on the low end of the published range for mammalian cardiomyocytes. Perfusion with anoxic Ringer equilibrated with 3% CO2, resulted in a significant increase in free [Ca2+]i to 941 +/- 494.6 nM after 60 min. Increasing the CO2 in the perfusion solution to 5% or 6% blunted this rise (peak levels after 60 min of anoxia were 420.5 +/- 176.0 nM and 393.8 +/- 132.8 nM, respectively). A further increase to 8% CO2 increased the maximal value for free [Ca2+]i to 610.9 +/- 297.5 nM. In eight cells from the 5% CO2 protocol in which [Ca2+]i was monitored during recovery, reperfusion with normoxic Ringer rapidly lowered intracellular calcium to 92.8 +/- 9.7 nM within 15 min. Anoxia at relatively high extracellular (and hence intracellular) pH results in an increase in free [Ca2+]i comparable in magnitude and time course to that seen in some mammalian cardiomyocyte preparations. Perfusion of anoxic myocytes with Ringer equilibrated with either 5% or 6% CO2 blunted this increase in intracellular calcium, possibly an example of the pH paradox effect. A more severe combination of respiratory acidosis and anoxia (8% CO2) removed this protective effect.

Animals↗
PubMed1997

31P-NMR determinations of cytosolic phosphodiesters in turtle hearts.

As part of our ongoing research on cardiac hypoxia tolerance we have conducted 31P nuclear magnetic resonance (NMR) studies of isolated, perfused, working hearts from freshwater turtles, animals that are well known for their ability to tolerate prolonged periods of anoxia. A striking feature of turtle heart spectra is an extremely high concentration of NMR visible phosphodiesters (PDEs). Cardiac spectra from mammals, on the other hand, typically exhibit only a small resonance in the PDE region. Our aim in this study was to compare myocardial PDE profiles between the highly hypoxia tolerant western painted turtle (Chrysemys picta bellii) and the relatively hypoxia sensitive softshelled turtle (Trionyx spinifer) in order to begin to rest the hypothesis that high constitutive levels of cytosolic PDEs may play a role in conferring hypoxia and ischemia tolerance on the myocardium. We also collected 31P-NMR spectra of PCA extracts of tissue from these species and from Kemp's ridley sea turtles (Lepidochelys kempi), as well as spectra from isolated hearts and PCA extracts of red-eared sliders (Trachemys [formerly Pseudemys] scripta]). Total NMR visible phosphodiesters make up 24 +/- 8.6% of the total NMR visible phosphorus in Chrysemys hearts, 20.7 +/- 5.9% in Trachemys hearts, but only 12.2 +/- 5.1% in Trionyx hearts (P < 0.05). We have identified three distinct PDEs in turtle hearts: glycerophosphorylcholine (GPC); glycerophosphorylethanolamine (GPE); and serine ethanolamine phosphodiester (SEP). SEP is the dominant compound in Chrysemys and Trachemys (79.3 +/- 10.2% and 84.7 +/- 3.7% of total PDE, respectively), while GPC is most abundant in Trionyx (74.0 +/- 4.3% of total PDE) and Lepidochelys (not quantitated). The function of this class of compounds is unclear but it has been suggested that cytosolic PDEs may function as lysophospholipase inhibitors, a role that would decrease the rate of membrane phospholipid turnover. Our comparative data suggest that cytosolic PDEs could play a role in phospholipid sparing during anoxic or ischemic stress in turtles but a direct test of this hypothesis awaits future experimentation.

Animals↗
PubMed1997

In vitro tolerance to anoxia and ischemia in isolated hearts from hypoxia sensitive and hypoxia tolerant turtles.

Although freshwater turtles as a group are highly anoxia tolerant, dramatic interspecific differences in the degree of anoxia tolerance have been demonstrated in vivo. Painted turtles (Chrysemys picta bellii) appear to be the most hypoxia-tolerant species thus far studied, while softshelled turtles (Trionyx spinifer) are the most hypoxia-sensitive. We have assumed that this dichotomy persists in vitro but have not, until now, directly tested this assumption. We therefore, directly compared the responses of isolated, perfused, working hearts from these two species to either 240 min of anoxia, 90 min of global ischemia, or 240 min of global ischemia followed by reoxygenation/reperfusion. Isolated hearts were perfused at 20 degrees C and monitored continuously for phosphocreatine (PCr), adenosine triphosphate (ATP), inorganic phosphate (Pi), and intracellular pH (pHi) by 31P-nuclear magnetic resonance spectroscopy as well as for ventricular developed pressure and heart rate. Contrary to our expectations, we observed few significant differences in any of these parameters between painted and softshelled turtle hearts. Hearts from both species tolerated 240 min of anoxia equally well and both restored PCr, pHi, and Pi contents to control levels during reoxygenation. We did observe some significant interspecific differences in the 90 min (pHi and Pi) and 240 min (PCr) ischemia protocols although these seemed to suggest that Trionyx hearts might be more tolerant to these stresses than Chrysemys hearts. We conclude that: (a) the observed in vivo differences in anoxia tolerance between painted and softshelled turtles must either be due to differences in organ metabolism in organs other than the heart (e.g., brain) or to some integrative physiologic differences between the species; and (b) isolated hearts from a species known to be relatively anoxia sensitive in vivo can exhibit an apparent high degree of anoxia and ischemia tolerance in vitro.

Adenosine Triphosphate↗
PubMed1995

The effect of prolonged anoxia at 3 degrees C on tissue high energy phosphates and phosphodiesters in turtles: a 31P-NMR study.

Selected tissues (skeletal muscle, heart ventrical, and liver), sampled from turtles (Chrysemys picta bellii) at 3 degrees C either under normoxic conditions or after 12 weeks of anoxic submergence were quantitatively analysed for intracellular pH and phosphorus metabolites using 31P-NMR. Plasma was tested for osmolality and for the concentrations of lactate, calcium, and magnesium to confirm anoxic stress. We hypothesized that, in the anoxic animals, tissue ATP levels would be maintained and that the increased osmolality of the body fluids of anoxic turtles would be accounted for by a corresponding increase in the concentrations of phosphodiesters. The responses observed differed among the three tissues. In muscle, ATP was unchanged by anoxia but phosphocreatine was reduced by 80%; in heart, both ATP and phosphocreatine fell by 35-40%. The reduction in phosphocreatine in heart tissue at 3 degrees C was similar to that observed in isolated, perfused working hearts from turtles maintained at 20 degrees C but no decrease in ATP occurred in the latter tissues. In liver, although analyses of several specimens were confounded by line-broadening, neither ATP nor phosphocreatine was detectable in anoxic samples. Phosphosdiesters were detected in amounts sufficient to account for 30% of normoxic cell osmotic concentration in heart and 11% and 12% in liver and muscle, respectively. The phosphodiester levels did not change in anoxia. Heart ventricular phosphodiester levels in turtles at 3 degrees C were significantly higher than those determined for whole hearts from turtles at 20 degrees C.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed1993

Maintenance of high extracellular pH does not influence cell pH or metabolism in submerged anoxic bullfrogs.

We compared extracellular and intracellular acid-base states in paralyzed bullfrogs subjected to 4 h of anoxic submergence at 15 degrees C with or without maintenance of extracellular pH at preanoxic levels by bicarbonate infusion. We also assessed anaerobic metabolism under these conditions by measuring tissue lactate and glycogen concentrations in liver, heart, and skeletal muscle. Although bicarbonate infusion resulted in a significantly higher arterial blood pH (pHe) than saline infusion, intracellular pH (pHi) of heart and skeletal muscle, as determined by the DMO equilibration technique, were not significantly different after 4 h of anoxia. We were also unable to demonstrate any differences in anaerobic metabolic rate, since both tissue lactate accumulation and glycogen depletion were identical in bicarbonate- and saline-infused frogs in the tissues studied. We conclude that (1) alterations in the extracellular acid-base state by bicarbonate infusion are not necessarily reflected in the intracellular compartment, perhaps due to powerful intracellular buffering processes, and (2) maintenance of an alkaline extracellular pH during anoxia in bullfrogs does not influence the anaerobic metabolic rate. We could not, however, rule out a possible role for intracellular pH in regulating anaerobic metabolism during anoxia in frogs.

Anaerobiosis↗
PubMed1992

Metabolic and cardiodynamic responses of isolated turtle hearts to ischemia and reperfusion.

We used 31P and 1H nuclear magnetic resonance spectroscopy to measure intracellular pH, high energy phosphates, and lactate levels in hearts of turtles (Chrysemys picta bellii) subjected to 1.5 h of global ischemia followed by reperfusion. We simultaneously monitored maximum ventricular developed pressure (Pmax), maximal rate of pressure development (dP/dtmax), rate-pressure product (RPP), cardiac output, and heart rate and also measured lactate efflux from the hearts during reperfusion. Our goal was to test the hypothesis that turtle hearts would prove tolerant of prolonged global ischemia at 20 degrees C and would recover completely on reperfusion without any indication of ischemia-or reperfusion-related injury. The 1.5 h of ischemia resulted in decreases in phosphocreatine and ATP to 31.4 +/- 2.8 and 87.3 +/- 6.3% of control, respectively, while Pi rose to 236.6 +/- 26.3%. Intracellular pH decreased during this period from 7.38 +/- 0.02 to 6.87 +/- 0.04. Most of these changes occurred during the first 30 min. Tissue lactate rose during 1.5 h of ischemia from approximately 1.5 to 22.3 mumol/g wet tissue wt. However, the rate of lactate production was much higher during the first 21 min of ischemia (0.41 mumol.g-1.min-1) than during the remaining 70 min (0.10 mumol.g-1.min-1). With the onset of ischemia, Pmax, dP/dtmax, RPP, and heart rate all decreased dramatically with roughly the same time course as the changes in high-energy phosphates and intracellular pH. On reperfusion, turtle hearts rapidly restored high-energy phosphates, intracellular pH, lactate, and cardiodynamics to control levels, usually within 15-30 min, with no evidence of reperfusion injury.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Extracellular and intracellular acid-base effects of submergence anoxia and nitrogen breathing in turtles.

We compared extracellular and intracellular acid-base state in turtles (Chrysemys picta bellii) subjected to anoxic submergence to turtles made anoxic by N2-breathing. Measurements made on control animals and on animals after 1, 2, 4, or 6 h of anoxia included blood pH, PO2, PCO2, and lactate as well as liver, heart, skeletal muscle, and brain pHi (using DMO equilibration), lactate, and glycogen concentrations. We hypothesized that the anaerobic metabolic rate of submerged turtles would be depressed by the more severe extra- and intracellular acidosis, and that this would be indicated by reduced lactate accumulation and glycogen depletion. Submerged turtles became extremely acidemic due to a combined metabolic and respiratory acidosis and had significantly lower arterial pH than N2-breathing animals (6.98 and 7.34, respectively, after 6 h). In spite of this disparity in pHa, 6 h pHi values for liver, heart, and brain were similar. Likewise, our data on glycogen depletion and lactate accumulation at h 6 in these tissues suggest no dramatic differences in anaerobic metabolic rate. While skeletal muscle pHi was somewhat lower at h 6 in the submerged group (6.73 vs 6.91 for N2-breathers), we observed no differences in either glycogen depletion or lactate accumulation in this tissue between our two treatments. Thus, at h 6, in spite of a 0.37 pH unit difference in pHa and a nearly 70 mm Hg difference in arterial and presumably cytosolic PCO2, pHi and tissue lactate and glycogen concentrations were similar. These results can be explained if the in vivo intracellular buffer values (beta) of turtle tissues are very high. We conclude that extracellular acid-base state is not necessarily reflected intracellularly in vivo in turtles and care must be taken in extrapolating from one compartment to another when attempting to make inferences about metabolic depression or acid-base regulation in this species.

Acid-Base Equilibrium↗
PubMed1991

Effects of anoxia and graded acidosis on the levels of circulating catecholamines in turtles.

We measured circulating levels of catecholamines in painted turtles subjected to anoxia with different degrees of concomitant acidosis at 20 degrees C and in turtles subjected to long-term submergence at 3 and 10 degrees C. Blood levels of both epinephrine (E) and norepinephrine (NE) increased during N2-breathing, N2/CO2 breathing and submergence, with NE generally being present in higher concentrations than E. During submergence at 20 degrees C, anoxic turtles experienced an extreme acidosis and NE levels exceeded 18,000 pg/ml. The greater the degree of acidosis in anoxic turtles the higher were the levels of plasma NE (log [NE; pg/ml] = 1.640 x pHa + 15.776, r = -0.826). Elevation of plasma E under anoxic conditions was more modest and the correlation between plasma E and pHa was less pronounced (log [E; pg/ml] = -0.329 x pHa + 6.069, r = -0.285). Submergence at lower temperatures also resulted in increases in plasma levels of NE, but while plasma E generally increased during anoxia, this elevation was less dramatic than that observed for NE. Exposure of turtles to either mild (6.5% CO2) or severe (14.5% CO2) normoxic hypercapnia resulted in no increase in E and only modest increases in NE. Upon resumption of air-breathing in all of the 20 degrees C protocols, turtles rapidly restored E and NE to control levels. The function of elevated plasma catecholamines during anoxia and acidemia in turtles is unknown but may be important in stimulating respiratory and cardiovascular recovery once air-breathing is resumed. Catecholamines may also play a role in mediating the rise in blood glucose we observed in this study, which may be an important factor in maintaining tissue viability during anoxic stress.

Acidosis↗
PubMed1991

31P-NMR study of normoxic and anoxic perfused turtle heart during graded CO2 and lactic acidosis.

We studied the effects of graded acidosis (both CO2 and lactic acid) and anoxia on intracellular pH (pHi) regulation, high-energy phosphates, and mechanical function of isolated perfused hearts of the turtle (Chrysemys picta bellii) at 20 degrees C using 31P-nuclear magnetic resonance (NMR) spectroscopy. During CO2 acidosis, anoxia had no effect on apparent nonbicarbonate buffer value (d[HCO3-]/dpHi = 71 and 89 mM/pH in normoxia and anoxia, respectively) or on pHi regulation (dpHi/dpHe = 0.52 and 0.43 in normoxia and anoxia, respectively, where pHe is extracellular pH). During normoxic lactic acidosis, dpHi/dpHe was similar to the values observed in CO2 acidosis and averaged 0.55 overall. During anoxic lactic acidosis, however, similar regulation occurred over only a narrow range of pHe, and then dpHi/dpHe increased to greater than 1.0 at pHe less than 7.1. Creatine phosphate (CP), calculated as the area of the NMR peak, fell more in response to normoxic CO2 acidosis than to normoxic lactic acidosis; in anoxia, the fall in CP was further increased but to similar extreme levels (10-20% of control) in both acid perfusions. Cardiac output and maximum rate of pressure development each fell during acidosis in similar fashion in all protocols, and the responses were similar in normoxic and anoxic hearts. Heart rate, in contrast, decreased during acidosis, but this effect was more pronounced when hearts were anoxic. We conclude that the effect of acidosis on cardiac function can depend on the type of acidosis imposed. Based on the heart's insensitivity to anoxia alone, we suggest that anoxia may normally depress function indirectly via its effect on intracellular acid-base state.

Acidosis, Lactic↗