RPE drift during cycling in 18 degrees C vs 30 degrees C wet bulb globe temperature.

AIM: The potential influence of a hotter vs cooler environment on ratings of perceived exertion (RPE) estimations during longer duration exercise is not well-understood. This study compared overall and differentiated RPEs during cycling in 18 degrees C vs 30 degrees C wet bulb globe temperature (WBGT). METHODS: Male volunteers (n=16) completed a maximal cycling trial (60 rev . min(-1), 25 Watts . min(-1)) to determine VO(2) max and ventilatory threshold (VT) before completing 2 (counterbalanced) longer duration cycling trials. At 30 degrees C WBGT (30C) and 18 degrees C WBGT (18C), subjects cycled 60 min (60 rev . min(-1), 90% individualized VT). Heart rate (HR, b . min(-1)) and rectal temperature (Tre, degrees C) were recorded every 5 min with corresponding RPE-overall (RPE-O), RPE-legs (RPE-L) and RPE-chest (RPE-C) estimations. RESULTS: HR was not significantly different at 5 min but was greater (P<0.05) for 30C at all other time points. During 30C, Tre was significantly greater (25, 30, 35, 40, 45, 50, 55 and 60 min), RPE-O was significantly greater (5, 40, 45, 50, 55 and 60 min), RPE-L was significantly greater (55 and 60 min) and RPE-C was significantly greater (35, 40, 45, 50, 55 and 60 min). CONCLUSIONS: Greater cardiovascular (HR) and thermal (Tre) strain partially explain greater perceptual ratings during 30C. Discernible RPE differences resulted mid-way through 60 min cycling with minimal differences initially. Results suggest RPEs are magnified in a 30 degrees C (vs 18 degrees C) environment beyond 30 min duration. Additionally, a 30 degrees C environment resulted in a less pronounced impact on RPE-L (vs RPE-C and RPE-O).

Influence of aerobic fitness on ratings of perceived exertion during graded and extended duration cycling.

AIM: Ratings of perceived exertion (RPE) have been shown similar across subjects of varying fitness when estimations are made at relative physiological criteria. Because few studies have investigated the influence of fitness during longer duration bouts, the current investigation compared overall exertion (RPE-O), leg exertion (RPE-L) and breathing/chest exertion (RPE-C) between aerobically fit and unfit subjects. METHODS: Aerobically fit (61.6+/-2.5 mL . kg . min(-1)) (n=7) and unfit (41.8+/-6.3 mL . kg . min(-1)) (n=6) males completed a maximal bike test and then cycled for 60 min at approximately 90% of individualized ventilatory threshold (VT) (V(E)/VO(2) vs V(E)/VCO(2)). Heart rate (HR, b . min(-1)), rectal temperature (Tre, degrees C) and RPE estimations were collected during graded testing every 2 min and every 10 min during 60 min bouts. RESULTS: During graded testing, RPE estimations at VT were not significantly different between groups. During 60 min cycling, HR and Tre were not significantly different between groups. Also, there were no significant differences for HR increase (HR 60 min HR 5 min) or Tre increase (Tre 60 min Tre 5 min). Interactions between groups were; RPE-O (P=0.09), RPE-L (P=0.06) and RPE-C (P=0.19). Analyses suggest groups experienced similar relative cardiovascular (HR) and thermal (Tre) strain. CONCLUSIONS: Although RPE responses between groups were similar at 10, 20 and 30 min, RPE drift was magnified in aerobically unfit subjects (vs aerobically fit subjects) beyond the 30 min point. Contrary to previous studies suggesting aerobic fitness does not influence RPE, current results show lower aerobic fitness magnifies RPE at individualized relative intensities when cycling extends beyond 30 min.

Sweat lactate response during cycling at 30 degrees C and 18 degrees C WBGT.

Sweat lactate reflects eccrine gland metabolism. However, the metabolic tendencies of eccrine glands in a hot versus thermoneutral environment are not well understood. Sixteen male volunteers completed a maximal cycling trial and two 60-min cycling trials [30 degrees C = 30 +/- 1 degrees C and 18 degrees C = 18 +/- 1 degrees C wet bulb globe temperature (WBGT)]. The participants were requested to maintain a cadence of 60 rev min(-1) with the intensity individualized at approximately 90% of the ventilatory threshold. Sweat samples at 10, 20, 30, 40, 50 and 60 min were analysed for lactate concentration. Sweat rate at 30 degrees C (1380 +/- 325 ml x h(-1)) was significantly greater (P < 0.05) than at 18 degrees C (632 +/- 311 ml x h(-1)). Sweat lactate concentration was significantly greater (P < 0.05) at each time point during the 18 degrees C trial, with values between trials tending to converge across time. During the 30 degrees C trial, both heart rate (20, 30, 40, 50 and 60 min) and rectal temperature (30, 40, 50 and 60 min) were significantly higher than in the 18 degrees C trial. Higher sweat lactate concentrations coupled with lower sweat rates may indicate a greater relative contribution of oxygen-independent metabolism within eccrine glands during exercise at 18 degrees C. Decreases in sweat lactate concentration across time suggest either greater dilution due to greater sweat volume or increased reliance on aerobic metabolism within eccrine glands. The convergence of lactate concentrations between trials may indicate that time-dependent modifications in sweat gland metabolism occur at different rates contingent partially on environmental conditions.

Sweat lactate response between males with high and low aerobic fitness.

Sweat lactate indirectly reflects eccrine gland metabolism. However the potential influence of aerobic fitness on sweat lactate is not well-understood. Six males with high aerobic fitness [peak oxygen consumption ( VO(2)peak): 61.6 (2.5) ml.kg(-1).min(-1)] and seven males with low aerobic fitness [ VO(2)peak: 41.8 (6.4) ml.kg(-1).min(-1)] completed a maximal exertion cycling trial followed on a different day by 60 min of cycling (60 rev.min(-1)) in a 30 degrees C wet bulb globe temperature environment. Intensity was individualized at 90% of the ventilatory threshold ( V(E)/ VO(2) increase with no concurrent V(E)/ VCO(2) increase). Sweat samples were collected from the lumbar region every 10 min and analyzed for lactate concentration. Sweat rate (SR) was significantly greater ( p<0.05) for subjects with a high [1445 (254) ml.h(-1)] versus a low [1056 (261) ml.h(-1)] fitness level. Also, estimated total lactate excretion (SRxmean sweat lactate concentration) was marginally greater ( p=0.2) in highly fit males. However, repeated measures ANOVA showed no significant differences ( p>0.05) between groups for sweat lactate concentration at any time point. Current results show highly fit (vs. low fitness level) males have a greater sweat rate which is consistent with previous literature. However aerobic fitness and subsequent variations in SR do not appear to influence sweat lactate concentrations in males.

Psychosocial interventions for cancer: review and analysis using a three-tiered outcomes model.

This study describes a three-tiered measurement model for psychosocial interventions with cancer patients and compares this model to extant measurement strategies. Progress has been made toward demonstrating that psychosocial interventions reduce depression, anxiety, functional impairment, and symptoms. However, Chambless and Hollon (1998) note that the literature on psychosocial interventions for cancer fails to meet criteria for establishing treatment "efficacy" and does not address issues of cost-effectiveness. The lack of a timely model of clinical outcomes may be hindering demonstration of efficacy and wider implementation of these interventions. Outcomes assessed by 65 interventions were classified as Global Health Outcomes (medical endpoints, health-related quality of life (HRQOL), or resource utilization), Dimensions of HRQOL (distress, symptoms, functional ability, or interpersonal well-being), or Mechanisms of Action (evaluation of psychological or physiological processes). A total of 28% of reviewed studies assessed Global Outcomes, 82% assessed Dimensions of HRQOL, and 49% assessed Mechanisms of Action. While most studies assessed patients' symptoms and distress, measurements of resource utilization, HRQOL, and interpersonal HRQOL were under-reported. A greater emphasis on treatment costs, quality of life, and mediating/moderating processes associated with improvement in outcomes could inform decisions regarding allocation of health-care resources and lead to more widely available and efficient interventions for patients.

Knowledge about genetic risk for breast cancer and perceptions of genetic testing in a sociodemographically diverse sample.

Informed consent for genetic testing for breast-ovarian cancer susceptibility requires that women understand basic concepts about the inheritance of cancer susceptibility and the benefits and risks associated with genetic testing. Women awaiting routine medical services (N = 220) were surveyed about their knowledge of breast cancer and cancer genetics and their perceptions of genetic testing and personal risk. There were no racial differences in median income or mean level of education. Compared to Caucasian women, African American women knew significantly less about breast cancer and about genetic risk for breast cancer. African American women had different psychological, social, and economic concerns as evidenced by how they weighted the benefits and risks of genetic testing. This study is the first to assess several dimensions of informed consent for genetic testing among a sociodemographically diverse group. The findings should enable health professionals to target the African American and lower-income populations with the appropriate education and counseling.

Endogenous origin of glomerular endothelial and mesangial cells in grafts of embryonic kidneys.

To address origins of glomerular endothelial and mesangial cells in embryonic mammalian kidneys, we established interspecies grafts between rats and mice, in which fetal kidneys were implanted into the anterior eye chamber of adult hosts. After 5-7 days, hosts bearing grafts received intravenous injections with species-specific monoclonal antibodies (MAbs) to matrix components. In all cases, glomerular basement membranes and mesangial matrices labeled solely for donor-derived matrix. Additionally, microvessel extracellular matrices within grafts were usually of donor origin. To examine directly the origin of glomerular endothelial and mesangial cells, we grafted embryonic gestational days 11-12 (E11-12) kidneys from normal mice into anterior eye chambers of host reverse-orientation splice acceptor 26 mice, which are transgenic animals that express beta-galactosidase in every cell. When grafts were developed for beta-galactosidase activity, host cells were seen in peripheral vessels, but the majority of glomerular endothelial cells were of donor, not host, origin. Where host-derived-endothelial cells were found in glomeruli, donor endothelial cells were present as well. Mesangial cells were always of donor origin. When E11 mouse kidneys were labeled with the endothelial cell-specific Bandeiraea simplicifolia isolectin B4, we determined that endothelial cells are present from the inception of metanephrogenesis. Together, the evidence shows that cells of endogenous kidney origin were almost entirely responsible for development of the glomerular microvasculature in oculo. External vessels from the host, although important for graft maintenance, were not major contributors to the glomerulus.

Influence of graft innervation on neovascularization of embryonic heart tissue grafted in oculo.

We have shown that sympathetic denervation increases subendocardial capillarity during left ventricular hypertrophy. To determine the direct effects of sympathetic innervation on development of the coronary microvasculature in the absence of hemodynamic load, we grafted avascular fetal rat atrial or ventricular tissue into the anterior eye chamber of host rats which had undergone unilateral superior cervical gangliectomies. Innervation to the contralateral eye chamber remained intact. The grafts were harvested 14 or 35 days later, and volume densities of blood vessels, myocytes, and extracellular matrix were determined using standard point-counting techniques on low-power electron micrographs. Graft perfusion and metabolism were assessed simultaneously with thallium-201 and 2-[14C]deoxy-D-glucose uptake, respectively. Innervation did not significantly alter the vascular volume densities or cellular composition of atrial or ventricular tissue compared with noninnervated tissue after either 14 or 35 days in oculo. Similarly, innervation did not significantly alter graft perfusion or metabolism. We conclude that sympathetic innervation does not directly influence the growth of the microvasculature or myocardial metabolism in hemodynamically unloaded, developing heart tissue.

Sympathetic innervation modulates the expression of angiotensin II receptors in embryonic rat heart grafted in oculo.

Angiotensin II acts as a cardiac growth factor, and causes both inotropic and chronotropic changes within the heart. In the present study, we used an in oculo model system to examine the effects of sympathetic innervation on the density of cardiac angiotensin II receptors. Quantitative autoradiography was used to determine the density of angiotensin II receptors in embryonic rat hearts grafted into either sympathetically innervated or sympathetically denervated eye chambers of adult host rats. The density of specific binding to angiotensin II receptors was nearly three-fold higher in sympathetically non-innervated compared to sympathetically innervated heart grafts (30.8 +/- 4.2 v 11.5 +/- 3.2 fmol/mg protein). Specific binding to angiotensin II receptors in heart grafts was displaced by addition of the AT1 receptor antagonist losartan, but not by addition of the AT2 receptor competitor PD 123177. Thus, only AT1 receptors were present in sympathetically innervated and sympathetically non-innervated embryonic rat hearts grafted in oculo. We conclude that changes in sympathetic innervation caused changes in the density of cardiac angiotensin II receptors in the present study. Our results may have implications for growth and function not only during cardiac development, but also during cardiac disease.

Glucocorticoid stimulation interacts with sympathetic innervation to affect cardiac development in oculo.

The effects of chronic glucocorticoid stimulation and sympathetic innervation on myocardium developing in the absence of hemodynamic load were tested by grafting embryonic rat hearts into the anterior eye chamber (in oculo) of adult host rats. Myocardial grafts in control rats with normal hormonal milieu were compared with grafts in rats with chronic glucocorticoid stimulation (dexamethasone 40 micrograms/d) or glucocorticoid receptor type II blockade (RU 38486, 330 micrograms/d). Unilateral superior cervical ganglionectomy of one eye chamber prevented sympathetic innervation to one graft in each host. Two indices of growth, graft size (projected area) and terminal graft weight, were obtained. Dexamethasone treatment increased both size and weight of sympathetically innervated grafts, whereas RU486 treatment significantly decreased graft weight. Conversely, dexamethasone treatment decreased graft size in denervated eye chambers, whereas RU486 treatment had no effect. No differences in graft beating rate were observed among conditions. Sympathetic innervation modulated the effect of glucocorticoids on developing myocardium, suggesting that growth of sympathetically innervated myocardium is enhanced with glucocorticoid exposure, but growth of noninnervated myocardium (e.g. fetal heart) may be compromised by excessive glucocorticoid exposure.

Timing of sympathetic innervation affects growth of myocardium in oculo.

The effects of sympathetic innervation on myocardial growth during the proliferative and hypertrophic phases of cardiac growth were examined with the use of embryonic day 12 whole hearts or ventricles cultured in the anterior eye chamber of adult rats for 8 wk. Sympathetic innervation of whole heart and ventricular grafts was prevented by removing the superior cervical ganglion 1 wk before grafting or was limited to the cellular proliferation phase of growth by superior cervical ganglionectomy after grafts had been in oculo for 4 wk. Grafts in sympathetically innervated eye chambers were significantly larger than grafts in eye chambers denervated at 4 wk and grafts in eye chambers sympathectomized 1 wk before grafting. Innervation of grafts was delayed until 5-6 wk in oculo by crushing the internal carotid nerve. Delayed innervation produced grafts that were as large as those in innervated eye chambers. Together, these experiments suggest that the effects of sympathetic innervation on myocardial growth in oculo are most apparent during the second 4 wk in oculo (i.e., during the cellular enlargement phase of growth.

Rapid conversion from beta-MHC to alpha-MHC mRNA expression in embryonic rat ventricle cultured in oculo is not dependent on thyroid hormone or testosterone.

We investigated the expression of myosin heavy chain (MHC) isoenzymes in embryonic rat ventricles cultured in the anterior eye chamber of an adult rat. In oculo, these grafts beat and mature in an environment where the hormonal milieu can be manipulated. S1 nuclease protection assays were performed on pooled samples of ventricle grafts and compared to normally growing ventricles. At the time of grafting (embryonic day 12, E-12), 23 +/- 4% of the MHC mRNA was of the alpha isoform. While the proportion of ventricular alpha-MHC mRNA did not increase in utero, embryonic ventricles cultured in oculo showed a rapid increase in the relative amount of alpha-MHC mRNA expression (to 84 +/- 10% by 3 days and 86 +/- 5% by 8 days in oculo). alpha-MHC mRNA expression predominated through 8 weeks of culture in oculo, being 76% at 8 weeks in oculo. Additional experiments were performed to determine whether the rapid conversion to alpha-MHC expression resulted from exposure to adult levels of testosterone or thyroid hormone. Reduction of testosterone exposure to nondetectable levels by host orchiectomy did not affect the rapid conversion to alpha-MHC mRNA expression. Exposure to a hypothyroid milieu (i.e., PTU-treated hosts) decreased but did not prevent the conversion from beta- to alpha-MHC mRNA expression at 8 days in oculo; with 83% of the MHC mRNA being of the alpha isoform in hypothyroid hosts compared to 95% in euthyroid hosts. After 8 weeks of culture in hypothyroid hosts, however, alpha-MHC mRNA expression was undetectable in grafted ventricles. These data suggest that E-12 myocardial grafts respond to the hormonal milieu of an adult rat with rapid conversion from beta- to alpha-MHC mRNA expression and that alpha-MHC expression in early developing heart may show reduced sensitivity to downward modulation by a hypothyroid hormonal milieu.

Quantification and localisation of angiotensin II receptors and angiotensin converting enzyme in the developing rat heart.

OBJECTIVE: The aim was to determine the quantification and localisation of angiotensin II receptors and angiotensin converting enzyme (ACE) in the developing rat heart. METHODS: Quantitative autoradiography was used to determine the density of [125I]Sar1-angiotensin II binding to angiotensin II receptors and the density of [125I]351A binding to ACE. RESULTS: Angiotensin II receptors were first detected in the myocardium on embryonic day 14, and reached a maximum density within the first postnatal week. During the perinatal period, the density of angiotensin II receptors was twofold higher in atrial than in ventricular myocardium [27(SEM 7) v 11(1) fmol.mg-1 protein]. By adulthood, however, the density of angiotensin II receptors did not differ between atria and ventricles. A high density of angiotensin II receptors was first detected in the cardiac vasculature on embryonic day 19, with binding density decreasing during development. During the embryonic and early postnatal periods, most of the binding in the cardiac vasculature was to AT2 receptors. ACE was first detected in the myocardium on the day of birth, with the density of binding to ACE increasing during development. On postnatal day 56, the density of binding to ACE was fourfold higher in atrial than in ventricular myocardium [99(22) v 22(4) fmol.mg-1 protein]. A moderate density of binding to ACE was first detected in the cardiac vasculature and heart valves on embryonic day 19, with binding density increasing during development. By adulthood, the density of binding to ACE was 10- to 25-fold higher in the cardiac vasculature and heart valves than in the myocardium. CONCLUSIONS: The density of angiotensin II receptors and the density of binding to ACE are developmentally regulated in the heart. Both AT1 and AT2 receptors were present in the rat heart by late gestation and could, therefore, mediate the effects of angiotensin II on early cardiac growth and development.

Binding of insulin-like growth factors (IGF-I and IGF-II) to the IGF-II/mannose 6-phosphate receptor in fetal rat myocardium.

Previous studies indicate that fetal rat heart tissue contains large amounts of insulin-like growth factor (IGF)-II/mannose 6-phosphate (Man 6-P) receptor messenger RNA, with receptor messenger RNA levels falling by 20 days after birth. We examined the amount of IGF receptor protein in developing rat myocardium. To establish a model in which the role of neural, hormonal, and hemodynamic controls of IGF receptor binding could be studied, we compared binding of IGF-I and IGF-II in normally growing rat atria and ventricles with embryonic day 12 (E-12) atria and ventricles maturing in the anterior eye chamber of an adult host rat. In oculo, embryonic myocardium matures without hemodynamic load or exposure to the fetal hormonal milieu. In fetal rat hearts (E-12 to E-19), both IGF-I and IGF-II intensely bound to a protein with a molecular weight corresponding to the IGF-II/Man 6-P receptor. Receptors were identified using sodium dodecyl sulfate/polyacrylamide gel electrophoresis autoradiography and western blot analysis using Ab3637, a specific polyclonal antibody against rat IGF-II/Man 6-P receptor antigens. This antibody competed for binding of both IGF-I and IGF-II to the band with molecular radius corresponding to 260,000 (reduced). In normally growing rat atria, IGF-I binding to the IGF-II/Man 6-P receptor was similar to ventricular tissue; however, there was significantly greater binding of IGF-II than of IGF-I in both atrial and ventricular tissue. High levels of IGF-II binding to the IGF-II/Man 6-P receptor were observed in both fetal rat atrial and ventricular grafts until 6-8 weeks in oculo. As in normally growing heart tissue, there was similar IGF-I binding to the IGF-II/Man 6-P receptor in atrial grafts compared with ventricular grafts from 2-8 weeks after implantation. For the first 2 weeks after grafting, the ventricular grafts had relatively higher IGF-I binding to the IGF-II/Man 6-P receptor compared with later time points examined. The present data indicate that atrial and ventricular binding of IGFs to the IGF-II/Man 6-P receptor decreases with age, suggesting that decreased IGF binding may be independent of postnatal hemodynamic changes. The decrease is similar in in oculo embryonic rat cardiac grafts and normally growing heart tissue.(ABSTRACT TRUNCATED AT 400 WORDS)

Neovascularization of embryonic rat hearts cultured in oculo closely mimics in utero coronary vessel development.

Coronary neovascularization was studied following grafting of avascular hearts from gestation day-12 (E-12) rat embryos to the anterior eye chambers of adult rats. Volume densities (Vv) of vessels, myocytes, and the extracellular matrix (ECM) after 3-7, 14, 21, and 35 days in oculo were compared to Vv in hearts developing in utero at E-15, E-18, and E-20. The myocardium in both models exhibited similar vessel Vv and capillary developmental stages: (1) clustering of endothelial cells and red blood cells; (2) endothelial cell migration, and (3) tube formation/maturation. The Vv of myocytes increased while that of the ECM remained constant over time. Cross-species grafting utilizing species-specific antibodies determined that the majority, but not all, of the 10-day graft vasculature was of graft origin. Therefore, both de novo growth (vasculogenesis) and sprouting (angiogenesis) were occurring in oculo. Tracer molecules infused into host rats reached the outermost graft vessels only after 10 days in oculo, suggesting a functional link with the host circulation after this time. Thus, we have shown that both models exhibit similar: (1) vascular Vv; (2) shifts in Vv of nonvascular components; (3) stages of neovascularization, and (4) mechanisms of neovascularization. In conclusion, coronary neovascularization occurring in oculo closely mimics normal coronary vessel development.

Possible paracrine facilitation of ventricular growth in oculo by atrial tissue.

Load-independent growth controls were investigated in embryonic atria and ventricles cultured in the anterior eye chamber of adult rats. At embryonic day 12, the mass of atria was half that of ventricles (0.11 vs. 0.24 mg), whereas after 8 wk in oculo, atrial grafts were threefold larger than ventricular grafts (2.26 +/- 0.36 vs. 0.69 +/- 0.16 mg). To examine possible paracrine communication between atria and ventricles, two grafts were cocultured in the same eye chamber. Atrial grafts cocultured with either another atrial graft or a ventricular graft did not differ in projected area or mass from atrial grafts cultured alone. Ventricular grafts cocultured with another ventricular graft did not differ in projected area or mass from ventricular grafts cultured alone. However, ventricular grafts cocultured with an atrial graft grew larger than single ventricular grafts. At 1 wk in oculo, DNA synthesis (bromodeoxyuridine incorporation) was higher in ventricular grafts cocultured with atrial grafts than in single ventricular grafts (6.84 +/- 0.88 vs. 4.40 +/- 0.10%). Thus atria may stimulate growth, including DNA synthesis, in developing ventricles via a paracrine mechanism.

Developmental sensitivity to high dietary sodium chloride in borderline hypertensive rats.

The present study compared the postweaning blood pressures and body weights of borderline hypertensive rats exposed to a high (8%) sodium chloride maternal diet either from conception to weaning or only during the weaning period with borderline hypertensive rats consistently exposed to a normal (1%) sodium chloride maternal diet. Because the effects of early sodium chloride exposure may be most evident during a subsequent challenge, rats from each group were assigned to receive either an 8% sodium chloride or a 1% sodium chloride diet from 8 to 17 weeks of age. Exposure to an 8% sodium chloride diet from conception through weaning increased the adult blood pressure of borderline hypertensive rats compared with that of controls exposed to a 1% sodium chloride diet; exposure to an 8% sodium chloride diet only during weaning did not increase blood pressure. An 8% sodium chloride diet beginning at 8 weeks of age increased systolic blood pressure. The effects of perinatal and adult exposure to high dietary sodium chloride were additive. Behavioral observations and urinary electrolyte measures confirmed that pups exposed to an 8% sodium chloride diet during weaning ingested the high-sodium chloride diet. The blood pressure and heart rate response to autonomic nervous system ganglionic blockade were assessed at 17 weeks of age. Borderline hypertensive rats exposed to an 8% sodium chloride diet from conception through weaning showed an increased bradycardic response, but no difference in depressor response, to ganglionic blockade. These data suggest that the window of developmental sensitivity for modulation of blood pressure regulation by high dietary sodium chloride occurs during prenatal and early postnatal development.

Effects of long-term air jet noise and dietary sodium chloride in borderline hypertensive rats.

The hypothesis that simultaneous exposure to a high (8%) sodium chloride diet and behavioral stress (air jet noise) would act synergistically to increase blood pressure was investigated in male borderline hypertensive rats. Rats were fed either a 1% or an 8% sodium chloride diet beginning at 6 weeks of age. Rats in the Air Noise condition were restrained and exposed to random blasts of air jet noise for 2 h/d, 5 d/wk, from 7 to 17 weeks of age. Controls either were placed in identical restrainers and test chambers but not exposed to air jet noise (Restrained Control) or were left undisturbed (Maturation Control). Biweekly indirect blood pressure measurements showed that by 17 weeks of age, the high-sodium chloride diet and air jet noise exposure produced additive increases in blood pressure. Direct blood pressure measurements at 18 weeks of age confirmed the higher systolic pressures in borderline hypertensive rats exposed to both an 8% sodium chloride diet and air jet noise. After ganglionic blockade, the blood pressure of rats in the Air Noise group remained higher than that of Restrained and Maturation Controls, suggesting that the increased blood pressure of air jet noise-exposed rats was not maintained by increased autonomic activity. Blood pressure after maximal vasodilation by hydralazine was increased in rats exposed to both an 8% sodium chloride diet and air jet noise compared with other groups. Baroreceptor reflex sensitivity (tested by graded doses of angiotensin II) did not differ among groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of thyroid hormones on cardiac development in oculo.

Embryonic rat myocardium was grafted into the anterior eye chamber (in oculo) of adult host rats in a series of two experiments that studied the effects of thyroid hormones [triiodothyronine (T3) and thyroxine (T4)] on heart tissue developing without hemodynamic load. In each experiment, surgical sympathectomy of one eye chamber was used to define possible interactions between thyroid hormones and sympathetic innervation to the graft. In the first experiment, propylthiouracil (PTU, 20 mg/kg sc) greatly suppressed growth and beating rate of whole heart grafts, while excess T4 (0.1 mg/kg sc) transiently increased beating rate but not growth. In the second experiment, T3 (5 mg/21 days, slow-release pellet) failed to promote growth in ventricular grafts. However, the size of atrial grafts in surgically sympathectomized eye chambers was larger in T3-treated compared with control rats. T3 administration increased beating rate in ventricular grafts. In both experiments, thyroid hormone treatments were effective in increasing heart weight-to-body weight ratios in the host rats. The data suggest that exposure to normal levels of thyroid hormones may be necessary for optimal cardiac growth. The data also support the hypothesis that a hemodynamic load is required for thyroid hormone-induced cardiac growth.

Effects of sympathetic innervation on size of myocytes in embryonic rat heart cultured in oculo.

Embryonic rat myocardium cultured in the anterior eye chamber of an adult rat increases in mass and differentiates into mature myocardium by most morphological criteria [1]. When sympathetic innervation of grafted heart tissue was prevented by superior cervical ganglionectomy (SCGx), growth of the grafts was severely compromised. The present study used morphometric methods to examine the contribution of myocyte size to the differential growth of grafts in sympathetically denervated and intact eye chambers. For this purpose, atria or ventricles from 12-day gestation rat hearts were grafted into sympathetically denervated and intact eye chambers of male host rats. Tissue was harvested after either 2 or 8 weeks in oculo. Myocyte diameter and the ratio of cytoplasmic area to nuclear area increased between 2 and 8 weeks in oculo in both atrial and ventricular grafts. In these unloaded heart grafts, estimated myocyte size did not differ between atrial and ventricular myocytes. Grafts into sympathetically innervated and denervated eye chambers did not differ in myocyte diameter or in the ratio of cytoplasmic to nuclear area, suggesting that myocyte size cannot explain the smaller mass of grafts in sympathetically denervated eye chambers. Thus, it is likely that other factors such as myocyte proliferation, myocyte survival or altered tissue composition underlie the lesser growth of grafts not innervated by sympathetic nerves.