Cardiovascular and hormonal responses to swimming and running in the rat

1988 ◽  
Vol 65 (1) ◽  
pp. 116-123 ◽  
Author(s):  
D. Geenen ◽  
P. Buttrick ◽  
J. Scheuer

Hemodynamic and hormonal responses were studied during swimming (SW) and running (R) and in cage-confined (C) female Wistar rats at base line and 4 and 8 wk of training. Myocardial tissue levels of norepinephrine (NE) and epinephrine (EPI) were also measured at the end of 8 wk of training. Mean arterial blood pressure (BP), heart rate (HR), and blood samples for arterial lactate, plasma NE and EPI, and blood gases were obtained at rest and at 20, 40, and 60 min of exercise. After 4 wk of SW, a resting bradycardia was observed, and HR response for the remaining 4 wk was attenuated with SW compared with HR during R. BP and blood gases remained unchanged between the two groups. R resulted in increased arterial lactate concentrations compared with C and SW at base line but was not different from SW at 4 wk. SW elicited higher plasma levels of NE and EPI compared with C at base line and C and R at 4 wk. Myocardial tissue NE and EPI concentrations were markedly increased in both the left and right ventricle of the SW group compared with both R and C. These results indicate that BP and blood gases are not different between chronic R and SW and suggest a possible sympathoadrenal role in the differences observed in cardiac adaptations between R and SW.

1978 ◽  
Vol 44 (4) ◽  
pp. 534-537 ◽  
Author(s):  
M. Maskrey ◽  
P. P. Hoppe ◽  
O. S. Bamford

Five adult male dik-dik (Madoqua kirkii) were exposed in a climatic chamber to an air temperature of 45 degrees C. Measurements were made of rectal temperature (Tre) and respiratory frequency (f) and arterial blood samples taken before and during heat exposure were analyzed for pH, PCO2 and PO2. During exposure, Tre and f increased in all animals. In the first 80 min dik-dik displayed thermal tachypnea and minor changes in blood gases. Continued exposure lead to hyperpnea accompanied by a fall in PaCO2 and a rise in pH. PaCO2 at first fell and then increased toward or above control levels. The dik-dik did not display second phase breathing. This observation confirms that second phase breathing is not essential to the development of respiratory alkalosis. The main conclusion of the study is that the dik-dik, unlike another heat-adapted antelope, the wildebeest (Taylor, Robertshaw, and Hoffmann. Am. J. Physiol. 217:907–910, 1969), is unable to resist alkalosis during heat stress.


1989 ◽  
Vol 67 (5) ◽  
pp. 1747-1753 ◽  
Author(s):  
A. T. Scardella ◽  
T. V. Santiago ◽  
N. H. Edelman

In a previous study in unanesthetized goats, we demonstrated that cerebrospinal fluid levels of beta-endorphin were significantly elevated after 2.5 h of inspiratory flow-resistive loading. Naloxone (NLX) (0.1 mg/kg) administration partially and transiently reversed the tidal volume depression seen during loading. In the current study, we tested the hypothesis that endogenous opioid elaboration results in depression of respiratory output to the diaphragm. In six studies of five unanesthetized goats, tidal volume (VT), transdiaphragmatic pressure (Pdi), diaphragmatic electromyogram (EMGdi), and arterial blood gases were monitored. A continuous NLX (0.1 mg/kg) or saline (SAL) infusion was begun 5 min before an inspiratory flow-resistive load of 120 cmH2O.l-1.s was imposed. Our data show that the depression of VT induced by the load was prevented by NLX as early as 15 min and persisted for 2 h. At 2 h, Pdi was still 294 +/- 45% of the base-line value compared with 217 +/- 35% during SAL. There was no difference in EMGdi between the groups at any time. However, the augmentation of Pdi was associated with a greater increase in end-expiratory gastric pressure in the NLX group. We conclude that the reduction in VT and Pdi associated with endogenous opioid elaboration is not mediated by a decrease in neural output to the diaphragm, but it appears to be the result of a decrease in respiratory output to the abdominal muscles.


1989 ◽  
Vol 257 (3) ◽  
pp. H912-H917 ◽  
Author(s):  
M. L. Hudak ◽  
M. D. Jones ◽  
A. S. Popel ◽  
R. C. Koehler ◽  
R. J. Traystman ◽  
...  

Cerebral blood flow (CBF) rises as hematocrit (Hct) falls. We previously attributed this rise in CBF to two independent factors of equal importance, decreased arterial O2 content and decreased blood viscosity. We hypothesized that decreased arterial O2 content would dilate cerebral arterioles and that the magnitude of the vasodilation would depend on the magnitude of the passive fall in vascular resistance attributable to decreased viscosity. The present study was designed to test the hypothesis that anemia is accompanied by cerebral vasodilation. Using a closed cranial window, we measured the diameters of 42 pial arterioles (35-305 microns) in 7 cats as serial isovolemic hemodilution lowered Hct by 44% from 31 +/- 4 to 17 +/- 3%. Hemodilution increased CBF (microsphere technique) but did not change mean arterial blood pressure or arterial blood gases. Anticipated vasodilation did not occur; instead, pial arterioles constricted as Hct fell. Maximum vasoconstriction was observed when Hct reached 65-70% of the initial value. Vasoconstriction lessened as Hct was lowered further, but arteriolar diameters at the lowest Hcts remained less than base-line levels. Constriction was greater in small (less than 100 microns) than in large (greater than or equal to 100 microns) arterioles. The initial constriction of pial arterioles may represent myogenic vasoconstriction in response to flow-induced vasodilation of more proximal portions of the cerebrovascular bed and/or to washout of an endogenous vasodilator. Arteriolar relaxation with more profound hemodilution may reflect superimposed metabolic vasodilation.


1988 ◽  
Vol 255 (1) ◽  
pp. R67-R72 ◽  
Author(s):  
N. M. Rawashdeh ◽  
N. D. Ray ◽  
D. K. Sundberg ◽  
J. C. Rose

We studied norepinephrine (NE) and plasma renin activity (PRA) responses to sodium nitroprusside (NP)-induced hypotension in seven chronically catheterized fetal lambs 0.79-0.94 gestation (mature) and in seven fetuses 0.64-0.72 gestation (immature) 4 or 5 days after surgery. We infused intravenously 5% dextrose in water (DW) or NP in DW to reduce arterial pressure 30% in fetuses for 10 min. Initial infusion choice was random, and the two infusions were separated by 24-48 h. In both groups, basal NE levels were similar and doubled in response to hypotension. In mature fetuses, PRA basal levels were 6.89 +/- 1.80 ng.ml-1.h-1 and increased two- to threefold with hypotension. In immature fetuses, PRA basal levels were 2.42 +/- 0.86 ng.ml-1.h-1 and did not change with hypotension. No changes were observed with DW infusion in either group. Arterial blood gases were normal and remained unchanged. We conclude that in the lamb fetus, NE responses to hypotension are present before and are independent of the development of PRA responses and that before 0.72 gestation there is a functional deficit in the renin-angiotensin system.


Neurosurgery ◽  
1982 ◽  
Vol 10 (2) ◽  
pp. 167-169 ◽  
Author(s):  
Duke Samson ◽  
Chester W. Beyer

Abstract The effect of furosemide in the intraoperative reduction of intracranial pressure was measured in 25 patients undergoing the operative repair of a ruptured intracranial aneurysm. Seven patients with similar intracranial lesions served as controls. A single bolus of 80 mg of furosemide was administered intravenously after the induction of anesthesia, and sequential measurements were made of intracranial pressure, mean arterial pressure, and arterial blood gases. A mean decrease of intracranial pressure of 56% was measured in the furosemide-treated patients, whereas the control patients demonstrated a mean decline of subarachnoid pressures of 18%. These changes are significant at the P < 0.005 confidence level, whereas changes in mean arterial pressure, mean arterial pCO2, and base line arterial pCO2 were statistically insignificant. This study suggests that intravenous furosemide is a quick, dependable, and effective mechanism for the intraoperative reduction of intracranial pressure in the postsubarachnoid hemorrhage aneurysm patient.


1989 ◽  
Vol 66 (6) ◽  
pp. 2895-2900 ◽  
Author(s):  
T. I. Musch ◽  
B. S. Warfel ◽  
R. L. Moore ◽  
D. R. Larach

We compared the effects of three different anesthetics (halothane, ketamine-xylazine, and diethyl ether) on arterial blood gases, acid-base status, and tissue glycogen concentrations in rats subjected to 20 min of rest or treadmill exercise (10% grade, 28 m/min). Results demonstrated that exercise produced significant increases in arterial lactate concentrations along with reductions in arterial Pco2 (PaCO2) and bicarbonate concentrations in all rats compared with resting values. Furthermore, exercise produced significant reductions in the glycogen concentrations in the liver and soleus and plantaris muscles, whereas the glycogen concentrations found in the diaphragm and white gastrocnemius muscles were similar to those found at rest. Rats that received halothane and ketamine-xylazine anesthesia demonstrated an increase in Paco2 and a respiratory acidosis compared with rats that received either anesthesia. These differences in arterial blood gases and acid-base status did not appear to have any effect on tissue glycogen concentrations, because the glycogen contents found in liver and different skeletal muscles were similar to one another cross all three anesthetic groups. These data suggest that even though halothane and ketamine-xylazine anesthesia will produce a significant amount of ventilatory depression in the rat, both anesthetics may be used in studies where changes in tissue glycogen concentrations are being measured and where adequate general anesthesia is required.


1975 ◽  
Vol 38 (4) ◽  
pp. 581-587 ◽  
Author(s):  
W. E. Pepelko ◽  
G. A. Dixon

Adult male rats were anesthetized and catheters were implanted in the caudal artery. Soon after recovery from short-lasting anesthesia, a total of 20 groups of six each were individually exposed to five different oxygen levels varying from 21.0 to 9.0% combined with four CO2 levels ranging from 0 to 12.9% at a mean barometric pressure of 744 Torr. Arterial blood samples were collected and analyzed for pH, Po2, and Pco2 before and near the end of 20-min exposures. During an air-breathing control period, pH averaged 7.466 plus or minus 0.020 SD, Paco2 41.2 plus or minus 1.9 Torr and Pao2 91.8 plus or minus 3.5 Torr. During hypoxia, Pao2 levels were similar to that of acutely hypoxic humans. Rats apparently differ from man in that blood buffering is greater, resulting in a higher pH during air breathing and a smaller [H-+] increase with increasing Paco2. Differences between arterial and inspired CO2 were about 10 Torr at 60 and 90 Torr Plco2 and were not influenced by Plo2.


1989 ◽  
Vol 66 (1) ◽  
pp. 128-134 ◽  
Author(s):  
F. L. Glauser ◽  
D. E. Bechard ◽  
G. G. DeBlois ◽  
A. A. Fowler ◽  
R. E. Merchant ◽  
...  

Recombinant interleukin 2 (rIL-2) administration, a new form of therapy for patients with far-advanced cancer, is associated with a "third space" syndrome, i.e., pulmonary edema, respiratory distress, and hypoxemia, which limits the dose and duration of treatment. To extend our knowledge regarding this toxicity, we established a sheep chronic lung lymph fistula model and measured hemodynamics, arterial blood gases, caudal mediastinal (lung) lymph flow (QL), and blood and lung lymph cellular changes before, during, and after (recovery) a 3-day continuous rIL-2 infusion (9 x 10(5) U/kg). Moderate systemic hypotension, mild pulmonary hypertension, and an increase in alveolar-arterial PO2 gradient was present on day 3 of rIL-2 infusion. QL increased from a base line of 1.9 +/- 0.2 to a maximum of 4.3 +/- 1.1 ml/15 min on day 3 of rIL-2 infusion. At no time was there a change in lymph-to-plasma protein ratio. The leukocyte count increased significantly to 16.1 +/- 4.5 x 10(3) cells/mm3 at recovery day 1. The percentage of blood lymphocytes decreased significantly by day 1 of rIL-2 infusion, returned to base-line levels on day 3, and significantly increased on day 2 of recovery. Lung lymph lymphocytes decreased significantly on days 1 and 2 of rIL-2 infusion. There was a shift in their size; i.e., their area increased from 32 +/- 7 to 57 +/- 19 micron 2 (P less than 0.05) by day 2 of rIL-2 infusion. By day 1 of recovery, lung lymph lymphocyte counts increased significantly.(ABSTRACT TRUNCATED AT 250 WORDS)


1965 ◽  
Vol 208 (4) ◽  
pp. 798-800 ◽  
Author(s):  
Hugo Chiodi ◽  
James W. Terman

Individual blood samples were collected anaerobically from the brachial arteries of adult White Rock hens and were analyzed for Po2, Pco2, pH, oxygen content and capacity, and CO2 content and capacity. A dissociation curve was constructed from data on equilibration of pooled venous blood. The average arterial oxygen saturation was 90%, the Pco2 was about 32 mm Hg, the Po2 was between 94 and 99 mm Hg, and the pH averaged 7.49. The dissociation curve, as has been shown before, was shifted to the right of most homeothermic species.


1981 ◽  
Author(s):  
N J Dodd ◽  
J H Turney ◽  
M J Weston

In order to test certain hypotheses regarding the cause of arterial hypoxia during haemodialysis(HD),we investigated the effect of:- 1 Heparin bolus-infusion; or heparin plus:- 2.Prostacyclin ( PGI2 ) infusion ( 5ng/Kg/mi n );3. Methyl Prednisolone bolus(30mg/Kg) 30 minutes prior to dialysis; 4. Ultrafiltration for one hour followed by dialysis(UF/HD); 5.40mmo1/l Bicarbonate dialysate instead of standard acetate dialysate . Seven patients on long term HD were examined by all methods. Arterial blood samples were taken before,and at intervals during ,dialysis for blood gases, platelet count,and neutrophil count. All results are expressed as percentage of pre-dialys is value (means).Results fo r each group were tested fo r significance against the Heparin group(l.)using a paired t tes t . The only significant sparing of hypoxia occurred at 60 minutes during UF/HD.PGI2 spared platelets , as we have previously shown. Methyl Prednisolone failed to prevent dialysis induced neutropenia. The mechanism of haemodialysis induced hypoxia remains obscure


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