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N C Gonzalez

Publications and source records attributed to N C Gonzalez.

At least 37 records · Page 2Linked to original sources
PubMed1994

Distribution of pulmonary blood flow in conscious resting rats.

The pattern of pulmonary blood flow (PBF) distribution was determined in the rat, in which lung gravitational forces are minimal. Microspheres were infused into the inferior vena cava of 15 conscious, and 5 anesthetized rats. Relative scatter of specific PBF [(sample activity/sample weight)/(total activity/total weight)] in 28 lung samples was calculated. In 5 of the conscious rats, consecutive determinations were made 30 min apart. In 5 anesthetized rats, PBF was determined in prone and supine positions. Relative scatter of specific PBF varied from 0.84 to 1.12, with PBF being distributed preferentially to the hilar, central regions. There was a high correlation between consecutive measurements: y = 0.88 x +0.11 (n = 140, r = 0.92). By changing from prone to supine position, PBF to the topmost regions increased, and that to the lowermost regions decreased, by only 3 percent. The results indicate that in the conscious resting rat, PBF has a small but significant preferential distribution to the hilar, central regions, with lower blood flow to the peripheral regions of the lung.

Animals↗
PubMed1994

Pulmonary gas exchange during hypoxic exercise in the rat.

Pulmonary gas exchange and O2 transport were studied at rest and during maximal treadmill exercise in rats in acute hypoxia (PIO2 approximately 71 Torr), and in littermates acclimatized to PB = 380 Torr (PIO2 approximately 71 Torr) for 3 weeks (chronic hypoxia). To obtain valid estimates of blood gas partial pressures, particularly during exercise, the temperature coefficients of blood pH, PO2 and PCO2 were determined (Appendix). In both acute and chronic hypoxia, the following changes were observed: alveolar and arterial PO2 increased considerably, but the difference, A-aPO2, did not change significantly; arterial O2 concentration (CaO2) decreased, and apparent pulmonary diffusing capacity for O2, Dapp, increased. The increase in Dapp, together with hyperventilation, may prevent further drop in CaO2 due to a large rightward shift in the blood-O2 equilibrium curve caused by lactic acidosis in conjunction with a large Bohr coefficient characteristic of this species. Comparison with corresponding results obtained in man reveals that during hypoxic exercise, the rat shows a larger increase in PAO2, an increase, instead of a decrease, in PaO2, and a larger increase in Dapp.

Acclimatization↗
PubMed1994

Effect of hematocrit on systemic O2 transport in hypoxic and normoxic exercise in rats.

The effect of hematocrit (Hct) on O2 transport in hypoxic [inspired PO2 (PIO2) approximately 70 Torr] and normoxic (PIO2 approximately 145 Torr) exercise was studied in rats acclimatized to 3 wk of PIO2 at approximately 70 Torr (A rats) and in nonacclimatized littermates (NA rats). Isovolumic exchange transfusion of plasma or red blood cells was used to lower Hct in A rats from approximately 60 to 45% and to raise Hct of NA rats from 45 to 60%: Controls were A and NA rats exchange transfused with whole blood at constant Hct. Lowering Hct of A rats lowered the arterial O2 concentration (CaO2) and the arterial-mixed venous O2 difference and increased the maximal cardiac output (Qmax) without changes in maximal O2 uptake (VO2 max) or in the product of Qmax x CaO2, circulatory O2 convection at maximal exercise (TO2 max). Raising Hct in NA rats produced the opposite changes in CaO2, arterial-mixed venous O2 difference, and Qmax, but VO2 max and TO2 max increased significantly, both in hypoxia and normoxia, because of relatively small changes in Qmax. In NA rats, a steeper slope of the line relating VO2 max to calculated mean capillary PO2 at high Hct suggested a higher tissue O2 diffusing capacity with high Hct. For a given Hct and Qmax, systemic arterial pressure was higher in A rats. The data suggest that 1) the effect of Hct on systemic hemodynamics is different in A and NA rats, resulting in different effects on VO2 max; 2) factors in addition to Hct contribute to the high systemic vascular resistance of A rats; and 3) increased diffusive conductance for O2, as well as increased TO2 max, could be responsible for the effect of Hct on VO2 max of NA rats.

Acclimatization↗
PubMed1993

Effect of chronic hypoxia on hemodynamics, organ blood flow and O2 supply in rats.

Aortic blood flow, heart rate, blood pressure and blood flow distribution were measured in 10 chronically hypoxic rats (3 weeks, PB 370-380 Torr) breathing 10% O2 (chronic hypoxia) and after 30 min of breathing air (acute normoxia). Controls were 10 normoxic littermates breathing air (normoxia) and 10% O2 for 30 min (acute hypoxia). Acute hypoxia resulted in increased aortic blood flow and heart rate, and decreased total peripheral resistance. Blood flow and oxygen supply to vital organs increased, indicating that blood flow redistribution plays an important role in oxygen supply. In chronic hypoxia, aortic blood flow and heart rate remained elevated, and total peripheral resistance remained decreased. Blood flow distribution returned towards normoxia levels. Oxygen supply was maintained via increased arterial oxygen concentration. Acute normoxia resulted in decreased aortic blood flow and heart rate, and increased blood pressure and total peripheral resistance. Blood flow distribution was similar to that of chronic hypoxia except skeletal muscles, in which blood flow decreased markedly. Oxygen supply remained unchanged or increased.

Acid-Base Equilibrium↗
PubMed1993

Regional blood flow in conscious resting rats determined by microsphere distribution.

To determine organ blood flow in the resting state, a box was designed to keep conscious untrained rats minimally disturbed. Blood pressure, heart rate, and organ blood flow, determined by the microsphere distribution and reference sampling technique, were measured in 11 Sprague-Dawley rats. After an acclimation period, 15-microns-diameter microspheres labeled with 113Sn were infused into the ascending aorta, a reference blood sample was withdrawn from the caudal artery, and organ blood flows were computed according to standard procedures. The average values of heart rate (365 beats/min) and blood flow to the brain (45 ml.min-1.100 g-1) and hindlimb muscles (15 ml.min-1.100 g-1) were significantly lower than most values reported earlier, whereas splanchnic blood flow was significantly higher (106 ml.min-1.100 g-1). Blood flow to the soleus muscle, which is considered the most active for postural maintenance, was relatively high (99 ml.min-1.100 g-1). The combination of low skeletal muscle and high visceral blood flows observed in these experiments suggests a low sympathetic tone, which is consistent with the low level of circulating catecholamines also observed in this study. It is hypothesized that the difference between our present and previous results is a lower level of stress, attributable to a more complete acclimation to the experimental environment.

Animals↗
PubMed1993

Changes in regional blood flow distribution and oxygen supply during hypoxia in conscious rats.

The effects of acute hypoxia on central hemodynamics, regional blood flow, and regional oxygen supply (blood flow x arterial O2 concentration) were studied in conscious resting rats. Regional blood flow was determined by the radiolabeled microsphere technique. Blood pressure, heart rate; and aortic blood flow increased and total peripheral resistance decreased significantly during hypoxia. Blood flow to brain, respiratory muscles, and liver increased both in absolute value and as a fraction of the aortic blood flow. Fractional blood flow to the gastrointestinal tract, spleen, pancreas, skin, fat, and hindlimb bones decreased during hypoxia; blood flow decreased in absolute values only in stomach and fat. Oxygen supply to brain, respiratory muscles, and liver increased during hypoxia, whereas it decreased in the remaining organs investigated.

Animals↗
PubMed1993

Determinants of maximal oxygen uptake in rats acclimated to simulated altitude.

The effect of acclimation to hypoxia on maximal O2 uptake (VO2max), maximal cardiac output (Qmax), and arteriovenous O2 concentration difference (a-vCO2) was studied in male Sprague-Dawley rats acclimated for 3 wk to a barometric pressure of approximately 380 Torr (A rats). Nonacclimated control animals were pair-fed littermates maintained at an ambient barometric pressure of approximately 740 Torr (NA rats). Both A and NA rats exercised maximally on a treadmill with inspired PO2 maintained at either approximately 72 or 145 Torr. Arterial blood O2 concentration was significantly higher in A than in NA rats (16.0 +/- 0.6 vs. 12.4 +/- 0.3 ml/dl in hypoxia and 28.4 +/- 1.5 vs. 20.1 +/- 0.9 ml/dl in normoxia, respectively; both P < 0.05). During hypoxic exercise VO2max was slightly but significantly higher in A than in NA subjects (55.3 +/- 1.3 vs. 48.8 +/- 1.1 ml STPD.min-1 x kg-1; P < 0.05). In hypoxia a-vCO2 was 16.6 +/- 0.6 and 12.4 +/- 0.4 ml/dl and Qmax was 401 +/- 17 and 489 +/- 9 ml.min-1 x kg-1 in A and NA subjects, respectively (both P < 0.05). A rats showed both lower maximal heart rate and lower maximal stroke volume during hypoxic exercise. In normoxia there was no significant difference in VO2max between A and NA rats (71.8 +/- 2.7 vs. 73.9 +/- 3.1 ml.min-1 x kg-1). As with hypoxia, in normoxia a-vCO2 was significantly higher and Qmax was significantly lower in A than in NA animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Acclimatization↗
PubMed1992

Mechanism of the effect of alkalosis on maximum oxygen uptake in hypoxic exercise.

Maximum oxygen uptake (VO2max) of rats is increased in alkalosis; this increase is larger in hypoxic than in normoxic exercise (Gonzalez et al. (1991b). J. Appl. Physiol., 71: 1050-1056). The objective of the present experiments was to determine the mechanism of this phenomenon. NaHCO3 (0.3 M, 9 mmol/kg) was given 15 min before exercise to rats acclimated to PB 380 Torr for 3 weeks (HxBic) and to normoxic rats (NxBic). Additional groups of acclimated and normoxic rats received 0.3 M NaCl (HxNaCl and NxNaCl, respectively). Hx rats exercised at PIO2 approximately 70 Torr; Nx rats at PIO2 approximately 140 Torr. VO2max was higher after NaHCO3 than after NaCl; this effect was larger in hypoxia. The increase in VO2max was mediated through an increased arterio-venous oxygen concentration difference ((Ca - Cv)O2), due, in turn, to a higher CaO2 without changes in CvO2. (Ca - Cv)O2 after NaHCO3 was larger in hypoxia because a change in pH results in a larger change in HbO2 saturation at the values prevalent in arterial blood of the hypoxic rats (i.e. PO2 approximately 40-50 Torr, SO2 50-60%), than at either the values of normoxic arterial blood or of venous blood during maximum exercise. These results suggest that an increase in hemoglobin-oxygen affinity improves oxygen uptake in the lungs during hypoxia, without hindering its release in the tissues, and therefore has a beneficial effect in hypoxic exercise.

Acid-Base Equilibrium↗
PubMed1991

Maximum oxygen uptake and arterial blood oxygenation during hypoxic exercise in rats.

The objectives of these experiments were 1) to describe the effect of maximum treadmill exercise on gas exchange, arterial blood gases, and arterial blood oxygenation in rats acclimated for 3 wk to simulated altitude (SA, barometric pressure 370-380 Torr) and 2) to determine the contribution of acid-base changes to the changes in arterial blood oxygenation of hypoxic exercise. Maximum O2 uptake (VO2max) was measured in four groups of rats: 1) normoxic controls run in normoxia (Nx), 2) normoxic controls run in acute hypoxia [AHx inspiratory PO2 (PIO2) approximately 70 Torr], 3) SA rats run in hypoxia (3WHx, PIO2 approximately 70 Torr), and 4) SA rats run in normoxia (ANx). VO2max (ml STPD.min-1.kg-1) was 70.8 +/- 0.9 in Nx, 46.4 +/- 1.9 in AHx, 52.6 +/- 1.1 in 3WHx, and 70.0 +/- 2.4 in ANx. Exercise resulted in acidosis, hypocapnia, and elevated blood lactate in all groups. Although blood lactate increased less in 3WHx and ANx, pH was the same or lower than in Nx and AHx, reflecting the low buffer capacity of SA. In AHx and 3WHx, arterial PO2 increased with exercise; however, O2 saturation of hemoglobin in arterial blood (SaO2) decreased. In vitro measurements of the Bohr shift suggest that SaO2 decreased as a result of a decrease in hemoglobin O2 affinity. The data indicate that several features of hypoxic exercise in this model are similar to those seen in humans, with the exception of the mechanism of decrease in SaO2, which, in humans, appears to be due to incomplete alveolar-capillary equilibration.

Acclimatization↗
PubMed1991

Effect of alkalosis on maximum oxygen uptake in rats acclimated to simulated altitude.

The objective of the present experiments was to determine whether prevention or moderation of exercise acidosis would influence arterial blood oxygenation and exercise capacity in hypoxia. The effect of administration of 0.3 M NaHCO3 (3 ml/100 g) on maximum O2 uptake (VO2max) and arterial blood oxygenation was determined in rats acclimated to simulated altitude (370-380 Torr barometric pressure) for 3 wk (HxBic) and in normoxic littermates (NxBic). Controls were simulated-altitude (HxNaCl) and normoxic rats (NxNaCl) given 0.3 M NaCl. Inspiratory PO2 during treadmill exercise was approximately 70 Torr for hypoxic rats and 140-145 Torr for normoxic rats. VO2max was 18% higher in HxBic than in HxNaCl (62.8 + 1.6 vs. 53.1 + 1.0 ml STPD.min-1.kg-1, respectively, P less than 0.05) and only 8% higher in NxBic than in NxNaCl (74.0 + 1.1 vs. 68.7 + 1.5 ml STPD.min-1.kg-1, respectively, P less than 0.05). Exercise in HxNaCl resulted in a decrease in arterial O2 concentration (CaO2), which was largely due to a pH-induced decrease in O2 saturation of arterial blood, and occurred despite an increase in arterial PO2. NaHCO3 moderated the acidosis of exercise and largely attenuated the decrease in CaO2. The effects of acidosis and bicarbonate on CaO2 were much less evident in the normoxic controls. There was an almost linear relationship between VO2max and the corresponding CaO2 for all four groups, suggesting that the effect of NaHCO3 on VO2max may be related to moderation of the decrease in CaO2.

Acclimatization↗
PubMed1990

Compensation of respiratory alkalosis induced after acclimation to simulated altitude.

Conscious intact rats previously acclimated for 3 wk to barometric pressure of 370-380 Torr (3WHx) were made alkalotic for 3 h by a decrease in inspired O2 fraction from 0.10 to 0.075 at ambient barometric pressure (730-740 Torr). Controls were normoxic littermates (Nx) in which inspired O2 fraction was lowered from approximately 0.21 to 0.10 for 3 h. Arterial PCO2 decreased progressively and similarly in both groups (65-70% of control at 15 min). Initially, arterial pH increased less in 3WHx (0.09 +/- 0.004 vs. 0.15 +/- 0.008). As hypocapnia continued, delta[HCO3-]/delta pH (mmol.l-1.pH) became more negative in Nx, from -15.2 +/- 2.5 at 15 min to -37.0 +/- 2.9 at 3 h, indicating nonrespiratory compensation of alkalosis. In 3WHx, delta[HCO3-]/delta pH did not change during alkalosis. Cumulative renal excretion of base (mueq/100 g) during alkalosis increased by 73.2 +/- 11.1 in Nx and 25.4 +/- 7.3 in 3WHx. This difference was mainly due to a larger increase in HCO3- excretion in Nx. The data suggest that the smaller compensation of hypocapnic alkalosis in 3WHx is partly due to the smaller increase in renal base excretion. Because base availability limits renal base excretion, the smaller renal response of 3WHx may be secondary to the low plasma HCO3- concentration that accompanies altitude acclimation.

Acid-Base Equilibrium↗
PubMed1986

Intracellular pH regulation during prolonged hypoxia in rats.

Conscious rats maintained for three weeks at PB 370-380 Torr were studied in a chamber where PIO2 was maintained at 68-70 Torr at ambient barometric pressure (740-750 Torr). Controls were pair-fed rats maintained at ambient barometric pressure and studied at ambient PIO2 for 4 h. Steady-state intracellular pH (pHi) of left and right ventricle, and of tibialis anterior, quadriceps and diaphragm was determined from the distribution of 5,5-dimethyl-2,4-oxazolidinedione (DMO). Apparent non-bicarbonate buffer value (beta app) was calculated as the ratio of the change in HCO3- concentration to the change in pH elicited by the increase in PCO2. beta app of plasma, tibialis anterior, quadriceps and diaphragm was approximately 2, 3, 6 and 12 times higher, respectively, in hypoxic than in normoxic rats. Neither left nor right ventricular beta app was significantly changed by prolonged hypoxia. In the hypoxic animals, bilateral nephrectomy abolished the increase in beta app of plasma, tibialis anterior and quadriceps, and moderated the increase in beta app of diaphragm. No significant effect of nephrectomy was observed in beta app of either left or right ventricle. The results indicate that in the skeletal muscles studied under conditions of an acid load in the form of increased PCO2, intracellular pH is better regulated in hypoxic than in normoxic rats. The effects of nephrectomy suggest that this is due, at least in part, to a more effective renal compensation in hypoxic than in normoxic rats. Prolonged hypoxia, on the other hand, does not affect the cell pH regulation of right or left ventricle.

Acid-Base Equilibrium↗
PubMed1986

Renal compensation of hypercapnia in prolonged hypoxia.

We previously showed that rats made hypoxic for three weeks were able to regulate their plasma pH better than normoxic rats during acute hypercapnia. This improved pH regulation was abolished by nephrectomy, suggesting that it was due, at least in part, to a more effective renal compensation of hypercapnia in hypoxic rats. To test this possibility renal acid excretion was measured in conscious rats that had been kept at PB 370-380 Torr for three weeks. The rats were studied in a chamber where PIO2 was kept at 68-70 Torr at ambient PB (740-750 Torr). Controls were pair-fed normoxic rats. After a 2 h control period, inspired PCO2 was increased for 4 h. The apparent non-bicarbonate buffer value of arterial blood plasma was twice as high in the hypoxic than in the normoxic rats. Renal excretion of ammonium increased to a similar extent during hypercapnia in both normoxic and hypoxic rats. Titratable acid excretion of normoxic rats did not change significantly during hypercapnia. In the hypoxic rats, on the other hand, total excretion of titratable acid in the 2 h control period was 90.9 +/- 16.4 mumol/rat; and increased to 150.0 +/- 13.4 mumol/rat in the first 2 h and to 232.9 +/- 26.0 mumol/rat in the last 2 h of hypercapnia. In spite of this large increase in acid excretion, urine pH of hypoxic rats did not change significantly, indicating a higher buffer value of the urine of hypoxic rats. These results confirm our previous observations and support the idea that the improved pH regulation of hypoxic rats is due in part to a more effective renal compensation of hypercapnia.

Animals↗
PubMed1986

Acid-base regulation in prolonged hypoxia: effect of increased PCO2.

Conscious rats maintained for 3 wk at PB 370-380 Torr were studied in a chamber where PIO2 was kept at 68-70 Torr at ambient barometric pressure (740-750 Torr). Blood samples were obtained through an arterial catheter. Controls were pair-fed rats maintained at ambient barometric pressure and studied at PIO2 68-70 Torr for 4 h (acute hypoxia) or at ambient PIO2 (normoxia). Arterial blood pH of 3-wk hypoxic rats was not different from that of normoxic rats. Hypercapnia was produced by increasing PICO2 for 4 h. The 3-wk hypoxic rats showed the highest apparent non-bicarbonate buffer value of arterial blood (beta app): 77 mmol/(pH X kg), compared to 38 in normoxia and 43 mmol/(pH X kg) in acute hypoxia. Comparison of beta app at different times of hypercapnia in intact and in nephrectomized rats suggests that the high beta app of prolonged hypoxia is largely due to an increased renal compensation, and, to a smaller extent, to increased chemical buffering. While the extracellular fluid of normoxic and acute hypoxic rats showed a net gain of base of non-renal origin during hypercapnia, the 3-wk hypoxic rats showed a net non-renal base loss, which may be masked by the increased renal compensation.

Acid-Base Equilibrium↗
PubMed1984

Catecholamine effect on HCO3-/Cl- exchange and rabbit myocardial cell pH regulation.

The possible effect of isoproterenol on a HCO3-/Cl- exchange in mammalian myocardium and its role on intracellular pH (pHi) regulation was studied in isolated perfused rabbit hearts. pHi was determined from the distribution of 5.5-dimethyl-2,4-oxazolidinedione (DMO). Perfusates contained either 137.4 or 4.4 mM Cl-. In the latter case, Cl- was replaced by glucuronate. Hearts were perfused with low [Cl-] Ringer for 1 h in order to deplete the cell of Cl-. Isoproterenol (10(-5) M) was infused for the last 15 min of perfusion in approximately half of the preparations. Reduction of [Cl-], both in the untreated and in the isoproterenol-treated preparations resulted in an increase in pHi. Isoproterenol increased tissue cAMP concentration by approximately 2.5 fold both in hearts perfused with normal and with low [Cl-] Ringer. In the presence of normal [Cl-], isoproterenol had an alkalinizing effect when acid loads were introduced. This effect was abolished by the reduction of [Cl-]. These results support the idea that the catecholamine-cAMP system stimulates a HCO3-/Cl- exchange in mammalian myocardium.

Acid-Base Equilibrium↗