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Biomedical subjects

H Nose

Publications and source records attributed to H Nose.

At least 73 records · Page 4Linked to original sources

Role of cardiopulmonary baroreflexes during dynamic exercise.

To examine the role of cardiopulmonary (CP) mechanoreceptors in the regulation of arterial blood pressure during dynamic exercise in humans, we measured mean arterial pressure (MAP), cardiac output (Q), and forearm blood flow (FBF) during mild cycle ergometer exercise (77 W) in 14 volunteers in the supine position with and without lower-body negative pressure (LBNP). During exercise, MAP averaged 103 +/- 2 mmHg and was not altered by LBNP (-10, -20, or -40 mmHg). Steady-state Q during exercise was reduced from 10.2 +/- 0.5 to 9.2 +/- 0.5 l/min (P less than 0.05) by application of -10 mmHg LBNP, whereas heart rate (97 +/- 3 beats/min) was unchanged. MAP was maintained during -10 mmHg LBNP by an increase in total systemic vascular resistance (TSVR) from 10.3 +/- 0.5 to 11.4 +/- 0.6 U and forearm vascular resistance (FVR) from 17.5 +/- 1.9 to 23.3 +/- 2.6 U. The absence of a reflex tachycardia or reduction in arterial pulse pressure during -10 mmHg LBNP supports the hypothesis that the increase in TSVR and FVR results primarily from the unloading of CP mechanoreceptors. Because CP mechanoreceptor unloading during exercise stimulates reflex circulatory adjustments that act to defend the elevated MAP, we conclude that the elevation in MAP during exercise is regulated and not merely the consequence of differential changes in Q and TSVR. In addition, a major portion of the reduction in FBF in our experimental conditions occurs in the cutaneous circulation. As such, these data support the hypothesis that CP baroreflex control of cutaneous vasomotor tone is preserved during mild dynamic exercise.

Adult↗

Change in salt appetite due to rehydration level in rats.

Thermally dehydrated rats were given a choice of tap water and saline (0.9% or 1.8% NaCl), and the change in the salinity of their choice during rehydration was measured up to 15 hr. The rats consumed more water than saline for about 2 hr after the start of fluid replacement (about 55 mEq/l), while they consumed more saline than tap water (about 120 mEq/l) thereafter. Urine output and urinary Na output were only about 20% of their intake during the initial 4 hr of rehydration, while after 4 hr the output became almost equal with the intake. The change in salt intake occurred when about 90% of Na loss and 60% of fluid loss was regained. The results indicate that rats choose dilute salt solution to lower plasma osmolality during the initial period of the rehydration and then regain body fluid isotonically. Urine volume and urinary Na output increased only after volume repletion. Thus, osmoregulation with salt appetite has priority over fluid volume regulation in restitution from thermal dehydration.

Animals↗

Changes in blood volume and plasma sodium concentration after water intake in rats.

Changes in blood volume (BV) and Na+ concentration of plasma ([Na+]) were measured continuously during recovery from thermal dehydration in rats. At least 5 days prior to the experiments rats were cannulated into both the jugular vein and the descending aorta. After thermal dehydration (DBT: 36 degrees C, RH: 20%) amounting to approximately 6% of body wt, catheters were connected to a system for continuous monitoring of BV and [Na+]. Water was made available and water intake, BV, and [Na+] were recorded at 30-s intervals for 4 h. The rats took 2-3 ml of water/100 g of body wt in the first 10 min and then drank 1 ml at 30- to 60-min intervals to reach equilibrium in 2-3 h. The relations between water intake and delta BV and between delta[Na+] were analyzed for 2 h after the start of water supply. BV was unchanged until 18.9 +/- 3.6 min after access to water, whereas [Na+] started to decrease after 3.6 +/- 0.6 min. The retention ratio of ingested fluid in the vascular space was 20.8 +/- 2.8%, and the decrease of [Na+] was 1.5 +/- 0.2 meq X l-1 X ml ingested fluid-1 X 100 g body wt-1. These results indicate that drinking causes the change of [Na+] more rapidly than that of blood volume.

Animals↗

Diminished baroreflex control of forearm vascular resistance in physically fit humans.

The stimulus-response characteristics of cardiopulmonary baroreflex control of forearm vascular resistance (FVR) were studied in five unfit [UF, maximal O2 consumption (VO2 max) = 38.5 ml X min-1 X kg-1] and six fit (F, VO2 max = 57.0 ml X min-1 X kg-1) subjects. We assessed the relationship between reflex stimulus, i.e., changes in central venous pressure (CVP) and response, i.e., FVR, during selective unloading of the cardiopulmonary mechanoreceptors with lower body negative pressure (0 to -20 mmHg). The linear relationship between FVR and CVP, the gain of this baroreflex, was significantly diminished in the F subjects, -2.42 +/- 0.57 U/mmHg, compared with the UF, -5.15 +/- 0.58 U/mmHg. Both groups, F and UF, had similar resting values for CVP and FVR; thus the diminished gain in F subjects was not simply an artifact resulting from a shift of the set point along the baroreflex stimulus-response curve. We also found a linear relationship between baroreflex gain and total blood volume (r = 0.59, P less than 0.05). We conclude that the gain of this vascular reflex is attenuated in trained individuals and is related to cardiovascular adaptations, such as an increased blood volume, associated with exercise training.

Blood Pressure↗

Estimation of plasma volume from hematocrit and plasma oncotic pressure during volume expansion in dogs.

Changes in hematocrit and plasma oncotic pressure were measured continuously during and after isotonic volume expansion in splenectomized dogs in order to test the potential of these types of measurements to predict changes in plasma volume. A volume of Ringer's solution amounting to 15% of the initial blood volume was infused over 10 min. At the end of the infusion, 54% of infused fluid remained within the intravascular space and 9% of the infused volume was retained within the intravascular space at 50 min after the end of the infusion. Hematocrit and plasma oncotic pressure decreased by 2.4% and 2.4 mmHg, respectively, at the end of infusion and then variables returned to their control levels gradually. Changes in plasma volume were estimated indirectly from hematocrit and plasma oncotic pressure based on the dilution of the erythrocytes and the protein. Highly significant correlations were observed between the measured plasma volume (Y) and the plasma volume (X) calculated from hematocrit (Y = 0.95X + 0.22, r = 0.96) and the plasma oncotic pressure (Y = 0.86X + 0.46, r = 0.91). We therefore conclude that either hematocrit and plasma oncotic pressure measured continuously are reliable parameters for predicting the time course of the plasma volume change during an isotonic volume expansion of up to 15% of the initial blood volume.

Animals↗

Recovery of blood volume and osmolality after thermal dehydration in rats.

Changes in blood volume and fluid intake were assessed continuously during recovery from thermal dehydration (approximately 6 ml/100 g body wt) in rats. Catheters chronically implanted into the jugular vein and descending aorta were connected with the system for continuous monitoring of blood volume. Changes in blood volume and fluid consumption were recorded for 2-6 h while tap water (TW group) or 0.45% NaCl solution (Na group) was provided ad libitum. As soon as the fluids became available, the rats in both groups drank a relatively large volume (2-3 ml/100 g) within 10 min. Thereafter, Na group consumed approximately 1 ml X 100 g body wt-1 X 30-60 min-1 and regained almost all water loss in 2 h, whereas TW group drank only approximately 50% of their water deficit. The percent of ingested fluid that remained in vascular space was 17% on average in both groups. Thus TW group replenished 80% of the depleted blood volume, whereas Na group regained almost all of it. Rehydration for 2 h decreased plasma Na concentration to the control level in TW group, whereas in Na group the level remained high. These results suggest that the lower fluid intake in TW group is due to the dilutional inhibition of drinking and that the osmoregulation has priority over blood volume regulation in restitution from thermal dehydration.

Animals↗

Continuous determination of blood volume on conscious rats during water and food intake.

A method to measure circulating blood volume continuously on a conscious rat was developed using the dilution method of 51Cr-labelled red cell and changes in blood volume after drinking and food intake were monitored. In splenectomized rats, the blood volume showed a transient decrease of 0.1-0.2 ml/100 g body wt. about 30 min after food intake, while increasing by 0.1-0.4 ml/100 g body wt. after water ingestion. Thus, blood volume showed fluctuations following water and food intake ranging from 2-8% of the circulating blood volume.

Animals↗

Continuous recording of plasma sodium concentration and blood volume in awake rats.

A new continuous measuring system for blood sodium concentration and blood volume in conscious rats is described. A small extracorporeal circulation was made and the blood was passed through a sodium sensitive glass electrode and a gamma-counter. Applying the system to conscious rats, the effect of various salinities of drinking water was detected from the change in blood sodium concentration.

Animals↗

Osmotic factors in restitution from thermal dehydration in rats.

The degree of voluntary dehydration after thermal dehydration was assessed while supplying drinking water of varying NaCl concentrations. Adult male albino rats were exposed to a hot-dry environment (dry bulb temp 36 degrees C; relative humidity 20%) for 6-8 h, and dehydration of 7% body wt was induced. After dehydration the rats were divided into three groups, and distilled water and 0.45 or 0.9% NaCl solution was given ad libitum. The amount of fluid intake reached an equilibrium in 6-12 h; the 0.45 and 0.9% NaCl groups regained almost all lost water, whereas the distilled water group regained only half. During rehydration the 0.45 and 0.9% NaCl groups gained Na by approximately 430-650 mueq and lost K by 90-130 mueq, whereas the distilled water group lost Na slightly and K by 80 mueq/100 g body wt. As for the electrolyte balance during thermal dehydration, rats excreted Na and K into urine and saliva. Na loss was 200 mueq/100 g, almost all of which was derived from the interstitial space of skin and skeletal muscle, and K loss was 230 mueq/100 g, almost all of which was derived from intracellular space of skeletal muscle. Total cation loss (Na, K) during thermal dehydration, including K excretion during rehydration, was 510-560 mueq/100 g, which was almost identical to the Na gained by rats given 0.45 or 0.9% NaCl solution. These results suggest that voluntary dehydration is caused by the dilutional inhibition of drinking due to loss of electrolytes during thermal dehydration.

Animals↗

Responses of the vascular-interstitial-lymph system to saline loading in the rat.

The responses of the vascular-interstitial-lymph system to saline loading were examined in rats by continuous monitoring of circulating blood volume and simultaneous collection of thoracic duct lymph. About 90% of the infused volume shifted out of the intravascular space, of which 72% was imbibed in the interstitial space, 21% was drained through the thoracic duct, and 7% was excreted in the urine by the 50th min after the infusion amounting to 4% of body weight. The drainage of lymph protein following the infusion was about 50% of that expected from the interstitial protein concentration and even distribution of the infused saline. This result can be explained partly by the increase of lymph from skin and muscle after the infusion.

Animals↗

Transvascular fluid shift and thoracic duct lymph: analysis of lymph formation in the rat.

To analyze the effect of changes in interstitial fluid on lymph production, intravascular infusions of saline were given to splenectomized rats under pentobarbital anesthesia at 3 different rates (2, 3, and 4 ml/100 g of body weight) over 10 min. Change of blood volume was continuously monitored and, simultaneously, thoracic duct lymph was collected during and after the infusion. Equilibrium was attained approximately 40 min after the infusion; regardless of the infusion rate, 10% of the infused volume was incorporated into the vascular space and 90% was filtered into the extravascular space. Thus, the amount of transvascular fluid shift showed a linear relationship with the infused volume. However, the drainage from thoracic duct lymph amounted to 5.9%, 11.4%, and 17.8% of the infused saline volume when given at the rate of 2, 3, and 4 ml/100 g, respectively. The relation of lymph flow and infused volume could be regarded as a nonlinear system. By means of a simulation study, this relation was found to be attributed to the nonlinearity of conductance for fluid movement from tissue to lymph duct, which was only one sixth of that determined for the capillary membrane. The drainage of lymph protein following the infusion was only about 50% of that expected from the interstitial protein concentration in even distribution of the infused saline. These characteristics of interstitial fluid space play an important role in absorbing water and, hence, buffering changes in circulating blood volume after volume loading.

Animals↗

Transcapillary protein flux following blood volume modification in dog.

The net fluid and protein movements between intravascular and interstitial space following blood withdrawal and retransfusion of 15% of circulating blood volume were measured in dogs using a continuous monitoring method of circulating blood volume. A significant (p less than 0.01) increase in transvascular fluid shift was observed after the start of blood withdrawal and a new equilibrium state was reached within 15 to 20 min. Associated with the fluid shift, a significant increase in plasma protein of about 1 g was observed. On the other hand, blood retransfusion caused significant (p less than 0.01) increases in the shift of fluid and protein from intravascular space to interstitial space. The magnitudes of the shift of fluid and protein were almost identical in both blood withdrawal and retransfusion. The Kedem-Katchalsky transport equation was applied to the results obtained in the present study in order to analyze the relative role of diffusion and convection and to estimate the reflection coefficient for protein. A significant (p less than 0.01) linear relationship was observed between fluid and protein movement. These results suggest that the convective process is involved in the shift of protein between intravascular and interstitial space observed after blood volume modification.

Animals↗

Canine blood volume and cardiovascular function during hyperthermia.

The effect of acute hyperthermia on hemodynamic functions and blood volume regulation was examined on eight splenectomized dogs. Elevation of core body temperature by 2 degrees C over 90 min caused significant increase in cardiac output (11.2 +/- 12.5 ml X min-1 X kg-1 or about 10%) and significant decrease in total peripheral resistance (TPR; -1.3 +/- 1.0 mmHg X s X ml-1 or about 20%), whereas blood volume (BV), plasma oncotic pressure, and intravascular protein mass remained unchanged. Thus the raised core temperature caused peripheral vasodilation with decreased TPR and compensatory increase in cardiac output. Because BV remained unchanged during warming, mobilization of extravascular fluid did not occur; only the redistribution of blood to the vasodilated cutaneous circulation took place. To assess the effects of heat stress on transvascular fluid equilibrium, Ringer solution (10.7 ml X kg-1 X 10 min-1) was infused under normothermic and hyperthermic conditions. The volume of fluid retained within the intravascular space under equilibrium state was 33.5% in hyperthermia and 9.4% in normothermia. In hyperthermia, the transvascular fluid shift and urinary output were decreased both during and after infusion. The role of preferential fluid retention within the intravascular space observed during hyperthermia was discussed in relation to the mechanism to maintain cardiovascular function and BV under heat stress.

Animals↗

Distribution of water losses among fluid compartments of tissues under thermal dehydration in the rat.

Dehydration amounting to about 10% of body weight was induced in adult male rats by exposure to a hot, dry environment (D.B.T., 36 degrees C; R.H., 20%) over 6 to 8 hr. The volumes of total water (TW), extracellular fluid (ECF), and plasma (PV) were determined both on individual tissues and on the whole body using the constant dry weight as well as 51Cr-EDTA and 125I-RIHSA dilution methods. Total body water (TBW), intracellular (ICF), and interstitial (ISF) fluid volumes were calculated from these data. The 10% loss of body weight caused a decrease in TBW by 17% from the control value; 41% of this loss was from ICF, 47% from ISF, and 12% from PV. The decrease of ISF was proportional to that of PV and the water loss from ICF was caused by an increase in plasma osmolality. As to the water loss from organs, 40% of the whole body water loss came from muscle, 30% from skin, 14% from bone, and 14% from viscera. The G.I. tract had the highest tendency to lose water while the brain and liver showed the least. These findings suggest that under heat-induced dehydration, both the extra- and intracellular fluid compartments of muscle and skin play an important role in the compensation of water loss and in the maintenance of circulation to the brain and liver.

Animals↗