The Distribution of Cardiac Output in the Anaesthetized Spontaneously Hypertensive Rat

1978 ◽  
Vol 55 (3) ◽  
pp. 317-320 ◽  
Author(s):  
C. R. Hiley ◽  
M. S. Yates
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Cardiac Output ◽  
Spontaneously Hypertensive Rats ◽  
Spontaneously Hypertensive Rat ◽  
Regional Distribution ◽  
Tissue Blood Flow ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Distribution Of Cardiac Output

1. Radioactive 15 μm and 50 μm diameter microspheres were used to determine cardiac output, its regional distribution and tissue blood flow in adult normotensive Wistar and Okamoto spontaneously hypertensive rats. 2. Cardiac output in the spontaneously hypertensive rats was the same as in Wistar normotensive rats, but its distribution in the hypertensive rats appeared to differ: there was a significant increase in the proportion of microspheres trapped in the liver whereas fewer were found in the gastrointestinal tract. This indicates that a greater fraction of the cardiac output passes along the hepatic artery and less through the splanchnic bed. 3. Blood flow in skin and skeletal muscle in spontaneously hypertensive rats was approximately 50% of that in Wistar normotensive rats.

Prolonged tissue Po2 reduction after contraction in spinotrapezius muscle of spontaneously hypertensive rats

2004 ◽  
Vol 287 (1) ◽  
pp. H401-H407 ◽  
Author(s):  
Lane M. Smith ◽  
R. Wayne Barbee ◽  
Kevin R. Ward ◽  
Roland N. Pittman
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Muscle Contraction ◽  
Spontaneously Hypertensive Rats ◽  
Primary Role ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Tissue Po2 ◽  
Significant Difference ◽  
Delayed Recovery

We tested the hypothesis that a deficit in oxygen extraction or an increase in oxygen demand after skeletal muscle contraction leads to delayed recovery of tissue oxygen tension (Po2) in the skeletal muscle of hypertensive rats compared with normotensive rats. Blood flow and Po2 recovery at various sites in the spinotrapezius muscle of spontaneously hypertensive rats (SHRs) were evaluated after a 3-min period of muscle contraction and were compared with corresponding values in Wistar-Kyoto rats (WKYs). The recovery of tissue Po2 [75 ± 7 (SHRs) vs. 99 ± 12% (WKYs) of resting values] and venular Po2 [72 ± 13 (SHRs) vs. 104 ± 10% (WKYs) of resting values] were significantly depressed in the SHRs 30 s postcontraction. The delayed recovery persisted for 120 s postcontraction for both tissue [86 ± 11 (SHRs) vs. 119 ± 13% (WKYs) of resting values] and venular [74 ± 2 (SHRs) vs. 100 ± 9% (WKYs) of resting values] Po2 levels. There was no significant difference in the recovery of arteriolar Po2 between the two groups 30 s postcontraction [95 ± 7 (SHRs) vs. 84 ± 8% (WKYs) of resting values]. Values for resting diameter of arcade arterioles in the two groups were not different [52 ± 3 (SHRs) vs. 51 ± 3 μm (WKYs)], but the arteriolar diameter after the 3-min contraction period was greater in the SHRs (71 ± 4 μm) than the WKYs (66 ± 4). Likewise, red blood cell (RBC) velocity [5.8 ± 0.3 (SHRs) vs. 4.7 ± 0.2 mm/s (WKYs)] and blood flow [23.0 ± 0.8 (SHRs) vs. 16.0 ± 1.0 nl/s (WKYs)] measurements were significantly greater in the SHRs at 30 s postcontraction. The delayed recovery of tissue Po2 in the SHRs compared with the WKYs can be explained by a decrease in oxygen diffusion from the rarefied microvascular network due to the increased RBC velocity and the shorter residence time in the microcirculation and the consequent disequilibrium for oxygen between plasma and RBCs. The delayed recovery of venular Po2 in the SHRs is consistent with this explanation, as venular Po2 is slowly restored to baseline by release of oxygen from the RBCs. This leaves the arterioles in the primary role as oxygen suppliers to restore Po2 in the tissue after muscle contraction.

Excess oxygen delivery during muscle contractions in spontaneously hypertensive rats

1995 ◽  
Vol 78 (1) ◽  
pp. 101-111 ◽  
Author(s):  
J. M. Lash ◽  
H. G. Bohlen
Keyword(s):  
Blood Flow ◽  
Oxygen Saturation ◽  
Oxygen Delivery ◽  
Spontaneously Hypertensive Rats ◽  
Muscle Contractions ◽  
Hypertensive Rats ◽  
Hemoglobin Oxygen Saturation ◽  
Spontaneously Hypertensive ◽  
Tissue Po2 ◽  
Wistar Kyoto

These experiments determined whether a deficit in oxygen supply relative to demand could account for the sustained decrease in tissue PO2 observed during contractions of the spinotrapezius muscle in spontaneously hypertensive rats (SHR). Relative changes in blood flow were determined from measurements of vessel diameter and red blood cell velocity. Venular hemoglobin oxygen saturation measurements were performed by using in vivo spectrophotometric techniques. The relative dilation [times control (xCT)] of arteriolar vessels during contractions was as large or greater in SHR than in normotensive rats (Wistar-Kyoto), as were the increases in blood flow (2 Hz, 3.50 +/- 0.69 vs. 3.00 +/- 1.05 xCT; 4 Hz, 10.20 +/- 3.06 vs. 9.00 +/- 1.48 xCT; 8 Hz, 16.40 +/- 3.95 vs. 10.70 +/- 2.48 xCT). Venular hemoglobin oxygen saturation was lower in the resting muscle of SHR than of Wistar-Kyoto rats (31.0 +/= 3.0 vs. 43.0 +/- 1.9%) but was higher in SHR after 4- and 8-Hz contractions (4 Hz, 52.0 +/- 4.8 vs. 43.0 +/- 3.6%; 8 Hz, 51.0 +/- 4.6 vs. 41.0 +/- 3.6%). Therefore, an excess in oxygen delivery occurs relative to oxygen use during muscle contractions in SHR. The previous and current results can be reconciled by considering the possibility that oxygen exchange is limited in SHR by a decrease in anatomic or perfused capillary density, arteriovenular shunting of blood, or decreased transit time of red blood cells through exchange vessels.

Cochlear blood flow in relation to age in normotensive and spontaneously hypertensive rats

1987 ◽  
Vol 104 (3-4) ◽  
pp. 243-250 ◽  
Author(s):  
Maria Hillerdal ◽  
Erik Borg ◽  
Berit Engstrom ◽  
Elisabeth Hultcrantz
Keyword(s):  
Blood Flow ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Cochlear Blood Flow ◽  
Spontaneously Hypertensive

Mechanism of exaggerated diuresis in spontaneously hypertensive rats

1978 ◽  
Vol 235 (5) ◽  
pp. F409-F416 ◽  
Author(s):  
Gerald F. DiBona ◽  
Linda L. Rios
Keyword(s):  
Volume Expansion ◽  
Spontaneously Hypertensive Rats ◽  
Spontaneously Hypertensive Rat ◽  
Renal Perfusion ◽  
Sodium Reabsorption ◽  
Loop Of Henle ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Single Nephron ◽  
Wistar Kyoto

The mechanism of exaggerated diuresis and natriuresis was studied in spontaneously hypertensive rats (SHR) by renal clearance and micropuncture techniques. Control normotensive rats of the same age and sex [Wistar-Kyoto rats (WKY)] were also studied. During the hydropenic control and the volume-expansion experimental periods absolute and fractional water and sodium excretion were greater in SHR than in WKY. Although fractional and absolute water and sodium reabsorption were similar along the proximal convolution in SHR and WKY, fractional and absolute water reabsorption in Henle's loop was less in SHR than in WKY. Hydrostatic and colloid osmotic pressures in the cortical peritubular microvasculature were similar in WKY and SHR. Acute normalization of renal perfusion pressure by aortic constriction reversed the exaggerated diuresis and natriuresis in SHR by halving the filtered load of water and sodium; whole kidney and single nephron glomerular filtration rates and blood flows decreased by 50%. It is concluded that the exaggerated diuresis and natriuresis of the spontaneously hypertensive rat is caused by a decreased reabsorption in the loop of Henle. The mechanism of this decreased reabsorption in the loop of Henle cannot be explained by alterations in the measured physical forces in the renal cortical microvasculature. natriuresis; autoregulation; volume expansion Submitted on November 15, 1977 Accepted on June 7, 1978

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