Regional sciatic nerve and muscle blood flow in conscious and anesthetized rats

1986 ◽  
Vol 251 (6) ◽  
pp. H1211-H1216 ◽  
Author(s):  
H. Sugimoto ◽  
W. W. Monafo ◽  
S. G. Eliasson

The regulation of peripheral nerve blood flow is incompletely understood. Regional blood flow in the rat sciatic nerve (NBF) and hamstring muscle (MBF) was measured in both conscious and anesthetized normal rats and in rats that had undergone surgical exposure of one sciatic nerve just prior to measurement. The distribution of [14C]butanol following its bolus intravenous injection was used to determine the flows in a modification of the “indicator fractionation” technique. NBF in normal rats was similar in limb pairs and was unaffected by pentobarbital sodium anesthesia. The pooled value was 12.5 +/- 1.1 ml X min-1 X 100 g-1. NBF was unaffected by sham operation in the conscious rats but was doubled in operated limbs of anesthetized rats (P less than 0.001). MBF in conscious normal rats was five times that measured during anesthesia. As in NBF, sham operation significantly increased MBF only in anesthetized rats (P less than 0.01). [14C]butanol distribution is a sensitive indicator of NBF and MBF. Mere surgical exposure of the nerve significantly increases NBF and MBF in anesthetized, but not in conscious rats.

1993 ◽  
Vol 265 (4) ◽  
pp. H1155-H1159
Author(s):  
Y. Kinoshita ◽  
W. W. Monafo

The spinal cord vasculature is innervated by noradrenergic nerve fibers, the role of which in the regulation of regional spinal cord blood flow (RSCBF) is presently unclear. We used the distribution of [14C]butanol to simultaneously measure RSCBF at seven cord levels and the regional blood flow in sciatic nerve (NBF), truncal skin, and biceps femoris muscle. The subjects were control rats and rats that had been given parenteral guanethidine sulfate for 5 wk to induce selective postganglionic "chemical sympathectomy." Flows were measured under basal conditions (group I) and immediately after an arterial hemorrhage (group II). The results indicate that RSCBF was unchanged from control after guanethidine administration in both groups; however, NBF was elevated after guanethidine by 47% in group I and by 41% in group II. We conclude that in the spinal cord as in the brain, sympathetic inflow does not appear to have an important role in the regulation of regional blood flow. Sympathetic inflow appears to partly regulate NBF, however, probably by varying vascular tone.


1995 ◽  
Vol 82 (1) ◽  
pp. 135-143 ◽  
Author(s):  
David H. Sigmon ◽  
Ivan Florentino-Pineda ◽  
Russell A. Van Dyke ◽  
William H. Beierwaltes

Background The endogenous vasodilator endothelium-derived nitric oxide (EDNO) contributes to the regulation of vascular tone and organ perfusion. It has been suggested that some volatile anesthetics may diminish the influence of EDNO and thereby decrease regional blood flow. Methods Radioactive microspheres were used to determine regional hemodynamics in rats. The authors tested the hypothesis that halothane inhibits EDNO and, therefore, should diminish the response to nitric oxide synthesis inhibition by NW-nitro-L-arginine methyl ester (L-NAME) compared with either conscious or barbiturate-anesthetized rats. Results NW-nitro-L-arginine methyl ester decreased blood flow to the brain by 23% (P < 0.005) in conscious rats to a level similar to that seen with either anesthetic agent. In both conscious and barbiturate-anesthetized rats, L-NAME increased blood pressure (BP) by 24 +/- 2 (P < 0.001) and 20 +/- 1 (P < 0.001) mmHg and total peripheral resistance (TPR) by 132% (P < 0.001) and 105% (P < 0.001), respectively. In contrast, during halothane anesthesia, both the pressor response (only 7 +/- 1 mmHg) and the increase in TPR (only 22%) were greatly diminished (P < 0.001). NW-nitro-L-arginine methyl ester decreased cardiac output (CO) by 47% (P < 0.001) and heart rate (HR) by 28% (P < 0.001) in conscious rats. In barbiturate-anesthetized rats, L-NAME decreased CO by 38% (P < 0.005) and HR by 13% (P < 0.001). In halothane-anesthetized rats, L-NAME changed neither CO nor HR. Thus halothane anesthesia largely eliminated the systemic response to EDNO synthesis inhibition. In conscious rats, L-NAME decreased blood flow to the heart (30%) and kidneys (47%). In barbiturate-anesthetized rats, L-NAME did not alter blood flow to the heart but decreased renal blood flow by 35% (P < 0.005). In halothane-anesthetized rats, L-NAME did not alter blood flow to either the heart or the kidneys. Overall, halothane blunted or blocked the systemic and regional hemodynamic responses to EDNO synthesis inhibition seen in conscious and barbiturate-anesthetized rats. Conclusions Halothane anesthesia greatly diminished or eliminated all systemic and regional hemodynamic responses to L-NAME. These data indicate that halothane anesthesia inhibits EDNO-mediated regulation of systemic and organ hemodynamics.


1987 ◽  
Vol 97 (2) ◽  
pp. 383-390 ◽  
Author(s):  
Hisashi Sugimoto ◽  
William W Monafo ◽  
Shuji Shimazaki

1997 ◽  
Vol 273 (1) ◽  
pp. E174-E184 ◽  
Author(s):  
Y. Ido ◽  
K. Chang ◽  
W. LeJeune ◽  
R. G. Tilton ◽  
W. W. Monafo ◽  
...  

The most widely used methods to assess nerve blood flow in diabetics rats are hydrogen clearance polarography and laser Doppler flowmetry, techniques requiring surgical exposure of the nerve. In these experiments, we examined the hypothesis that the trauma of surgical exposure introduces an important and hitherto largely unrecognized variable that could account for discordant reports on nerve blood flow changes induced by diabetes. We used the noninvasive (for sciatic nerve) reference sample microsphere method to quantify sciatic nerve blood flow in unexposed va. surgically exposed nerves in rats with streptozotocin-induced diabetes (at different temperatures and after curarization) and in unexposed vs. surgically exposed nerves in galactose-fed rats. Baseline resting blood flow in unexposed nerves in both animal models of diabetes was either normal or increased (but was decreased in diabetic rats given d-tubocurarine). Furthermore, the normal brisk hyperemic nerve blood flow response to the minimal trauma associated with surgical exposure of the nerve was markedly impaired in diabetic and in galactose-fed rats. Normalization of the blood flow response to trauma in galactose-fed rats by an aldose reductase inhibitor suggests that the impairment is linked to increased polyol pathway metabolism. These findings 1) confirm our previous findings that sciatic nerve blood flow in diabetic rats is increased or unchanged in unexposed nerves, while also confirming reports that in surgically exposed nerves blood flow is higher in control than in diabetic rats, and 2) indicate that blood flows in surgically exposed nerves are largely a measure of vascular responses to injury rather than (patho)physiological blood flow in undisturbed nerves.


1995 ◽  
Vol 268 (2) ◽  
pp. R492-R497 ◽  
Author(s):  
C. H. Lang ◽  
M. Ajmal ◽  
A. G. Baillie

Intracerebroventricular injection of N-methyl-D-aspartate (NMDA) produces hyperglycemia and increases whole body glucose uptake. The purpose of the present study was to determine in rats which tissues are responsible for the elevated rate of glucose disposal. NMDA was injected intracerebroventricularly, and the glucose metabolic rate (Rg) was determined for individual tissues 20-60 min later using 2-deoxy-D-[U-14C]glucose. NMDA decreased Rg in skin, ileum, lung, and liver (30-35%) compared with time-matched control animals. In contrast, Rg in skeletal muscle and heart was increased 150-160%. This increased Rg was not due to an elevation in plasma insulin concentrations. In subsequent studies, the sciatic nerve in one leg was cut 4 h before injection of NMDA. NMDA increased Rg in the gastrocnemius (149%) and soleus (220%) in the innervated leg. However, Rg was not increased after NMDA in contralateral muscles from the denervated limb. Data from a third series of experiments indicated that the NMDA-induced increase in Rg by innervated muscle and its abolition in the denervated muscle were not due to changes in muscle blood flow. The results of the present study indicate that 1) central administration of NMDA increases whole body glucose uptake by preferentially stimulating glucose uptake by skeletal muscle, and 2) the enhanced glucose uptake by muscle is neurally mediated and independent of changes in either the plasma insulin concentration or regional blood flow.


2004 ◽  
Vol 16 (1) ◽  
pp. 33-37 ◽  
Author(s):  
Tadashi Matsuzawa ◽  
Tsutomu Meguro ◽  
Katsuhiko Eguchi ◽  
Tsugio Yoshida ◽  
Touru Maejima ◽  
...  

1986 ◽  
Vol 250 (3) ◽  
pp. R499-R504 ◽  
Author(s):  
F. M. Faraci ◽  
M. R. Fedde

To investigate mechanisms that may allow birds to tolerate extreme high altitude (hypocapnic hypoxia), we examined the effects of severe hypocapnia and moderate hypercapnia on regional blood flow in bar-headed geese (Anser indicus), a species that flies at altitudes up to 9,000 m. Cerebral, coronary, and pectoral muscle blood flows were measured using radioactive microspheres, while arterial CO2 tension (PaCO2) was varied from 7 to 62 Torr in awake normoxic birds. Arterial blood pressure was not affected by hypocapnia but increased slightly during hypercapnia. Heart rate did not change during alterations in PaCO2. Severe hypocapnia did not significantly alter cerebral, coronary, or pectoral muscle blood flow. Hypercapnia markedly increased cerebral and coronary blood flow, but pectoral muscle blood flow was unaffected. The lack of a blood flow reduction during severe hypocapnia may represent an important adaptation in these birds, enabling them to increase O2 delivery to the heart and brain at extreme altitude despite the presence of a very low PaCO2.


1984 ◽  
Vol 247 (1) ◽  
pp. H35-H39 ◽  
Author(s):  
I. Kobrin ◽  
M. B. Kardon ◽  
W. Oigman ◽  
B. L. Pegram ◽  
E. D. Frohlich

The influences of the site of microsphere injection (intra-atrial vs. intraventricular) and positioning of the left ventricular catheter (aortoventricular vs. atrioventricular) on systemic, renal, and coronary hemodynamics were evaluated in anesthetized rats. The effect of anesthesia on aortoventricular catheter positioning was also evaluated. In anesthetized and open-chest preparations, the systemic and renal hemodynamics were not affected by catheter position or site of microsphere injection; however, myocardial blood flow was dependent on these variables. Variations in coronary blood flow were significantly greater when the catheter was in the aortoventricular position (34 +/- 3%) than with an atrioventricular catheter (11 +/- 2%, P less than 0.01), irrespective of whether the microspheres were injected into the atrium or ventricle. Comparison of anesthetized and conscious rats with aortoventricular catheter indicated lesser variability in coronary blood flow in the conscious rats (P less than 0.01). Therefore, the greater variability of coronary flow measurements in anesthetized rats was caused by the position of the cardiac catheter in the aortoventricular route. However, the variability caused by the aortoventricular catheter was much less in conscious rats. Therefore, coronary flow hemodynamic measurements (microsphere technique) are less variable when they are made in conscious rats.


1990 ◽  
Vol 259 (6) ◽  
pp. H1649-H1654
Author(s):  
T. Sakamoto ◽  
A. Iwai ◽  
W. W. Monafo

Regional blood flow (RBF) increases in the spinal cord and sciatic nerve of acutely hypothermic rats. To determine whether cord transection affects this response, we measured RBF in rat spinal cord and sciatic nerve 2 h after cord transection at vertebrae T8 (n = 18 rats) and T11 (n = 18 rats) using [14C]butanol distribution. Nine in each group were normothermic controls. In T11 transection-hypothermia (25-27 degrees C rectal temperature), RBF increased in the three rostral cord segments by 28-40% (P less than 0.05); caudally, cord RBF was depressed in two segments (P less than 0.05), unchanged in the other; RBF fell in nerve (P less than 0.05). In T8 transection-hypothermia, RBF was unchanged in the two rostral cord segments; caudally, RBF was depressed in one cord segment (P less than 0.05) and unchanged in the others; RBF was unchanged in nerve. We conclude that RBF does not rise in caudal spinal cord segments or in sciatic nerve during hypothermia in rats with prior spinal cord transection.


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