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Biomedical subjects

G A Meininger

Publications and source records attributed to G A Meininger.

At least 55 records · Page 3Linked to original sources
PubMed1991

Effect of vasodilation and vasoconstriction on microvascular pressures in skeletal muscle.

The effect of topically applied papaverine (PAP) and norepinephrine (NE), on the microvascular pressure distribution was studied in the cremaster muscle of anesthetized rats. The cremaster muscle was exteriorized into a tissue bath containing Krebs bicarbonate buffer, and microvessel diameters and pressures were measured using a video caliper and the resistance servo-null method, respectively. Pressures were measured in the 1st through 4th branch order arterioles (1A to 4A) and 1st through 4th branch order venules (1V to 4V). Resistances were calculated across each segment from pressure gradients and 1A blood flow which was estimated from red cell velocities. PAP (10 microM) produced approximately a 15% decrease in arteriolar pressures with a concomitant increase in venular pressures of between 15 and 50%. In contrast, NE (0.1 microM) significantly increased arteriolar pressure by approximately 30% and decreased venular pressure by about 25%. Changes in systemic pressure during treatment with PAP and NE were small or insignificant and could not account for the observed changes in microvascular pressure. Significant dilation was observed in 3A, 4A, and 3V vessels after papaverine. In comparison, NE caused significant constriction in all vessel orders except 4V. PAP decreased resistance across all segments between 1A and 4V by 22-42% and increased venular resistance by almost 400%. NE increased resistance in all microvascular segments with the largest changes occurring in 2A to 3A (+276%) and 4A to 4V (+277%) segments. These data demonstrate that PAP and NE induce significant and opposite changes in arteriolar and venular pressures. Such network alterations in microvascular pressure should be considered when evaluating microvascular reactivity and exchange in the presence of vasoactive agents.

Animals↗
PubMed1990

Altered cremaster muscle hemodynamics due to disruption of the deferential feed vessels.

Surgical preparation of the cremaster muscle for microvascular studies typically requires disruption of collateral vessels within the muscle and between the cremaster and the structures of the epididymis/ductus deferens. To study the effect of interrupting these vascular connections on cremaster hemodynamics, two modified preparations were examined in addition to the conventional open cremaster muscle preparation. One of these preparations enabled the measurement of feed vessel (1A) pressure and diameter with all cremaster vascular connections intact. The second preparation involved interruption of intramuscle collaterals to open the cremaster sac but with intact collateral pathways between the cremaster and deferential vessels. Intravascular pressures in the main cremasteric arteriole (1A) were similar in all three preparations with pressure in the 1A, expressed as a percentage of femoral artery pressure, varying between 53% in the intact preparation and 48% in the standard open preparation. These data support the existence of substantial upstream vascular resistance regardless of the extent of surgery. Selective occlusion of the branches of the deferential vessels significantly increased red cell velocity in the cremasteric 1A and major draining venule (1V) so that calculated blood flow increased by approximately 40% (P less than 0.01) in the 1A and 95% (P less than 0.01) in the 1V. Also, intravascular pressure fell significantly (P less than 0.01) in the 1A and increased in the 1V. Despite these compensatory changes total blood flow to the muscle was reduced by approximately 40% in the standard open preparation, compared to the preparation with the deferential feed pathway intact. Further studies where the 1A flow was transiently occluded indicated that the deferential pathway was capable of providing significant collateral blood flow to the muscle. Collectively these studies demonstrate that the surgical modifications of the cremaster vascular supply required for in vivo microscopy significantly alter normal hemodynamics within the vascular bed. The surgery does not, however, entirely explain the large pressure drop that exists upstream of the cremasteric 1A.

Analysis of Variance↗
PubMed1990

Cyclooxygenase inhibition potentiates myogenic activity in skeletal muscle arterioles.

The proposition that arteriolar constriction to increased intravascular pressure is mediated through either the increased local production of an eicosanoid constrictor factor or decreased production of a dilating factor was examined. The myogenic response of arterioles was studied by enclosing anesthetized rats in an airtight Plexiglas box with the cremaster muscle exteriorized into a tissue bath containing Krebs solution. Microvascular responses were observed by video microscopy. The arteriolar response to a 20-mmHg increase in intravascular pressure was examined in the absence or presence of cyclooxygenase inhibition. In the absence of cyclooxygenase inhibition, second-order arterioles (2As) responded passively to increased pressure by distending to 107 +/- 1% of control diameter. In the presence of the indomethacin, 2As constricted to 79 +/- 5% of control. Third-order arterioles (3As) constricted to 47 +/- 8% of control without indomethacin and similarly to 33 +/- 4% with indomethacin. To test whether inhibitors of endothelium-derived relaxation factor would potentiate the myogenic response of 3As, methylene blue or gossypol was topically applied to the cremaster muscle. Neither inhibitor was found to augment the myogenic vasoconstriction; however, these inhibitors were observed to significantly reduce basal vascular tone. In comparison, the tonic local production of dilating prostaglandins appears to attenuate myogenic activity as demonstrated by the appearance of myogenic activity in the normally passive 2As when exposed to cyclooxygenase inhibitors.

Animals↗
PubMed1990

Combined effects of autoregulation and vasoconstrictors on hindquarters vascular resistance.

Relative contributions of local autoregulatory tone and vasoconstrictor tone to skeletal muscle vascular resistance were studied in anesthetized rats during hypertension produced by vasoconstrictor infusion. Rats were instrumented with a Doppler flow probe on the sacral aorta (SA) to measure blood flow and to allow calculation of vascular resistance. An occluder was placed on the SA and used to produce stepwise reductions in local perfusion pressure. Pressure-flow curves for the hindquarters were obtained in the absence and presence of elevated mean arterial pressure (MAP) produced by infusion of angiotensin II (ANG II; 50-1,247 ng.kg-1.min-1) or phenylephrine (PE; 2.5-12.4 micrograms.kg-1.min-1). Both ANG II and PE infusion increased MAP. For example, MAP was increased by ANG II from 91 to 134 mmHg and by PE from 89 to 156 mmHg. In addition, infusions of ANG II and PE produced dose-dependent rightward shifts in the hindquarters pressure-flow relationship. To examine the effect of pressure on the dose-response relationships of ANG II or PE, local perfusion pressure was adjusted to remain constant at various pressure levels that were independent of MAP during drug infusions. This produced a series of distinct dose-response curves with each curve defined by a different pressure level and with each characterized by a different maximum change in vascular resistance. If local perfusion pressure was not held constant but was permitted to increase with MAP, a compound dose-response curve was obtained in which the combined effects of the change in local pressure (i.e., autoregulation) and vasoconstrictor dose on vascular resistance could be discerned. These data demonstrate that hindquarters blood flow autoregulation continues to occur in the presence of vasoconstrictors. Consequently, autoregulatory mechanisms may be stimulated by any increase in MAP whether associated with systemic vasoconstrictor infusion or activation of neurohumoral pressor systems. The result is an amplified rise in local vascular resistance.

Angiotensin II↗
PubMed1990

Selective interaction of alpha-adrenoceptors with myogenic regulation of microvascular smooth muscle.

The interaction of alpha 1- and alpha 2-adrenoceptor constriction of arterioles with the myogenic mechanism was examined in rat cremaster skeletal muscle using intravital microscopy. Intravascular pressure was increased or decreased by changing pressure from 0 to +30 and 0 to -20 mmHg in a chamber that surrounded the animal but not the cremaster. Arterioles of 110 microns in diameter were constricted by approximately 30% with the alpha 1-agonist, phenylephrine, or the alpha 2-agonist, UK-14304. Increases in microvascular (box) pressure caused stepwise constrictions of similar magnitude (10-30%) regardless of the prevailing type of alpha-adrenergic tone. In contrast, during alpha 2 tone, decreases in pressure caused a three- to fourfold greater dilation (myogenic inhibition) than during alpha 1 tone. Thus myogenic constriction, normally minimal in these large arterioles, was amplified similarly during either alpha 1 or alpha 2 tone; however, alpha 2 tone was much more susceptible than alpha 1 tone to myogenic inhibition. Similar results were obtained with tone produced by thromboxane A2 vs. the Ca2+ channel agonist, BAY K 8644. Thus the particular sensitivity of alpha 2 constriction to myogenic inhibition may relate to interactions between these stimuli at the postreceptor level. The degree and type of alpha-adrenoceptor tone at different microvasculature levels may be important in myogenic autoregulatory blood flow adjustments during changes in perfusion pressure.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1990

Evidence for protein kinase C involvement in arteriolar myogenic reactivity.

Little information exists as to the cellular events that couple the myogenic contractile response of an arteriole to an acute rise in intravascular pressure. The aim of this study was to examine whether protein kinase C (PKC), which has been implicated in the contractile response to agonists, contributes to myogenic vasoconstriction of cremaster muscle arterioles. Studies were performed on anesthetized rats, enclosed in an airtight Plexiglas box, with the cremaster exteriorized into a bath containing Kreb's solution. Pressure in the box was increased to elevate intravascular pressure by 20 mmHg. To examine PKC involvement, studies were performed in the absence or presence of inhibitors of PKC: H 7 (10(-9)-10(-5) M) or staurosporine (10(-10)-10(-7) M). Inhibitors were added to the tissue bath and produced no observable systemic effects or alterations in arteriolar diameter. Third-order arteriole (16 +/- 1 microns diam) responses to these agents and alterations in intravascular pressure were monitored by in vivo microscopy and vessel diameter was measured with a video caliper. H 7 produced a concentration-dependent inhibition of myogenic vasoconstriction, inhibiting the extent of constriction by 75% at 10(-5) M. Similarly, staurosporine caused a concentration-dependent inhibition of pressure-induced constriction. At 10(-7) M staurosporine the myogenic response was inhibited by 82%. Further support for a role for PKC in the myogenic response was provided by the observation that indolactam (10(-6) M), a stimulator of PKC activity, induced myogenic reactivity in first-order arterioles, which under basal conditions show passive distension to increased intravascular pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Vasoconstriction is amplified by autoregulation during vasoconstrictor-induced hypertension.

This study investigated the degree to which autoregulation of blood flow interacts with vasoconstrictors to determine vascular resistance. Anesthetized rats were instrumented with a Doppler flow probe on the superior mesenteric artery (SMA) to measure blood flow and for calculation of vascular resistance. An adjustable occluder was placed on the SMA to set local perfusion pressure at values independent of mean arterial pressure (MAP) even when MAP was increased by the vasoconstrictors. Infusion of angiotensin II (ANG II, 50-1,247 ng.kg-1.min-1) produced a dose-dependent rightward shift in the intestinal pressure-flow relationship and elevated MAP from 85 to 127 mmHg. Low doses of phenylephrine (PE, 2.5-12.4 micrograms.kg-1.min-1) failed to shift the pressure-flow curve but did increase arterial pressure from 83 to 102 mmHg. At higher doses (25-62 micrograms.kg-1.min-1), PE also shifted the pressure-flow curve to the right. Maintaining local perfusion pressure at different values during the infusion of ANG II or PE produced a family of dose-response curves, with each exhibiting a different maximum change in resistance. When local pressure was permitted to increase with MAP, the composite dose-response curve for resistance that was obtained reflected the influence of the rise in local pressure (i.e., auto-regulation) and vasoconstrictor dose. At low doses of PE the increase in vascular resistance was attributable solely to an autoregulatory response related to the rise in MAP and not due to the constrictor effects of PE. Thus these data indicate that the rise in MAP accompanying systemic infusion of a vasoconstrictor stimulates autoregulation to amplify the local increase in vascular resistance.

Angiotensin II↗
PubMed1987

Anatomic and hemodynamic characteristics of the blood vessels feeding the cremaster skeletal muscle in the rat.

The anatomic arrangement, pressure distribution, and resting vascular tone of the feed arteries located upstream from the rat cremaster microcirculation were determined to characterize the sites of the vascular resistance in this macrovessel segment of the cremaster circulation. The cremaster microcirculation and its feeding arteries were studied using an intravital video microscopy system. Vascular diameters and pressures were measured with an image shearing monitor and servo-null micropipet system, respectively. The central arteriole of the cremaster muscle was found to be a distal segment of the external spermatic artery which branched from the pudic-epigastric artery that in turn arose from the common iliac artery. Together the length of these vessels, from the aorta to the cremaster muscle, was 37 mm and they accounted for 42% of the total pressure drop across the cremaster vascular network. The largest pressure drop (31 mm Hg) upstream from the cremaster occurred across the external spermatic artery which was also the longest (17.7 mm) feed vessel. Topical application of adenosine (1 X 10(-3) M) significantly dilated the pudic-epigastric artery and the external spermatic artery, indicating that these vessels had significant tone. In summary, our data indicate that the large fraction of network vascular resistance located in the feed vessels upstream from the cremaster is the result of both architectural features and vascular tone.

Adenosine↗
PubMed1987

Responses of sequentially branching macro- and microvessels during reactive hyperemia in skeletal muscle.

Small artery and microvascular responses during reactive hyperemia were compared to determine which resistance-bearing vessels played a role in controlling blood flow and resistance for the cremaster skeletal muscle. Using an intravital video microscopy system, measurements of microvessel pressure, flow velocity, and diameter were obtained from cremaster muscles in anesthetized rats. These were compared with measurements of diameter that were obtained from the small arteries feeding the cremaster muscle. After a 60-sec occlusion of the sacral aorta, total cremaster blood flow increased approximately 28% and calculated microvascular resistance for the cremaster muscle fell 50%. During the period of occlusion, diameters of small arteries (159-292 micron) decreased despite the presence of smooth muscle tone. Likewise, the diameters of large arterioles (65-117 micron) decreased whereas small arterioles (16-30 micron) dilated. The decrease in diameter of the small arteries and large arterioles was accompanied by a significant fall in intravascular pressure, suggesting that the behavior of these vessels was largely passive. Immediately following the release of occlusion, small arteries and large arterioles returned to their control diameters while small arterioles remained in a dilated state for approximately 2 min. These results indicate that for the cremaster muscle, vascular responses vary along the length of the arterial tree during reactive hyperemia, small but not large arterioles are primarily responsible for the decrease in network resistance and subsequent hyperemia following occlusion, and the small feeder arteries did not dilate during reactive hyperemia but instead acted to set a limit on the decrease in network resistance and the increase in blood flow.

Animals↗
PubMed1987

Splanchnic circulatory changes during development of renal hypertension.

Total and regional splanchnic blood flows were measured with radiolabeled microspheres (15 micron) in one-kidney, one-clip renal hypertensive rats at 2, 4, and 6 wk after induction of hypertension. Arterial pressures (mean +/- SE, mmHg) for the normotensive rats (N) and age-matched hypertensive rats (H) were 110 +/- 5 and 114 +/- 6 at 2 wk, 104 +/- 4 and 148 +/- 13 at 4 wk, and 117 +/- 6 and 164 +/- 11 at 6 wk, respectively. Total splanchnic blood flow was increased in H compared with N at 4 wk but not at 2 or 6 wk. The blood flow changes among individual splanchnic organs varied in N and H. For example, at 2 and 4 wk, stomach, small intestine, large intestine, pancreas, hepatic artery, and portal venous blood flows in H were unchanged compared with N. At 6 wk, small intestinal and hepatic arterial blood flows were increased in H compared with N, and pancreatic blood flow was decreased. Vascular resistance was not different for any splanchnic organs between N and H at 2 wk, but it was elevated in H for all organs at 4 and 6 wk except for the hepatic artery. In another group of rats, the renal and superior mesenteric arteries (SMA) were instrumented with ultrasonic Doppler flow probes. Acute one-kidney, one-clip hypertension was produced by removing one kidney and mechanically reducing flow to the remaining kidney with a pneumatic occluder. After 2 h of stenosis, mean arterial pressure and SMA flow velocity was decreased by 6%.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1987

Myogenic vasoregulation overrides local metabolic control in resting rat skeletal muscle.

Microvascular reactions to increases in intravascular pressure were studied in the cremaster muscle of the anesthetized rat by enclosing the animal in an airtight box with the muscle exteriorized for observation of the microcirculation. Since the cremaster was exposed to atmospheric pressure, increasing pressure within the box produced equal increases in arterial and venous pressures. Thus, intravascular pressure was altered without affecting the pressure gradient for blood flow. Raising box pressure had no effect on respiration or heart rate and did not change the systemic activity of the sympathetic system, angiotensin II, or vasopressin. Diameters and flows were measured for first (107 +/- 3 micron, mean +/- SEM), second (87 +/- 5), third (29 +/- 2), and fourth (15 +/- 2) order arterioles during increases in intravascular pressure of +10, +20, and +30 mm Hg. No significant changes in the diameters of first or second order arterioles were elicited when pressure was increased. However, when box pressure was increased to +10, +20, or +30 mm Hg, a sustained constriction occurred in third (29%, 45%, and 63%, respectively) and fourth (5%, 38%, and 57%, respectively) order arterioles. Blood flow was significantly reduced in all arterioles, and perivascular PO2 was decreased adjacent to third and fourth order arterioles. Furthermore, the third order arteriole constrictor response was not abolished by local alpha-receptor blockade (phentolamine), indicating that it was not mediated by a local sympathetic axon reflex. Collectively, these data indicate that a potent, non-neural, pressure-dependent mechanism for vasoregulation is present in small arterioles of the cremaster. The sustained constriction in the presence of reduced blood flow and reduced periarteriolar oxygen tension indicates that the vascular response is independent of and capable of overriding flow-dependent (i.e., metabolic) control in resting skeletal muscle. The observations are compatible with the operation of a powerful myogenic mechanism in small arterioles.

Animals↗
PubMed1986

Hemodynamic characteristics of the intestinal microcirculation in renal hypertension.

This study investigated the microvascular changes that affect vascular resistance in the rat small intestine during two-kidney, one clip renal hypertension 4 weeks after renal artery stenosis. To study the intestinal microcirculation, a loop of the small intestine was exteriorized with intact circulation and innervation and a section of the bowel wall was prepared for observation with an intravital video microscopy system. Microvascular diameter, pressure, and flow velocity were measured for first, second, and third branch order arterioles and venules, using an image shearing monitor, servo-null micropipette system, and an optical Doppler velocimeter, respectively. The diameters of the first order arterioles and venules were significantly (p less than 0.05) reduced in hypertensive rats; however, diameters were unaltered in smaller second and third order arterioles and venules as compared with normotensive vessels. In hypertensive rats, mean arterial pressure was significantly (p less than 0.05) elevated (47%) and pressures also were elevated significantly (p less than 0.05) throughout the microcirculation, although by a proportionally smaller amount. Total network flow (i.e., first order arteriole flow) was significantly (p less than 0.05) reduced (40%) in hypertensive rats, but volume flows in individual second and third order arterioles were similar to flows measured in normotensive rats. Calculated total network resistance was increased (124%) in hypertensive rats. Thus, the intestinal microcirculation in rats with two-kidney, one clip renal hypertension is disturbed by elevated pressure and decreased total flow. The presence of normal flows in individual second and third order arterioles without any demonstrable difference in their diameters suggests that the predominant cause of elevated resistance across this segment of the intestinal microcirculation is a reduction in the number of perfused small arterioles.

Animals↗
PubMed1985

Altered skeletal muscle microvascular hemodynamics after one week of streptozotocin-induced diabetes.

The aim of this study was to examine alterations in skeletal muscle microvascular hemodynamics occurring one week after the onset of streptozotocin diabetes. Diabetes was induced in 9 male, Sprague-Dawley rats by intraperitoneal streptozotocin (60 mg/kg); 10 age-matched rats acted as controls. The animals were then studied 6-8 days after the induction of diabetes. For study of skeletal muscle microvascular hemodynamics the right cremaster muscle was exteriorized. Vessel diameters were measured with an image shearing monitor and red blood cell velocity was determined with an optical Doppler velocimeter. Measurements were taken in the resting and dilated (adenosine applied topically to the muscle) states. In the resting state, diabetic rats showed significant enlargement of venules less than 120 microM, while arteriolar diameters were comparable to those of controls. The extent of dilation in response to adenosine was significantly decreased in both the arterioles and venules of the diabetic animals. Blood flow through the main arteriole supplying the tissue was significantly decreased in the diabetic animals in both the resting and dilated states. The results of this study demonstrate changes in skeletal muscle hemodynamics after one week of streptozotocin diabetes. The diabetic animals are characterized by decreased perfusion and diminished ability to lower vascular resistance by vasodilation.

Animals↗
PubMed1984

Hemodynamic and microvascular responses in the hindquarters during the development of renal hypertension in rats. Evidence for the involvement of an autoregulatory component.

Microvascular responses in the cremaster muscle were compared with changes in mean arterial pressure and hindquarters vascular resistance during the development (initial 3 hours) of two-kidney one-clip renal hypertension in rats, to examine the possibility that an autoregulatory mechanism may contribute to the development of hypertension. Rats were anesthetized with urethane and chloralose and implanted with Doppler flow probes on the renal artery and abdominal aorta. Acute hypertension was produced by inflation of a balloon occluder on the renal artery to reduce renal flow by 50%. The cremaster muscle was isolated with intact innervation and circulation for measurement of microvessel diameters. To determine whether increased pressure contributed to the changes in hindquarters vascular resistance or in microvascular diameters during acute hypertension, arterial pressure was prevented from increasing in the hindquarters region after renal artery stenosis by servo-controlled inflation of a balloon occluder around the sacral aorta to maintain hindquarters pressure at normotensive levels. In hypertensive rats with unprotected hindquarters, mean arterial pressure and hindquarters vascular resistance increased 26% and 20%, respectively, after renal artery stenosis. In comparison, hypertensive rats with protected hindquarters exhibited a similar increase in mean arterial pressure, but hindquarters vascular resistance was significantly reduced compared to that in hypertensive rats with unprotected hindquarters. In the cremaster microcirculation, vasoconstriction was observed only in the small third- (mean +/- SEM: 29 +/- 4 micron) and fourth- (12 +/- 2 micron) order arterioles in rats with unprotected hindquarters. In general, microvessel diameters in rats with protected hindquarters that had lower hindquarters vascular resistance than those with unprotected hindquarters were larger for the second- (82 +/- 5 micron), third-, and fourth-order arterioles, suggesting less vasoconstrictor tone. Our data indicate that the increase in hindquarters resistance during the development of renal hypertension is, in part, dependent on the presence of a pressure-dependent autoregulatory process.

Animals↗
PubMed1984

Central and regional hemodynamics during the acute onset of renal hypertension in rats.

The purpose of this study was to quantitate the regional changes in flow and resistance which occur during the acute onset of two-kidney, one clip renal hypertension. Anesthetized rats were implanted with a Doppler flow probe and balloon occluder on one renal artery. To produce acute hypertension, the occluder was inflated to reduce renal flow velocity by 50%. After 90 minutes, mean arterial pressure increased 25% above the prestenosis control period value as a result of a 22% increase in peripheral resistance. Regional flows and resistances were determined prior to and 90 minutes after renal artery stenosis by injection of labelled microspheres into the left ventricle. Our major findings were that: 1) the regional hemodynamic changes in flow and resistance are unevenly distributed among individual organs; and 2) the major site of increased resistance resides in the splanchnic circulation with the largest increases occurring in the small intestine.

Animals↗
PubMed1983

Splanchnic circulation in hypertension.

The effect of arterial hypertension on the splanchnic circulation is assessed. In human essential hypertension, splanchnic vascular resistance rises in proportion to the blood pressure, and the transvascular escape rate of plasma proteins is increased. The various animal models of hypertension show variable results, but in general support the concept that vascular resistance changes in the splanchnic organs are similar in direction and magnitude to pressure changes. This is especially true in longer-term chronic experiments. These resistance changes appear to result from increased responsiveness of the arterioles to a variety of constrictor influences, and they may result from either structural or functional changes. Hypertension appears to alter splanchnic arteriolar permeability via a pressure-dependent mechanism. These vessels may also undergo degenerative histological changes. Capillaries and small venules experience increased endothelial permeability via a pressure-independent mechanism that is not mediated by angiotensin II. In addition to the resistive and exchange alterations, the capacitance function of splanchnic veins is reduced, probably via a structural change. Much work remains to be done before the characterization is complete. Especially needed are studies of individual organs with respect to vascular resistance, exchange, and capacitance alterations in the various models of hypertension.

Animals↗
PubMed1980

A model for hypokinesia: effects on muscle atrophy in the rat.

Hypokinesia in the hindlimbs of rats were induced by suspension; a newly developed harness system was used. The animal was able to use its forelimbs to maneuver, within a 140 degrees arc, to obtain food and water and to permit limited grooming of the forequarters. The hindlimbs were nonload bearing for 7 days; following a 7-day period of hypodynamia, selected animals were placed in metabolic cages for 7 days to study recovery from hypokinesia. During the 7-day period of hypokinesia there was evidence of muscle atrophy. Gastrocnemius weight decreased, renal papillary urea content increased, and daily urinary losses of urea, NH3, and 3-methylhistidine increased. During the 7-day recovery period muscle mass and excretion rate of urea, NH3 and 3-methylhistidine returned to control levels. Calcium balance was positive throughout the 7-day period of hypokinesia. Hypertrophy of the adrenals suggested the occurrence of some level of stress despite the apparent behavioral adjustment to the suspension harness. It was concluded that significant muscle atrophy and parallel changes in nitrogen metabolism occur in suspended rats and these changes are readily reversible.

Ammonia↗