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S S Segal

Publications and source records attributed to S S Segal.

At least 19 recordsLinked to original sources
PubMed1992

Microvascular architecture in rat soleus and extensor digitorum longus muscles.

Microvascular architecture was investigated in the slow-twitch soleus (SOL) and fast-twitch extensor digitorum longus (EDL) muscles. Rats (n = 5) were anesthetized and papaverine was infused into a carotid artery cannula to induce vasodilation. Microfil casting compound was then infused at an inflation pressure (caudal artery) of 100 mm Hg. Bilateral SOL and EDL muscles were excised 24-72 hr postcasting, dehydrated in ethanol, and cleared in methyl salicylate. Branch frequencies (BR) and segment lengths (SL) of intramuscular arterioles and venules were quantified along primary (1 degree), secondary (2 degrees), and tertiary (3 degrees) order microvessels using microscopy. In both muscles, BR decreased with increasing vessel order. Regional differences in network organization were observed within the EDL muscle. SL of 1 degrees arterioles was 47% shorter in the SOL muscle indicating more compact microvascular networks compared to the EDL muscle. These findings provide a structural basis for reported differences in blood flow between the SOL and EDL muscles at rest and during exercise.

Animals↗
PubMed1992

Intracellular recording and dye transfer in arterioles during blood flow control.

We tested for dye coupling between arteriolar smooth muscle cells (SMC) and endothelial cells (EC) and investigated the correspondence of vasomotor activity with changes in the membrane potential (Vm) of EC and SMC during blood flow control. Female golden hamsters (n = 8, 90-170 g) were anesthetized (pentobarbital sodium, 60 mg/kg ip). A cheek pouch was spread over an optical pedestal, transilluminated, and irrigated with physiological saline solution (37 degrees C, pH 7.4). Glass microelectrodes were filled with 3 M KCl or with Lucifer yellow dye (LY, mol wt 470; 106 mM). SMC or EC of arterioles (ID, 20-50 microns) containing blood flow were impaled under a stereomicroscope. Vm was similar [-48 +/- 3 and -52 +/- 4 mV (means +/- SE)] with KCl (n = 6) or LY (n = 13) microelectrodes, respectively. Acetylcholine (5 x 10(-6) M) increased Vm from -47 +/- 3 to -67 +/- 4 mV (n = 5; P less than 0.01) concomitant with vasodilation. Spontaneous slow waves in Vm (2/min, 15-30 mV) were observed in arterioles with vasomotion. In cells identified with LY microinjection, resting Vm was -52 +/- 8 and -44 +/- 2 mV for EC (n = 3) and SMC (n = 3), respectively. SMC injected with LY did not show evidence of dye transfer to other SMC or to EC. When an EC was injected, the dye spread to many contiguous EC but not to SMC.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Microvascular recruitment in hamster striated muscle: role for conducted vasodilation.

The influence of conducted vasodilation upon arteriolar diameter and capillary red blood cell (rbc) perfusion was investigated in the cremaster muscle of male hamsters anesthetized with pentobarbital. The muscle was surgically exposed, superfused with physiological saline solution (pH 7.4; 34 degrees C), and transilluminated for observation of microvessels using intravital video microscopy. The tip (2 microns ID) of a glass micropipette filled with acetylcholine (ACh; 1.0 M) was positioned adjacent to an arteriole. Microiontophoretic delivery of an ACh stimulus (200-1,000 nA; 200-750 ms) caused vasodilation at the pipette tip, which conducted rapidly along the arteriole and decayed with distance; this was characterized by length constants of 2.1 and 2.4 mm (P greater than 0.05) for arterioles with maximal diameters of 32 +/- 2 (means +/- SE; n = 8) and 63 +/- 2 microns (n = 5), respectively. When applied to the distal end of a terminal arteriole (TA) devoid of flow, ACh triggered a dilation that was conducted proximally (greater than 1,000 microns upstream) into the parent vessel (terminal arteriole feed, TAF) containing rbc flow, thereby inducing flow into the TA; stimulation of the TAF also induced rbc flow into TA. In capillaries fed by TA, rbc flux (rbc/s) increased from zero at rest to 23 +/- 6 during the peak of the TA dilation (n = 9); calculated tube hematocrit increased from 4 +/- 2 to 28 +/- 3%. Findings demonstrate that conduction of vasodilation can coordinate vasomotor responses between terminal and parent arterioles and promote rbc delivery to capillaries supplying striated muscle fibers.

Acetylcholine↗
PubMed1991

Preservation of endothelial cells in excised rat carotid arteries. Effects of transmural pressure and segment length.

When arteries are excised, they collapse and shorten spontaneously, which can result in damage to the endothelium. To determine if an intact endothelial cell layer could be preserved in excised vessels, we isolated and cannulated rat carotid artery segments (in situ length, Lis, 10-20 mm) at both ends while maintaining both transmural pressure (70 mm Hg) and Lis, while either transmural pressure or Lis, or after allowing vessel collapse and shortening (n = 4 vessels per treatment). After each treatment, vessel segments were perfused with fixative and stained with AgNO3 to visualize endothelial cells. The amount of endothelial cell loss was quantified using stereological analysis of video microscopic images of the luminal surface. Results demonstrated that maintenance of both Lis and transmural pressure minimized endothelial cell denudation (1.6 +/- 0.9%); permitting the vessel to collapse and shorten resulted in the greatest loss of endothelial cells (59.4 +/- 13.2%); and maintenance of either pressure or Lis resulted in intermediate endothelial cell loss (13-30%). We conclude that the spontaneous collapse and shortening that normally accompany the excision of arterial segments result in substantial endothelial cell loss, which can be virtually eliminated with the maintenance of transmural pressure and vessel segment length. These findings have implications for surgical and experimental procedures requiring intact endothelium.

Animals↗
PubMed1990

Intellective functioning and strategy use in children with insulin-dependent diabetes mellitus.

The cognitive development of children with either early or late onset insulin-dependent diabetes mellitus (IDDM) was investigated with tasks measuring intellectual ability, memory, and academic progress. In addition, children's perceptions of their competence and parents' perspectives on family functioning and their children's behavior were compared. It was found that children with IDDM scored within the normal range on standardized measures of intelligence and academic performance but evidenced some school difficulties, as reflected in subscale performance as well as in their need of remedial education services. Further, evidence was found to suggest deficiencies in children's use of strategies to organize and recall information, particularly for those with early onset of disease. Children's perceived self-competencies and parents' reports of family functioning were strikingly similar across groups. However, parents of those children whose illness began prior to age 5 reported their children to have poor attention spans and difficulty completing tasks.

Achievement↗
PubMed1989

Propagation of vasomotor responses coordinates arteriolar resistances.

We tested the hypothesis that a conduction pathway intrinsic to the arteriolar wall possesses the properties necessary to coordinate vasomotor responses in the microcirculation. Acetylcholine (ACh) or norepinephrine (NE) was iontophoresed onto cheek pouch arterioles (15-35 microns diam) of pentobarbital-anesthetized hamsters, and diameter responses were observed using intravital video microscopy. ACh and NE induced vasodilation and vasoconstriction, respectively, that propagated both upstream and downstream from the site of application. Propagated vasomotor responses decayed with distance along the arterioles; this decay was characterized by mechanical length constants of 1.9 and 1.8 mm for ACh and NE, respectively. Vasodilations and vasoconstrictions initiated on daughter vessels of a branch propagated into parent arterioles that were approximately twice the diameter of the daughter vessels. Iontophoretic stimuli applied simultaneously to paired daughter vessels induced propagated responses that summed linearly in the parent vessel. We conclude that the arteriolar network functions as a highly coordinated syncytium and that diverse vasomotor stimuli can be summed and integrated within the peripheral microvasculature.

Acetylcholine↗
PubMed1989

Conduction of vasomotor responses in arterioles: a role for cell-to-cell coupling?

Vasomotor responses of arterioles triggered by the iontophoretic application of acetylcholine (ACh) or norepinephrine (NE) are conducted along the vessel wall. The present experiments focus on elucidating the mechanism of conduction in arterioles of the superfused cheek pouch preparation in pentobarbital-anesthetized hamsters. Localized muscarinic or adrenergic receptor blockade on an arteriolar segment produced by atropine or phentolamine, respectively, did not affect propagation through the region of blockade but did block vasomotor responses to ACh or NE applied to the segment. Thus muscarinic and alpha-adrenergic receptors can trigger the propagation of vasomotor responses, but these receptors are not involved in their conduction. Tetrodotoxin did not affect either local or propagated responses to ACh or NE. Treatment of arteriolar segments with calcium antagonists (verapamil, diltiazem, nifedipine, or manganese) caused maximal dilation locally but did not affect propagation through the dilated region. The preceding findings argue against a neural pathway for propagation. A depolarizing solution (137 mM KCl) applied by micropipette to arteriolar segments caused both local and propagated vasoconstriction and significantly attenuated propagated vasodilation induced with ACh (P less than 0.05). Putative antagonists of gap-junctional communication (hypertonic sucrose solution, octanol, CO2) reversibly attenuated or abolished propagated responses. We hypothesize that propagation of vasomotor responses along arterioles is initiated via a local change in membrane potential secondary to receptor occupation and that changes in potential spread electrotonically through gap junctions coupling smooth muscle cells, endothelial cells, or both.

Animals↗
PubMed1989

The behavior of sonicated albumin microbubbles within the microcirculation: a basis for their use during myocardial contrast echocardiography.

The purpose of this study was to determine whether the behavior of sonicated albumin microbubbles accurately mimics red blood cell flow in the microcirculation and is thus consistent with their use as in vivo tracers of red blood cell flow during myocardial contrast echocardiography. Accordingly, microbubbles prepared from fluorescein-conjugated albumin and fluorescently labeled red blood cells were injected intravascularly in eight golden hamsters. Their intravascular distribution, velocities, arteriolar-to-venular transit and flux ratios at branch points were determined in the microcirculation of the cheek pouch. Albumin microbubbles (mean diameter, 4.9 +/- 3.6 microns) and red blood cells displayed a similar frequency of distribution across the arteriolar lumen (33% in the central 20% of the arterioles), and their arteriolar velocities were also similar (2.5 +/- 0.7 mm/sec and 2.3 +/- 0.7 mm/sec,p = NS). The mean velocities of microbubbles correlated well with those of red blood cells at baseline and after adenosine application (r = 0.97 and r = 0.89, respectively), as did the calculated maximum velocity (r = 0.98 and r = 0.80, baseline and adenosine, respectively). The velocity profiles across the lumen of the vessels for albumin microbubbles and red blood cells were similar at baseline and after adenosine-induced velocity changes. The flux ratios at branch points also correlated well (r = 0.92, p less than 0.001). Arteriolar-to-venular transit times of albumin microbubbles were similar to those of red blood cells in vessels ranging in size from 22 microns to 45 microns. We conclude that the behavior of albumin microbubbles in the microcirculation mimics that of red blood cells and supports their use as intravascular tracers of red blood cell flow during myocardial contrast echocardiography.

Animals↗
PubMed1987

Vasomotor control: functional hyperemia and beyond.

Historically, functional hyperemia has been viewed largely as an interaction between a parenchymal cell and its associated microvasculature. Locally released metabolites have been thought to produce relaxation of the smooth muscle and a vasodilation that increases blood flow in proportion to metabolic need. This symposium report presents evidence from a variety of disciplines and a number of different types of biological preparations that demonstrates that functional hyperemia is a complex process involving several classes of microvessels including capillaries, arterioles, and small arteries. These vessels do not function independently but are coordinated by a complex set of interrelations involving at least three different modes of interaction between parenchymal cells and the various segments of the vascular bed. These are local metabolic effects, propagated effects extending over long segments of the vasculature, and flow-dependent vasodilation induced by local changes in blood flow. In addition to these acute responses to metabolic demand it appears that tissues may be capable of more long-term structural alterations of the arterial and arteriolar network in response to sustained changes in the relationship between supply and demand. The vascular bed appears to be able to adapt either by increasing the maximal anatomic diameter of the large arteries or by inserting new arterioles into the parenchyma. Thus, classical functional hyperemia appears to be but one manifestation of a multifaceted process leading to highly coordinated responses of many vascular elements, resulting finally in vascular patterns that are optimized to meet parenchymal cell demands.

Animals↗
PubMed1987

Propagation of vasodilation in resistance vessels of the hamster: development and review of a working hypothesis.

In many tissues, a substantial fraction of total vascular resistance resides in the feed arteries that give rise to the microcirculation. We have explored the thesis that control of tissue blood flow is integrated over several levels of the vascular network, including feed arteries and microvessels. In response to muscular contraction, feed arteries (resting diameter 100-125 microns) of hamster cremaster and gracilis muscles dilated by 20-25%. Acetylcholine applied to distal microvessels of the cremaster induced a dilation that ascended into feed arteries not having direct contact with acetylcholine. In the hamster cheek pouch, iontophoretic application of acetylcholine onto an arteriole (diameter 20-30 microns) triggered a vasodilation that propagated along the arteriole. Propagation was not dependent on blood flow, indicating that the dilator response was conducted along the vessel wall. We found that preventing diameter changes in an arteriole segment along the apparent conducting pathway did not block propagated vasodilation, indicating that propagation was not mediated by a myogenic mechanism requiring changes in smooth muscle length. We investigated whether the conduction of a vasodilatory stimulus may be mediated by either a neural plexus intrinsic to microvessels or cell-cell coupling between the cells composing the arteriole. Tetrodotoxin (10(-6) M) did not block propagated vasodilation, indicating that propagation is not mediated by a neural pathway. Hypertonic sucrose solution applied to an arteriole segment along the apparent conducting pathway attenuated propagation significantly, which is consistent with its reported effect to decouple gap junctions between cells. Thus, propagated vasodilation in arterioles may be mediated by direct cell-cell conduction.

Acetylcholine↗
PubMed1986

Flow control among microvessels coordinated by intercellular conduction.

Optimal distribution of blood flow requires coordination of vasodilation among resistance vessels. During hyperemia, blood vessels dilate upstream from the initiating stimulus. Spreading vasodilation independent of flow changes has not been previously demonstrated. In the present study, iontophoresis of acetylcholine adjacent to single hamster cheek pouch arterioles in situ (diameter, 20 to 37 micrometers) induced a rapid bidirectional dilation that was not attenuated when blood flow was eliminated with vascular occlusion. This finding indicates that a vasodilatory stimulus is conducted along the arteriole and demonstrates the existence of a mechanism of intercellular communication that is capable of coordinating diameter changes among resistance vessels.

Acetylcholine↗
PubMed1986

Architecture, composition, and contractile properties of rat soleus muscle grafts.

Skeletal muscle grafts have a deficit in tension development compared with control muscles, even after accounting for reduced mass and total muscle cross-sectional area. Our purpose was to determine relationships among the architecture, tissue composition, and contractile properties of rat soleus muscle grafts. Data were compared with control soleus muscles obtained from littermates. Female Wistar rats were anesthetized with pentobarbital sodium for grafting of soleus muscles with nerve implant and for dissection of muscles 56 days after grafting. Compared with control values, the maximum specific tension (N/cm2) of grafts was 76%, the interstitial (inulin) space was 135%, and the connective tissue protein concentration was 177%. For grafts, total muscle length and fiber length were 91 and 123% of control values, respectively. The extrapolated shortening velocity at zero load (fiber lengths/s) for grafts was not different from the control value. The deficit in specific tension of grafts is explained by a greater concentration of noncontractile tissue components. Changes in muscle architecture and composition following grafting had little affect on contraction dynamics.

Animals↗
PubMed1986

Skeletal muscle fatigue in vitro is temperature dependent.

Our purpose was to determine the effect of temperature on the fatigability of isolated soleus and extensor digitorum longus (EDL) muscles from rats during repeated isometric contractions. Muscles (70-90 mg) were studied at 20-40 degrees C in vitro. Fatigability was defined with respect to both the time and number of stimuli required to reach 50% of the force (P) developed at the onset of the fatigue test. Fatigue was studied during stimulation protocols of variable [force approximately 70% of maximum force (Po)] and constant frequency (28 Hz). Results for soleus and EDL muscles were qualitatively similar, but fatigue times were longer for soleus than for EDL muscles. During the variable-frequency protocol, development of approximately 70% of Po required an increase in stimulation frequency as temperature increased. During stimulation at these frequencies, fatigue time shortened as temperature increased. For both fatigue protocols, the relationship between temperature and the number of stimuli required to reach fatigue followed a bell-shaped curve, with maximum values at 25-30 degrees C. The temperature optimum for maximizing the number of isometric contractions to reach fatigue reflects direct effects of temperature on muscle function.

Animals↗
PubMed1986

Communication between feed arteries and microvessels in hamster striated muscle: segmental vascular responses are functionally coordinated.

Pressures in the primary arterioles of the cremaster muscle are reported to be approximately 50% of systemic, indicating that arterial resistance proximal to microvessels is high and may limit maximal blood flow. With no change in arterial resistance, increases in perfusion normally associated with muscle work either could not occur or would require increments in systemic pressure far greater than those actually observed in vivo. Therefore, we hypothesized that the small arteries feeding the muscle may participate in the hyperemic response. To test this hypothesis, male golden hamsters (n = 31, 118 g) were anesthetized (pentobarbital, 70 mg/kg i.p.), and the right cremaster was opened to expose its feed arteries, which originated from the iliac artery. Preparations were superfused and maintained at 35 +/- 1 degree C. Feed arteries had substantial tone, as shown by the fact that topical acetylcholine, applied at supramaximal concentration, dilated these vessels from 115 +/- 8 microns at rest to 158 +/- 9 microns (mean +/- SE; n = 38 vessels; p less than 0.01), corresponding to an estimated 4.4-fold increase in conductance. Stimulation of the sectioned motor nerve (8 Hz, 30 seconds) induced striated muscle contraction and increased feed vessel diameter from 93 +/- 5 microns to 116 +/- 5 microns (n = 14; p less than 0.01), consistent with a 2.6-fold increase in conductance. A 5-minute occlusion of the iliac artery resulted in feed artery dilation of similar magnitude. Supramaximal doses of acetylcholine applied topically to the distal portions of the cremaster resulted in striated muscle contraction and a dilation that propagated upstream to increase feed artery diameter by 25%.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Temperature-dependent physiological stability of rat skeletal muscle in vitro.

Stability of rat skeletal muscle contractile properties with time in vitro as a function of incubation temperature was characterized. Female Sprague-Dawley rats (8 wk, 148 g) were anesthetized with pentobarbital sodium (40 mg/kg, ip). Intact soleus (SOL) and extensor digitorum longus (EDL) muscles of 70- to 90-mg mass were removed and studied at incubation temperatures of 20, 25, 30, 35, and 40 degrees C. The average muscle thickness was 2.0 mm. Each muscle was studied at one temperature only. At 5, 15, 30, 45, and 60 min following immersion in an oxygenated Krebs-Ringer bicarbonate solution, isometric contractile properties were measured. Peak twitch tension, maximum tetanic tension, and rate of tension development of both SOL and EDL muscles were stable with time at 20 and 25 degrees C but decreased with time as a function of bath temperature above 25 degrees C. The calculated critical radius for O2 diffusion declined from 1.19 mm at 20 degrees C to 0.51 mm at 40 degrees C. For SOL and EDL muscles incubated at 25 degrees C, the histochemical demonstration of glycogen content was similar to that of fresh muscles, whereas muscles incubated at 40 degrees C showed staining for glycogen only in peripheral fibers. Observed and calculated results both infer a progressively larger hypoxic core at incubation temperatures above 25 degrees C.

Animals↗
PubMed1985

Skeletal muscle protein synthesis and degradation in vitro: effects of temperature.

We compared the structure, function, protein synthesis, and degradation of 70- to 95-mg rat soleus muscles during 120 min of incubation at 20 and 37 degrees C. At 37 degrees C, muscles were characterized by a damaged central core region and a decline of isometric tension development during incubation. Protein synthesis in the core region at 37 degrees C was depressed relative to the peripheral region. At 20 degrees C, developed tension remained constant during incubation, and synthesis rates in the core region were not different from the peripheral region. Compared with fresh muscle, ATP concentration after incubation was not affected by temperature. After equilibration of phenylalanine specific activity between extracellular and intracellular spaces (60 min at 20 degrees C; 30 min at 37 degrees C), rates of protein synthesis at 20 [0.048 nmol tyrosine (Tyr) X mg wet mass-1 X 2 h-1] and 37 degrees C (0.160 nmol Tyr X mg wet mass-1 X 2 h-1) were linear up to 180 and 120 min, respectively. Rates of protein degradation at 20 (0.076 nmol Tyr X mg wet mass-1 X 2 h-1) and 37 degrees C (0.248 nmol Tyr X mg wet mass-1 X 2 h-1) measured after 60 min were linear up to 180 and 120 min, respectively. Incubation at 20 degrees C offers an approach to study 70- to 95-mg muscles in vitro without compromising structure and function.

Animals↗
PubMed1979

Effects of glycogen depletion and work load on postexercise O2 consumption and blood lactate.

To study a possible relationship between blood lactate and O2 consumption (VO2) after exercise, 11 male subjects exercised on a bicycle ergometer at moderate and heavy work loads in both normal glycogen and glycogen-depleted states. At rest, glycogen depletion resulted in significantly lowered blood glucose and lactate concentrations, CO2 production (VCO2), respiratory exchange ratio (R), and minute ventilation (VE). With the exception of glucose, these variables changed more in response to heavy exercise (HE: 2 min at a mean of 1,750 kg.m/min) than to moderate exercise (ME: 2 min at a mean of 1,000 kg.m/min). At either work load, VCO2, R, and lactate showed consistently greater responses in the normal glycogen state. The slope of the initial component of the postexercise VO2 curve was unaffected by either work load or lactate. Although the slope of the slow component of the postexercise VO2 curve became significantly more negative after HE, it was unaffected by the level of lactate. These results are inconsistent with the hypothesis of a "lactacid O2 debt." Exercise intensity was the predominant factor influencing the magnitude and kinetics of postexercise VO2. Glycogen depletion resulted in lower VCO2, R, and blood lactate, but higher VE during heavy exercise. The results suggest that factors, in addition to CO2 flux to the lungs, influence VE during exercise.

Blood Glucose↗