Biomedical subjects

M H Laughlin

Publications and source records attributed to M H Laughlin.

At least 91 records · Page 5Linked to original sources

PubMed1994

Differences in blood flow to uterine segments and placentae in relation to sex, intrauterine location and side in pregnant rats.

The effects of location within the left or right uterine horn, position within each uterine horn, and fetal sex on fetal bodymass, blood flow to individual uterine segments associated with fetuses, and blood flow to the maternal portion of the placenta were investigated in rats. Sprague-Dawley rats were anaesthetized on day 5, 10, 15, 20, 21 or 22 of pregnancy, and radioactive microspheres with diameters of 15 mm were injected via a left ventricular cannula to measure blood flow to tissues. Tissues were weighed wet, and the rate of blood flow, corrected for wet mass (ml min-1 g-1 tissue), was calculated. Microspheres were not detected in fetuses, suggesting that they did not pass from maternal into fetal blood. Uterine blood flow was greater at the cervical and ovarian ends than in the middle of the uterus; on day 15 the rate of blood flow at the cervical and ovarian ends of each uterine horn was over twice that in the middle. The blood flow to the right uterine horn was greater than to the left horn. Blood flow to placentae increased dramatically between day 15 and day 20. There were marked differences in architecture between the uterine artery feeding the ovarian end of the right and left uterine horn, and blood flow to placentae located at the ovarian end of the right uterine horn was greater than to placentae in the same location in the left uterine horn. The blood flow to placentae and fetal bodymass were greater for female than for male fetuses on day 20, but on day 22 the reverse was observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1994

Regional changes in capillary supply in skeletal muscle of interval-sprint and low-intensity, endurance-trained rats.

OBJECTIVE: Exercise training produces regional increases in blood flow capacity among muscle fibers that experience increased activity during exercise. We tested the hypothesis that this increase is partially due to capillary angiogenesis among muscle fibers with large increases in activity during exercise training bouts. METHODS: Two training programs were evaluated: a program consisting of 10-12 weeks of exposure to low-intensity (30 m/min, 0 incline, 60 min/day) (LET) exercise bouts, 5 days/week, and a second program consisting of 8-10 weeks of exposure to repetitive bouts (6/day) of sprint (60 m/min, 15% incline) exercise, alternating running (2.5 min) and recovery (4.5 min), 5 days/week (IST). Cage-confined rats were utilized (SED) as controls. After training was completed, rat hindquarters were perfusion-fixed with modified Karnovsky's fixative. Transverse sections from soleus (Sol), and red (GR), mixed (GM), and white (GW) portions of gastrocnemius muscle were prepared to evaluate capillarization. Sections were analyzed using the Olympus Cue 2 Image Analyzer to determine capillary/muscle fiber ratio (C/F), number of capillary profiles per square millimeter of muscle area (CND), capillary surface area per volume of tissue, and capillary volume density. RESULTS: Average area per muscle fiber and sarcomere length did not differ among groups. LET did not affect capillarization of the GW, whereas increasing C/F in GM (2.3 +/- 0.1 versus 2.1 +/- 0.1 for SED) and GR (3.0 +/- 0.1 versus 2.6 +/- 0.1 for SED). IST increased C/F and CND in GW (1.6 +/- 0.1 versus 1.3 +/- 0.0 for SED and 657 +/- 74 versus 418 +/- 53 for SED, respectively) and increased C/F ratio in GM (2.3 +/- 0.1 versus 2.1 +/- 0.1 for SED). IST did not increase capillarization of the GR. The capillarization of the soleus muscle was not affected by either exercise training program. CONCLUSION: IST increased capillarization in muscle tissue composed of a high percentage of fast glycolytic fibers (GW and GM) and LET increased capillarization of muscle tissue composed of a high percentage of fast oxidative-glycolytic fibers (GW and GR).

Animals↗

PubMed1994

Altered control of calcium in coronary smooth muscle cells by exercise training.

The increase in myoplasmic free Ca (Cam) is a primary trigger of contraction in vascular smooth muscle. We review data showing that the sarcoplasmic reticulum (SR) can buffer (attenuate) increases in Cam by: 1) sequestering a fraction of Ca entering the cell via sarcolemmal influx pathways, and 2) slowly releasing Ca from the SR toward the sarcolemma for extrusion from the cell, thereby decreasing subsequent agonist-induced Cam transients and contraction--so called "SR Ca unloading." Endurance exercise trained (EX), not sedentary (SED), Yucatan miniature pigs show SR Ca unloading via a ryanodine-sensitive SR Ca release pathway. The slow release of Ca from SR of EX cells may allow for efflux from the cell by close functional association with sarcolemmal Ca efflux mechanisms. In contrast, rapid, bolus release and resequestration of Ca by the SR of SED cells prevents Ca efflux from the cell. The endothelin-sensitive SR Ca store, a subset of the caffeine- and ryanodine-sensitive SR, is decreased in EX cells. Mildly increased resting Cam in EX cells may reflect a constant leak of Ca from the SR. The endothelin-sensitive SR Ca store was loaded above basal levels by depolarization-induced Ca influx. Collectively, these data indicate altered Cam regulation by the SR in coronary artery of EX animals. Future studies should focus on the molecular mechanisms of altered Cam regulation.

Animals↗

PubMed1994

Exercise training-induced increase in coronary transport capacity.

The objective of this study was to measure effects of exercise training on coronary flow heterogeneity, microvascular transport, and hemodynamics. Five miniature swine were trained on a treadmill (ET) for 16 wk; five control pigs (C) were confined to cages for the same period. At the end of that period we used the multiple indicator dilution method to measure permeability-surface area product (PS) to EDTA over a range of flow (F) in an anesthetized, open-chest preparation. We found that the heterogeneity of flow as measured by microspheres decreased with increasing F, but that ET had no clear effect on heterogeneity. We evaluated PS from the indicator concentration curves, taking into account flow heterogeneity and variations in capillary recruitment throughout the bed. In both C and ET pigs we observed an increase in PS with F until a maximum value of PS was reached at full recruitment. This relationship between PS and F was unaltered by ET. However, hemodynamic resistance was significantly reduced by ET, and F was higher at a given perfusion pressure after training. Since PS increases with F, ET pigs had higher PS values at typical coronary artery pressures.

Adaptation, Physiological↗

PubMed1994

Effects of exercise training on regulation of tone in coronary arteries and arterioles.

A large number of studies now support the concept that exercise training alters functional control of the coronary circulation. Recent work has approached this area using ex vivo coronary arterial preparations (proximal coronary arteries, near-resistance arteries, resistance arterioles) isolated from exercise-trained animals and contracting independently of confounding in vivo influences. The combined results of these studies indicate that training-induced alterations in vascular control mechanisms do not occur uniformly throughout the coronary vascular tree. Proximal epicardial coronary arteries (approximately 2.0 mm diameter) isolated from exercise-trained pigs exhibited significantly reduced contractile responsiveness to the alpha-adrenergic receptor agonist, norepinephrine, but unaltered contractile responsiveness to K+, acetylcholine, and endothelin. Also, proximal arteries from exercise-trained animals demonstrated enhanced sensitivity to the vasodilator effects of adenosine. At the other end of the vascular spectrum, in resistance arterioles (< 150 microns diameter) the relaxation responses to adenosine were unaffected by exercise training, but bradykinin-induced vasodilation (endothelium-dependent) was significantly enhanced. In near-resistance arteries (150-240 microns diameter) responses to both bradykinin and adenosine were enhanced by exercise training. Thus, exercise training is associated with intrinsic vessel size-dependent alterations in coronary smooth muscle and endothelium-mediated regulatory mechanisms.

Animals↗

PubMed1994

Cerebral and spinal cord blood flow dynamics during high sustained +Gz.

This study had two purposes. First, the use of Transonic flowprobes placed on the common carotid and internal carotid arteries of seven male baboons was evaluated for measuring cerebral blood flow (BF) during +Gz stress. The approach was to compare BF's obtained with these flowprobes to microsphere measurements of total cerebral BF. The second purpose was to measure regional variations in cerebral and spinal cord BF during +Gz to test the hypothesis that +Gz produces a differential perfusion deficit throughout the central nervous system so that BF's at the superior portion of the brain are decreased more than in areas of the brain that are nearer to the heart. The results indicate that internal carotid artery and microsphere measurements of total brain BF were related so that the relative decrease in internal carotid artery BF was consistently comparable to that measured with the labeled microsphere technique. Thus, Transonic flowprobes placed on the internal carotid artery of the baboon give reliable estimates of cerebral BF during +Gz stress. The microsphere BF data demonstrated that there were no regional differences in the relative decrease in BF measured in the brain or spinal cord during +Gz. We conclude that our results do not support the hypothesis of a gradient of BF deficit within the brain or spinal cord during +Gz.

Acceleration↗

PubMed1993

Comparison of muscle cell fiber types and oxidative capacity in gracilis, rectus femoris, and triceps brachii muscles in the ferret (Mustela putorius furo) and the domestic dog (Canis familiaris).

Muscle cell fiber types in gracilis, rectus femoris, and long head of triceps brachii muscles of ferrets and dogs were identified on serial sections stained for myosin ATPase after preincubation at pH values of 9.8, 4.6, and 4.3 and for NADH-tetrazolium reductase (NADH-TR) activity. Although fiber types I and II were identified, the ATPase stain did not demonstrate classic type IIA/IIB fiber differences in either species. However, two type II fiber subtypes could be distinguished in the ferret because they differed slightly in staining intensity with ATPase at pH 4.3 and markedly with NADH-TR. One ferret type II fiber (designated II dark or IID) was smaller, slightly darker on ATPase, more oxidative on NADH-TR, and comprised more muscle volume than the other type II fiber (designated II light IIL). The IID fibers of ferret may represent the IID/X fibers of other authors. Both ferret type II fiber subtypes stained darker at pH 4.3 than canine II fibers. The NADH-TR staining indicated high oxidative activity in canine and ferret type I fibers. In contrast, type II fibers in the dog and IIL fibers in the ferret were moderately oxidative. Canine type IIC fibers were intermediate between type I and type II, whereas in the ferret, type IIC fibers were highly oxidative, as were type IID fibers. Ferret muscles are more oxidative than canine muscles according to NADH-TR staining. Also, ferret muscles possess 40-100% higher citrate synthase activity as compared to canine muscles.

Animals↗

PubMed1993

Vasoactivity of isolated coronary arterial microvessels: influence of albumin.

Previous investigators have reported the development of spontaneous tone, a spontaneous decrease in diameter in response to application of intraluminal pressure, in isolated microvessels bathed in physiological salt solution (PSS) containing albumin. In contrast, myogenic activity and spontaneous tone are rare in microvessels bathed in albumin-free PSS. The purpose of this study was to determine whether albumin and/or the development of spontaneous tone altered coronary microvessel responsiveness to vasoactive agents. Microvessels (70-150 microns) were isolated from the hearts of domestic pigs and studied in vitro using video dimension analysis. Control microvessels were bathed in albumin-free PSS while albumin-treated vessels were bathed in PSS containing 10 mg/ml albumin. Vasoconstrictor responses were determined for acetylcholine (3 x 10(-10) to 1 x 10(-5) M) and KCl (20-120 mM). Concentration-response curves were generated for an endothelium-dependent vasodilator, bradykinin (1 x 10(-12) to 1 x 10(-7) M), and a direct smooth muscle dilator, sodium nitroprusside (1 x 10(-10) to 1 x 10(-4) M). Seventy-seven percent of the albumin-treated microvessels developed spontaneous tone, whereas only 20% of the control microvessels developed tone. KCl and acetylcholine induced contraction in both control and albumin-treated microvessels. Maximal response to acetylcholine (percentage constriction) was significantly greater in albumin-treated microvessels (79.93 +/- 2.53 and 68.86 +/- 3.20 in control and albumin-treated groups, respectively). Responses to bradykinin and sodium nitroprusside were not different between albumin-treated and control groups. The results indicate that microvessels develop spontaneous tone more frequently when bathed in PSS containing albumin.(ABSTRACT TRUNCATED AT 250 WORDS)

Albumins↗

PubMed1993

Skeletal muscle fiber types and their vascular support.

Different neural and thyroidal influences on mammalian skeletal muscle result in considerable heterogeneity in muscle-fiber characteristics. Muscle fibers can, nonetheless, be grouped into three relatively homogeneous classes, based primarily on their contractile properties. There is a remarkable matching of metabolic support systems to contractile properties and, in turn, appropriate vascular supply for the metabolic systems of each of the three muscle fiber types. The contractile, metabolic, and vascular characteristics of each fiber type are consistent with known patterns of muscle fiber recruitment for the performance of muscular work.

Animals↗

PubMed1993

Effects of chronic heart failure on skeletal muscle vascular transport capacity of rats.

The purpose of this study was to determine the effects of chronic heart failure (HF) on the vascular transport capacity of rat skeletal muscle. A large myocardial infarction (MI) was surgically produced in rats by ligating the left main coronary artery (n = 10). Sham operations were performed in control animals (Sham, n = 4). The vascular transport capacity of each animal's hindquarters was determined 8-9 mo post-MI to ensure that each rat was in a chronic state of left ventricular (LV) dysfunction and HF. With the use of an isolated, maximally vasodilated hindquarters preparation, we found that perfusion pressures, capillary pressures, capillary filtration coefficients, and precapillary vascular resistances were similar for the two groups under isogravimetric conditions. In contrast, postcapillary resistance was elevated (Sham, 0.9 +/- 0.2; MI, 1.5 +/- 0.2 mmHg.ml-1 x min x 100 g; P = 0.03), and flow to the hindquarters was reduced for rats in chronic HF compared with controls (Sham, 16.1 +/- 2.3; MI, 12.1 +/- 0.9 ml.min-1 x 100 g-1; P = 0.07). Vascular flow capacity (VFC) for the hindquarters was similar for control rats and rats with chronic HF across a wide range of perfusion pressures (20-60 mmHg). However, regional flow capacities were reduced in soleus and red gastrocnemius but not in white gastrocnemius muscles of rats in chronic HF compared with controls. These results suggest that the VFC of muscle comprised primarily of high oxidative fibers is selectively reduced in rats with chronic HF.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1993

Exercise training alters endothelium-dependent vasoreactivity of rat abdominal aorta.

We tested the hypothesis that adaptations in peripheral arterial vasoreactivity are induced by exercise training. Male rats were trained to run on a treadmill at 30 m/min (15 degrees incline) for 1 h/day 5 days/wk for 10-12 wk. Efficacy was indicated by a 51% increase (P < 0.05) in citrate synthase activity in soleus muscle of exercise-trained (ET) rats compared with that of sedentary (SED) control rats. Responses to vasoactive compounds were examined in vitro using rings of abdominal aorta. Maximal isometric contractile tension evoked by KCl, norepinephrine (NE), and phenylephrine were not different between groups; sensitivity to phenylephrine was also not different between groups. However, sensitivity was lower for both KCl and NE in vessels from ET animals. Endothelium removal did not influence KCl sensitivity but did abolish the difference in NE sensitivity of vessel segments between ET and SED animals. Maximal vasodilator responses induced by acetylcholine (ACh; NE or prostaglandin F2 alpha preconstriction) were greater in vessel rings from ET rats. However, dilatory responses by sodium nitroprusside (NE or prostaglandin F2 alpha preconstriction) and forskolin (NE preconstriction) were not different between groups, indicating that the augmented ACh-induced dilatory response resulted from an adaptation of the endothelium. Blockade of nitric oxide synthase activity diminished ACh-induced vasodilation by 79 and 100% in SED and ET rats, respectively. These results indicate that training alters vasomotor function in rat abdominal aortas through adaptations of both endothelium and smooth muscle.

Animals↗

PubMed1993

Vasoconstrictor properties of rat aorta are diminished by hindlimb unweighting.

Prolonged bed rest and exposure to weightlessness in humans result in cardiovascular alterations that are characterized by orthostatic intolerance and decreased exercise capacity. Modifications of cardiovascular function have been suggested to be causally related to changes in peripheral vascular reactivity. Rat hindlimb unweighting (HU) was used as an animal model to determine whether prolonged decreases in weight-bearing activity induce changes in vasoreactivity of peripheral arterial vessels. Responses to vasoactive compounds were examined in vitro using isolated abdominal and thoracic aortic rings. Maximal isometric contractile tension evoked by the vasoconstrictors KCl (10-100 mM), norepinephrine (NE; 10(-9)-10(-4) M), phenylephrine (10(-9)-10(-4) M), arginine vasopressin (10(-13)-3 x 10(-5) M), and CaCl2 (10(-6)-10(-2) M) was lower in abdominal aortic rings from HU rats. Sensitivity [agonist concentration that produced 50% of maximal vasoconstrictor response (EC50)] to KCl was enhanced in segments from HU animals but was not different for the other constrictors. Maximal contractile responses of thoracic aortic rings to KCl (10-100 mM) and NE (10(-9)-10(-4) M) were also attenuated by HU. In abdominal aortic rings preconstricted with 10(-4) M NE, maximal vasodilatory responses induced by sodium nitroprusside (10(-10)-10(-4) M) and 8-bromoguanosine 3',5'-cyclic monophosphate (10(-6)-10(-2) M) were greater in vessel rings from HU rats. However, with 10(-7) M NE preconstriction, maximal dilatory responses induced by sodium nitroprusside (10(-10)-10(-4) M) and acetylcholine (10(-9)-10(-4) M) were not different between groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1993

Exercise training alters myogenic responses in porcine coronary resistance arteries.

The purpose of this study was to test the hypothesis that myogenic responsiveness in porcine coronary resistance arteries is attenuated by exercise training. Twenty-four female Yucatan miniature swine were randomly separated into two groups of 12 pigs: exercise trained (ET) and sedentary control (SED). The ET pigs were trained on a motor-driven treadmill for 16-22 wk while the SED pigs remained confined to their pens. After training, heart weight-to-body weight ratio, skeletal muscle oxidative capacity, and exercise tolerance were significantly increased in ET pigs compared with SED pigs. Coronary resistance arteries 75-150 microns diam were isolated for in vitro evaluation of myogenic responses to changes in intraluminal pressure in the absence of intraluminal flow. Coronary resistance arteries from ET and SED pigs developed spontaneous tone at 40 mmHg intraluminal pressure. Active changes in diameter measured in response to intraluminal pressures < 40 mmHg were similar in coronary resistance arteries from ET and SED pigs. When pressure was raised above 40 mmHg, myogenic constriction was greater in coronary resistance arteries from ET pigs, as indicated by significantly greater reductions in diameter. At 60 and 70 mmHg intraluminal pressure, constriction was 8 and 16% greater, respectively, in resistance arteries from ET pigs. After maximal relaxation with sodium nitroprusside (100 microM), passive diameter changes measured in response to changes in intraluminal pressure from 10 to 80 mmHg were not significantly different in coronary resistance arteries from ET and SED pigs. We conclude that, contrary to our hypothesis, exercise training in pigs enhances myogenic constrictor responses in coronary resistance arteries.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1993

Coronary vascular function after hemorrhagic hypotension in dogs.

This study tested the hypothesis that hemorrhagic hypotension alters intrinsic contraction-relaxation mechanisms of coronary arteries. Coronary vascular smooth muscle (VSM) was evaluated ex vivo using left circumflex coronary artery preparations isolated from beagle dogs 4 hr after sham hemorrhage (controls) or maintained hemorrhagic hypovolemia. Hemorrhaged dogs exhibited systemic hypotension (mean arterial pressure approximately 65 mm Hg), tachycardia, and tachypnea during the 4 hr in vivo phase of the study, accompanied by 30-50% reductions in left ventricular myocardial blood flows (P < 0.05). Coronary arteries isolated from these dogs were stretched to the asymptote of their length-contractile tension relationship; no significant differences were observed in length-active tension or length-passive tension relations between hemorrhage and control arteries. Similarly, neither the maximal responses nor the EC50 values for isometric contractions produced by prostaglandin F2 alpha (PGF2 alpha) (10(-8) to 3 x 10(-5) M) or depolarizing concentrations of K+ (10-100 mM) were altered by hemorrhage (P > 0.05). Vasodilator responses to the cyclic guanosine monophosphate (GMP)-dependent VSM relaxant nitroprusside (10(-4) M) also were not prevented by the hemorrhage protocol. In contrast, coronary VSM relaxation induced by the endothelium-dependent vasodilator acetylcholine (10(-9)-10(-5) M) was significantly decreased by 25-50% in K(+)- and PGF2 alpha-precontracted coronary arteries from the hemorrhaged dogs (P < 0.01). We conclude that receptor (PGF2 alpha)-dependent and membrane depolarization (K+)-dependent contractile mechanisms remained operational in coronary arteries during hemorrhagic hypotension, as did basal cyclic GMP-dependent VSM relaxation mechanisms. However, diminution of acetylcholine-induced relaxation of coronary VSM suggests impaired endothelium-dependent vasodilation in the coronary vasculature during acute (4 hr) hemorrhagic hypotension.

Acetylcholine↗

PubMed1992

Estimating transit time for capillary blood in selected muscles of exercising animals.

The mean minimal capillary transit time was estimated in muscles of various animals using a combination of physiological and morphometric methods. Radioactive microspheres were injected intravascularly in various animals running on a treadmill at maximum oxygen consumption rate (VO2,max) to label blood flow to individual muscles. The muscles were then removed and preserved by standard methods for electron microscopy. The volume density of mitochondria was measured to assess muscle oxidative capacity. Capillary densities in muscle cross-sections, capillary diameters and tortuosities were incorporated into an estimate of capillary volume per unit muscle mass. Mean capillary transit time (tc) in the exercising muscles was estimated by dividing mass-specific capillary volume by mass-specific blood flow. Estimates of tc ranged from values near 1 s in horse heart and thigh muscles to 0.2 s in duck gastrocnemius. The relationship between muscle blood flow and tc was hyperbolic. The experimental data indicate a limiting value of 0.2 s for transit times at very high blood flows. There was no correlation between tc and body-mass-specific VO2,max.

Animals↗

PubMed1992

Endotoxin impairs flow-induced vasodilation of porcine coronary arterioles.

The purpose of this study was to test the hypothesis that endotoxemia impairs endothelium-dependent (both receptor-mediated and flow-induced) vasodilation in porcine coronary arterioles. Coronary arterioles were isolated from three groups of 4- to 8-wk old (10.3 +/- 0.8 kg) pigs: endotoxemic (E; 250 micrograms/kg endotoxin iv), control (C; equal volume of saline), and untreated pigs (UT). Subepicardial arterioles (60-120 microns) were isolated and cannulated with two micropipettes that were connected to two independent reservoir systems. Intraluminal pressure was set at 60 cmH2O throughout the experiments. All C vessels developed spontaneous tone and exhibited flow-induced vasodilation from 65 to 95% maximal diameter. Spontaneous tone developed in only three of five arterioles from E pigs, and flow-induced vasodilation was not observed in any arteriole from E pigs. Spontaneous tone developed in all six arterioles isolated from UT pigs but disappeared in four of these vessels as a result of 1 h of in vitro incubation with endotoxin (2.5 micrograms/ml). Flow-induced vasodilation was also abolished in these vessels after 1 h of endotoxin exposure. Incubation with 3 mM L-arginine, in vitro, restored flow-induced vasodilation in E arterioles and endotoxin-treated UT arterioles. Vasoconstriction induced by acetylcholine (ACh) and vasodilation induced by nitroprusside (NP) and bradykinin (BK) were similar in arterioles from all groups. In contrast, endotoxin impairs flow-induced vasodilation of coronary arterioles. The mechanism responsible for the impairment of flow-induced vasodilation seems to reside in disruption of the L-arginine/nitric oxide pathway.

Acetylcholine↗

PubMed1992

Effects of exercise training on vasomotor reactivity of porcine coronary arteries.

The purpose of this study was to determine whether exercise training induces changes in the contractile behavior of proximal coronary arteries. Female Yucatan miniature swine were either exercise trained (ET) on a motor-driven treadmill or allowed to remain sedentary (SED) for 16-22 wk. Responses to vasoactive compounds were evaluated in vitro using coronary arterial rings (approximately 2 mm diam) isolated from ET and SED pigs. Each ring was stretched to the apex of the length-active tension relationship. Concentration-response relationships for isometric contractions evoked with KCl (5-100 mM), prostaglandin F2 alpha (PGF2 alpha; 10(-8)-3 x 10(-5) M), acetylcholine (ACh; 10(-9)-10(-4) M), and endothelin (10(-10)-10(-7) M) were similar in arteries from SED and ET pigs. In contrast, arteries from the ET group developed 50-60% less maximal tension in response to norepinephrine (NE; 10(-6)-10(-4) M) than did controls. Vasodilator responses of rings precontracted with either KCl or PGF2 alpha were evaluated with adenosine (ADO; 10(-9)-10(-4) M), isoproterenol (10(-9)-10(-4) M), forskolin (10(-9)-10(-4) M), and sodium nitroprusside (NP; 10(-10)-10(-4) M). Vasodilator responses were similar in SED and ET groups for all agents except ADO and NP; arteries from ET pigs were more sensitive to ADO and less sensitive to NP. The ET-induced alterations in vasomotor responses to NE and ADO appear to be due to changes in vascular smooth muscle because they were still present after removal of endothelium. We conclude that chronic exercise training in pigs induces selective alterations in NE and ADO receptor-second messenger coupling and/or postreceptor-related events in epicardial coronary vascular smooth muscle.

Animals↗

PubMed1992

Effect of exercise training on intracellular free Ca2+ transients in ventricular myocytes of rats.

The purpose of this study was to test the hypothesis that exercise training induces enhanced intracellular free Ca2+ (Cai) availability to the contractile elements of cardiac cells. Cai transients were directly measured in single isolated contracting ventricular myocytes from exercise-trained (EX) and sedentary control (SED) rats. Male Sprague-Dawley rats underwent 16 wk of progressive treadmill exercise (32 m/min, 8% grade, 1.5 h/day) (EX) or were cage confined (SED). EX rats had lower resting heart rate and elevated skeletal muscle oxidative capacity. Cai was measured with the fluorescent Cai indicator fura-2. Simultaneous video monitoring indicated that myocytes suspended in physiological salt solution were quiescent until stimulated electrically at a frequency of 0.2 Hz (12-36 V, 2-ms duration). Stimulated Cai transients, measured from changes in fura-2 fluorescence, were similar in cells from EX and SED groups. Peak shortening, time to peak shortening, velocity of shortening, contraction duration, and time to half-relaxation were also similar in cells from EX and SED rats. Ryanodine (10 microM) was applied to eliminate the contribution of Ca2+ release from sarcoplasmic reticulum to the Cai transient. Verapamil was applied to eliminate the contribution of voltage-gated Ca2+ channels to Cai transients. Cai transients were also similar in cells from EX and SED groups after these pharmacological interventions. These results suggest that treadmill training of rats does not alter Cai availability to the contractile elements in isolated ventricular myocytes.

Animals↗