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PubMed2002

Torque-EMG relationships in normal and spastic muscles.

The linearity of the relationship between torque and electromyographic (EMG) activation has been widely debated for years, yet remains unresolved. Despite limitations and possible inaccuracies, an assumption of linearity is often made to simplify the relationship between these variables for computational and descriptive purposes. Although typically derived from isometric test conditions, these relationships have also been extrapolated, perhaps invalidly, to conditions where joint velocity and length are changing. The purpose of this study was to examine the degree of linearity between hamstring and quadriceps torques and their respective EMG signals, and to compare the slopes of these relationships in normal and spastic muscles at varying muscle lengths and conditions. We hypothesized that relationships would be linear for all muscles tested in both subject groups; however, slopes would differ across the two muscles, the three muscle lengths tested, and the two subject groups. We further hypothesized that the degree of linearity during an isotonic task would be less than for the isometric one, particularly for patients with spasticity who may demonstrate abnormal responses to changes in muscle length. Results indicated that torque--EMG relationships were linear for all subjects during isometric contractions, regardless of group, muscle, or knee angle. However, the degree of linearity was significantly less in CP in both conditions; and within the CP group, was less during isotonic compared to isometric conditions. Slope values differed between muscles at some lengths, across muscle lengths in the quadriceps, and subjects with CP showed consistently lower slopes for all quadriceps values. These data in general support the robustness of the linear assumption in isometric conditions for the knee musculature, caution against extrapolation to isotonic conditions particularly for those with movement abnormalities, and suggest that slope differences may provide valuable insights into pathology and warrant further investigation.

Adolescent↗
PubMed2005

Effects of dopamine in isolated rat colon strips.

The aim of the present work is to investigate the effects of dopamine on isolated rat colon strips, and whether dopamine receptors are involved in these effects. Experiments on spontaneous motility and under potassium contraction were performed with dopamine and isoprenaline, both in the absence and presence of antagonists (distal colon strips, isotonic recording, Tyrode solution, 31 degrees C, 1 g of resting tension). At higher concentration (10(-4) mol/L), dopamine abolished spontaneous motility of the rat colon and this effect was not modified by antagonists. In isolated rat colon strips that were depolarized with potassium, dopamine produced concentration-dependent relaxation, without significant differences in reserpinized rats. Preincubation with sulpiride or Sch 23390, dopamine antagonists, did not modify the effects of dopamine. Propranolol shifted the concentration-response curve to the right, though in a noncompetitive manner. Prazosin and yohimbine (alpha-antagonists) did not modify the response to dopamine. Isoprenaline produced a concentration-dependent relaxant response to the KCl-induced contraction antagonized by propranolol, but not by prazosin, in a noncompetitive manner. In conclusion, dopamine exhibits a relaxant effect on the isolated rat colon, which is not mediated by specific dopamine receptors or alpha-adrenoceptors but it may be mediated by atypical beta-adrenoceptors.

Animals↗
PubMed1992

The isometric athlete.

A number of normal daily and athletic activities require isometric or static exercise. Such sports as weight lifting and other high-resistance activities are used by athletes to gain strength and skeletal muscle bulk. However, static exercise also causes significant increases in blood pressure, heart rate, myocardial contractility, and cardiac output. These changes occur in response to central neural irradiation, called central command, as well as a reflex originating from statically contracting muscle. Studies have demonstrated that blood pressure appears to be the regulated variable, presumably because the increased pressure provides blood flow into muscles that have compressed their arterial inflow as a result of increases in intramuscular pressure created by contraction. Thus, static exercise is characterized by a pressure load to the heart and can be differentiated from dynamic (isotonic) exercise, which involves a volume load to the heart. Physical training with static exercise leads to concentric cardiac, particularly left ventricular, hypertrophy, whereas training with dynamic exercise leads to eccentric hypertrophy. Furthermore, the magnitude of cardiac hypertrophy is much less in athletes training with static than dynamic exercise. Neither systolic nor diastolic function is altered by the hypertrophic process associated with static exercise training. Many of the energy requirements for static exercise, particularly during more severe levels of exercise, are met by anaerobic glycolysis because the contracting muscle becomes deprived of blood flow. Training with repetitive static exercise therefore causes little increase in oxygen transport capacity, so that maximal oxygen consumption is either not or only minimally increased. Peripheral cardiovascular adaptations also can occur in response to static exercise training. Although controversial, these adaptations include modest decreases in resting blood pressure, smaller increases in blood pressure during a given workload, increases in muscle capillary-to-fiber ratio, improved lipid and lipoprotein profiles, and increases in glucose and insulin responsiveness. Some of these adaptations also have been found in cardiac patients and hypertensive patients and without any concomitant cardiovascular complications. However, in both healthy individuals and those with cardiovascular disease, the manner in which resistance training is performed may dictate the extent to which these adjustments take place. Specifically, training that involves frequent repetitions of moderate weight (and hence contains dynamic components) seems to produce the most beneficial results.

Cardiovascular Diseases↗
PubMed1995

Endothelium-dependent relaxations in sheep pulmonary arteries and veins: resistance to block by NG-nitro-L-arginine in pulmonary hypertension.

1. The effect of the nitric oxide synthase inhibitor, NG-nitro-L-arginine (L-NOARG), on endothelium-dependent relaxation to a receptor-independent agent, ionomycin, was examined in isolated pulmonary arteries and veins from control, short-term and chronic pulmonary hypertensive sheep. All vessel segments were contracted to optimal levels of active force with endothelin-1 to record endothelium-dependent relaxation. 2. Pulmonary hypertension was induced by continuous pulmonary artery air embolization for 1 day (short-term) and 14 days (chronic) and was associated with a 2 and 3 fold increase in pulmonary vascular resistance respectively. 3. L-NOARG (0.1 mM) reduced the maximum relaxation (Rmax) to ionomycin in large and medium-sized pulmonary arteries from control sheep by approximately 70%. By contrast, L-NOARG (0.1 mM) did not inhibit the Rmax to ionomycin in matched vessels from short-term and chronic pulmonary hypertensive sheep. 4. Resistance of ionomycin-induced relaxations to inhibition by L-NOARG, was confined to the arterial vasculature in chronic pulmonary hypertensive animals, as relaxations to ionomycin in large and medium-sized chronic pulmonary hypertensive veins were, like those in control veins, abolished by L-NOARG. Both large and medium-sized pulmonary veins from short-term pulmonary hypertensive sheep, however, were resistant to block by L-NOARG. 5. Neither sensitivity (pEC50) nor Rmax to ionomycin in large, short-term pulmonary hypertensive arteries was affected when the extracellular concentration of K+ was increased isotonically to 30 mM. Nifedipine (0.3 microM) was present throughout to prevent high K(+)-induced smooth muscle contraction. In the presence of this high extracellular K+, however, L-NOARG (0.1 mM) caused complete inhibition of the relaxation to ionomycin, whereas in normal extracellular K+ (4.7 mM), L-NOARG only weakly inhibited ionomycin relaxations. 6. In conclusion, the onset of pulmonary hypertension in sheep following air embolization, is associated with the development of resistance of endothelium-dependent relaxations to block by L-NOARG. The mechanism of L-NOARG resistance appears to be due to the up-regulation of a K+ channel-mediated backup vasodilator mechanism which can compensate for the loss of nitric oxide (NO)-mediated relaxation. Although this mechanism remains functionally 'silent' in the presence of NO it is able to maintain adequate endothelium-dependent vasodilatation during pulmonary hypertension if NO synthesis is compromised.

Animals↗
PubMed1973

Energetics of contraction in phasic and tonic skeletal muscles of the chicken.

Comparative energetics of chicken latissimus dorsi muscles, tonic anterior (ALD) and phasic posterior (PLD), were investigated by measuring initial heat production. Heat components were analyzed in terms of the equation: E = A + W + alpha(F)(DeltaL) + f(P, t) As the muscles were stretched by increments, heat produced in isometric twitches and tetani decreased in a linear fashion. Two processes are involved: one tension independent, the activation heat, or A; and the other tension dependent, W(i) + alpha(F)(DeltaL) + f(P, t). In twitches, A, per unit tension, is equivalent in the PLD and ALD. Tension-dependent heat, per unit tension, is greater in the PLD due to W(i); but tension-time-related heat, f(P, t), per unit tension, is similar in both muscles. In tetanic contractions, differences in A and f(P, t), per unit tension, are attributed to the greater V(max) in the PLD. The differences in the energetics of isometric contractions in the PLD and ALD, therefore, can be explained by inherent differences in tension development, compliance, and myosin and reticular ATPase activities. Data from isotonic twitches were quantified by means of the equivalent tension technique. Both muscles exhibited an extra heat associated with shortening, alpha(F)(DeltaL). In the PLD, the ratio alpha(F)/P(ot) is greater; it is load independent and (1/2) the value of a/P(o) in both muscles. Enthalpy efficiency, W(e) + W(i)/E, is comparable in both muscles. A Fenn effect is observed only when isotonic energy liberation is compared to a decreasing isometric energy expenditure base line.

Animals↗
PubMed1991

Ca2+ dependence of motilide-induced contractions in rabbit duodenal muscle strips in vitro.

Recent studies suggested that certain erythromycin A (EM-A) derivatives are motilin receptor agonists. As proposed by Itoh they may be called "motilides". We have investigated the Ca2(+)-dependence of contractions induced by two potent motilides, ME-34 [de(N-methyl) 8,9-anhydroeryhtromycin A 6,9-hemiacetal] and EM-523 [de(N-methyl)-N-ethyl-8,9-anhydroerythromycin A 6,9-hemiacetal], in duodenal tissues and compared the results with those previously obtained with motilin. Isometric and isotonic contractile responses of isolated longitudinal muscle sheets from the rabbit duodenum were tested under normal, Ca2(+)-free and depolarizing conditions. Prior to stimulation with motilides, the maximal response to acetylcholine was recorded and all responses were always expressed as a percentage of this response. Both motilides induced contractions in normally polarized tissue, with an EC50 of 26 +/- 5 nM for ME-34 (n = 7), and 27 +/- 5 nM for EM-523 (n = 16) and maximal responses of respectively 88 +/- 4% and 80 +/- 3%. Like motilin, both compounds induced an 'extra'-contraction in depolarized tissues. The EM-523 response in 140 mM K+ under isotonic conditions was 84 +/- 3% (n = 5) at 10(-5) M, with an EC50 that was shifted to 65 +/- 18 nM. Similar figures were obtained for ME-34. When Ca2+ was added to Ca2(+)-depleted strips, half-maximal Ca2+ values (in mM) were 1.10 +/- 0.11 (n = 9) for EM-523 and 1.13 +/- 0.12 (n = 3) for ME-34, as compared with 1.12 +/- 0.13 (n = 7) for motilin and 2.8 +/- 1.1 (n = 9) for K+. Both ME-34 and EM-523 also induced a transient contraction in Ca2(+)-free solutions under isometric conditions.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Discontinuous volume transitions induced by calcium-sodium ion exchange in anionic gels and their neurobiological implications.

Discontinuous volume transitions in poly (acrylic acid) gels were studied by determining equilibrium swelling curves of small gel beads immersed in salt solutions containing varying concentrations of Ca2+ and Na+. Reversible contractions of gel membranes associated with Ca(2+)-Na+ exchange were examined using both isometric and isotonic recording devices. A discontinuous change in electric conductance was demonstrated in association with Ca(2+)-Na+ exchange in gel membranes. These experimental findings provide a sound physicochemical basis for elucidating the mechanism of nerve excitation.

Action Potentials↗
PubMedDate not supplied

Experimental hypothyroidism: depression of myocardial contractile function and hemodynamics and their reversibility by substitution with thyroid hormones.

Hemodynamics and myocardial muscle mechanics have been studied in 22 euthyroid and 60 hypothyroid cats in which experimental hypothyroidism has been produced by thyroidectomy 61 days prior to the examination. Left ventricular to body weight ratio was altered due to a decrease in left ventricular weight and an increase in body weight. Heart rate, cardiac output and cardiac index were decreased (by 12-15 per cent), whereas stroke volume remained unchanges. Peak systolic pressure of the left ventricle was moderately decreased, the other pressures were in the normal range. There was a marked and significant reduction of isovolumic contractility indices indicating a depression of myocardial contractility in situ by 20-27 per cent. The isolated ventricular myocardium exhibited decreases of isotonic muscle shortening, of maximum isometric tension development and of the rates of both, isotonic shortening and isometric tension development by 12-35 per cent. Force-velocity relationships of contraction and relaxation were depressed to lower values of contraction and relaxation velocity as well as of maximum isometric muscle tension. The alterations in myocardial muscle mechanics and hemodynamics were completely reversible following substitution of the hypothyroid group with physiological doses of L-thyroxine (5 mug/kg/day for 8-18 days). Excess increases of parameters of myocardial performance were found following substitution of the hypothyroid group with L-thyroxine (500 mug/kg/day) in accordance with the induction of experimental hyperthyroidism in these animals. The results demonstrate impaired myocardial contractility and hemodynamics in experimental hypothyroidism. These changes are completely reversible by substitution with L-thyroxine in accordance with a reversible thyroid cardiomyopathy. The cellular mechanisms responsible for the altered cardiac activity in experimental hypothyroidism are discussed.

Animals↗
PubMed2006

Role of the sarcolemmal adenosine triphosphate-sensitive potassium channel in hyperkalemic cardioplegia-induced myocyte swelling and reduced contractility.

BACKGROUND: Hyperkalemic cardioplegia (Plegisol) has been shown to result in myocyte swelling and reduced contractility. We have demonstrated the elimination of these detrimental effects by the addition of an adenosine triphosphate-sensitive K+ (KATP) channel opener. To examine whether the mitochondrial or sarcolemmal KATP channel might be involved, volume and contractility in isolated myocytes from wild-type mice and mice lacking the sarcolemmal KATP channel (Kir6.2-/-) were evaluated. METHODS: Myocytes were perfused for 20 minutes each with control 37 degrees C Tyrode's solution, test solution, and then control solution. Test solutions were (n = 10 per group) either 9 degrees C Plegisol or 9 degrees C Plegisol with 100 micromol/L of diazoxide, a putative mitochondrial-specific KATP channel opener. Cell volume and contractility were measured by digital video microscopy at baseline and during the test solution and reexposure periods. RESULTS: Myocytes from wild-type mice, perfused with 9 degrees C Plegisol, demonstrated significant cell swelling (11.2% +/- 0.4%; p < 0.01) and diminished contractility (32.5% +/- 9.6% reduction in percent shortening, 47.2% +/- 10.1% reduction in peak velocity of shortening, and 52.0% +/- 8.8% reduction in peak velocity of relengthening; p < 0.05) versus baseline. Cell swelling and diminished contractility were significantly reduced by the addition of diazoxide. In Kir6.2-/- myocytes, Plegisol caused a greatly reduced level of cell swelling (3.2% +/- 0.1%; p < 0.01), and this was unaffected by diazoxide. Contractility was unchanged in Kir6.2-/- myocytes after Plegisol. CONCLUSIONS: The sarcolemmal KATP channel appears necessary for exaggerated cell swelling and reduced contractility to occur after hyperkalemic cardioplegia in mouse myocytes.

Animals↗
PubMed1967

Fluid transfer in the everted human gallbladder.

The rates of fluid transfer across human gallbladders obtained at cholecystectomy for cholelithiasis were determined by the measurement of weight changes of everted preparations under controlled conditions. Active transport of fluid from the mucosal to the serosal surface was indicated since weight gain occurred with the same solution on both sides of the membrane and against hydrostatic, osmotic, and potential differences. With respect to sodium, the fluid transferred was isotonic to the bathing solutions. Metabolic inhibitors and temperature extremes inhibited weight gain. In addition, muscle contractions in this in vitro preparation were related to the rates and direction of fluid movement. Cholecystokinin increased muscle activity and caused weight loss in preparations that previously had gained weight. Norepinephrine caused weight gain or increased weight gain in all preparations tested. The direction of net fluid movement in the isolated everted human gallbladder was determined by the opposing forces of active mucosal transport and a filtration pressure generated by muscle contractions.

Biological Transport, Active↗
PubMed1970

Hemodynamic effects of pneumonia. II. Expansion of plasma volume.

Previous work has demonstrated that approximately one-third of patients with pneumonia have a hypodynamic circulatory response. This response is characterized by an abnormally wide arteriovenous oxygen difference, a low cardiac output, increased peripheral resistance, and an increased hematocrit. This state was found to abate in convalescence. In an attempt to elucidate the pathogenesis of this hypodynamic state, nine additional patients were studied hemodynamically during the acute phase of pneumonia before and during acute expansion of blood volume by low molecular weight dextran (seven patients) or normal saline (two patients). Five patients were restudied before and during acute blood volume expansion in convalescence. Three patients with pneumonia had a normal arteriovenous oxygen difference (< 5.5 vol%), and six patients were hypodynamic in that their arteriovenous oxygen differences were greater than 5.5 vol%. With expansion of blood volume in the acute phase of pneumonia, all patients showed an increase in cardiac output, a decrease in arteriovenous oxygen difference, and a decrease in peripheral vascular resistance; however, the percentage change in the hypodynamic patients was not as great as occurred in the patients with normal hemodynamics nor as great as occurred when restudied in convalescence. Likewise, all patients had a normal or near normal hemodynamic profile in convalescence. In addition, ventricular function in the acute phase of pneumonia was depressed. The findings suggest that the hypodynamic state associated with acute pneumonia is due to depressed myocardial contractility to which relative hypovolemia may contribute.

Acute Disease↗
PubMed2005

The effects of isoflurane on airway smooth muscle crossbridge kinetics in Fisher and Lewis rats.

Our aim was to determine how isoflurane modified crossbridge (CB) number and kinetics in airway smooth muscle (ASM) and to compare its effects in Fisher and Lewis rats, two strains with differences in airway responsiveness. The effects of isoflurane (2 MAC) on isotonic and isometric contractility in tracheal ASM strips were investigated after methacholine (10(-6) M)-induced contraction. CB mechanics and kinetics were analyzed using the formalism of Huxley's equations adapted to ASM. After isoflurane, maximum velocity did not differ from baseline in Lewis rats, whereas it was significantly less than baseline in Fisher rats ( approximately 25%), the most reactive strain. Isoflurane totally reversed methacholine-induced increase in active CB number in Lewis rats (2.4 +/- 0.5 versus 1.8 +/- 0.4 10(9)/mm(2) after methacholine and isoflurane, respectively) whereas reversal was only partial in Fisher rats (2.7 +/- 0.4 versus 2.1 +/- 0.3 10(9)/mm(2) after methacholine and isoflurane, respectively). Isoflurane induced a 40% increase in attachment step duration in both strains and an almost twofold increase in the CB cycle duration compared with baseline in Lewis rats. The isoflurane-induced increase in detachment step duration was less in Lewis than in Fisher rats (P < 0.05). We concluded that isoflurane modulated CB number and CB cycling rates of isolated rat ASM differently depending on the level of airway responsiveness.

Algorithms↗
PubMed1978

[Mechanical characteristics of isotonic work and high-energy phosphates in frog ventricle after 1-fluoro-2,4-dinitrobenzene].

The blocking of the creatinphosphokinase by 1-fluoro-2,4-dinitrobenzene (FDNB) allows to investigate the relationship between ATP-supply, contractility and relaxability of the frog's myocardium. In isotonically working isolated ventricles of frogs the time of work, systolic and diastolic volume, velocity of contraction and relaxation as well as the levels of CP, ATP, ADP and AMP were measured at different intervals until termination of each experiment. CP shows a small variation, ATP decreases to 60% and ADP + AMP increase for the same amount under FDNB during the development of a slight inhibition of contractility and a continuously growing inhibition and retardation of relaxation until systolic arrest. ATP content and volume of relaxation correlated strictly. The contracture and the diminished contractility are caused by the decrease of ATP, producing a lack of substrate for Ca transport and actin-myosin-ATPase. This models the course of events during an insufficiency like in angina pectoris and in myocardial infarction.

Adenine Nucleotides↗
PubMed1988

Improving myocardial metabolic and functional recovery after cardioplegic arrest.

The myocardial oxidation of fatty acids and glucose, the predominant substrates for aerobic metabolism, is impaired after cardioplegic arrest for coronary revascularization. Because lactate can be readily metabolized to pyruvate, it may be the preferred substrate for aerobic metabolism after cardioplegic arrest when arterial concentrations are elevated. Nineteen patients undergoing elective coronary revascularization with blood cardioplegia were randomized to receive LOW (nine patients, no exogenous lactate) or HIGH (10 patients, a perioperative infusion of Ringer's lactate) arterial lactate concentrations. Coronary sinus catheterization and lactate labeled with carbon 14 permitted calculation of myocardial oxygen consumption and lactate oxidation which were significantly increased during reperfusion in the group with HIGH arterial lactate concentrations. Atrial pacing at 110 beats/min on cardiopulmonary bypass resulted in myocardial lactate production (suggesting ischemic anaerobic metabolism) in the LOW lactate group, but atrial pacing increased lactate consumption and oxidation in the HIGH lactate group (suggesting increased aerobic metabolism). Systolic function (the relation between end-systolic pressure and volume) as assessed by nuclear ventriculography 3 hours postoperatively was significantly better (p less than 0.05 by analysis of covariance) in the HIGH lactate group. Postoperative myocardial creatine kinase release was significantly lower in the HIGH lactate group, which suggested less perioperative ischemic injury. Lactate was the preferred substrate for myocardial oxidative metabolism after cardioplegic arrest, and the higher arterial lactate concentrations improved myocardial metabolic and functional recovery and reduced perioperative ischemic injury.

Cardiac Pacing, Artificial↗
PubMed1980

On the changes in the membrane potential and the contractile activity of the smooth muscle of the lower esophageal and ileo-caecal sphincters upon increased K in the nutrient solution.

The influence of increased K+ in the nutrient solution on the excitatory-contractile process in smooth-muscle strips from the lower esophageal sphincter (LES) and the ileo-caecal sphincter (ICS) of cats is studied. The changes in the membrane potential (MP) and the tension (T) are recorded by the sucrose gap method. The rise of the K+ concentration in the nutrient solution to 30 mM causes hyperpolarization and relaxation of LES, while in ICS depolarization is observed irrespective of the relaxation. In LES the higher K+ concentrations, as well as the isotonic K+ lead to initial brief hyperpolarization, followed by depolarization. A biphasic response in the contraction-relaxation and subsequent contraction corresponds to them. Irrespective of the fact that the response in ICS is also biphasic with respect to the contraction, the changes in MP are manifested only as depolarization. These responses of LES and ICS are not influenced by cholinergic and adrenergic blockers (atropinum sulfuricum, Propranolol, Phenoxybenzamine--(10(-6) to 10(-5) g/ml). In ouabaine-pretreated (10(-6) to 5 x 10(-6) M) smooth muscle from LES and ICS, in all K+ concentrations the response is depolarization and contraction. The effects of increased K+ in the nutrient solution on LES and ICS are connected with the ratio [K]i : [K]o ([K]i--intracellular, [K]o--extracellular). It is assumed that the Na-K pump in LES and ICS functions at a different level compared with the other smooth muscles of the gastro-intestinal tract.

Animals↗
PubMed1994

Chronic exposure to cyclosporine affects endothelial and smooth muscle reactivity in the rat aorta.

Chronic exposure to cyclosporine affects vascular reactivity. Experiments were designed to characterize the endothelium-dependent and endothelium-independent vascular reactivity of rats exposed to oral cyclosporin A (CyA). Two subsets of rats (n = 6) were treated with CyA (20 mg/kg/day) and olive oil (cyclosporine vehicle), respectively, for a period of 8 weeks. Aortic rings (4-5 mm) were suspended for isometric force measurement in organ chambers containing Krebs Ringer solution (37 degrees C, 95% O2, 5% CO2). The maximal endothelium-dependent relaxation to cumulative doses of acetylcholine was significantly decreased in the CyA-treated aortic rings compared to olive oil-treated ones (data expressed as percent of initial contraction; CyA, 50% +/- 3% versus olive oil, 37% +/- 7%; p < 0.05). However, endothelium-dependent relaxations to histamine and adenosine diphosphate and endothelium-independent relaxation to sodium nitroprusside were not affected in both groups. An endothelium-dependent contraction to serotonin and aggregating platelets were observed in the CyA group, but not in the control group. The endothelium-independent contraction to norepinephrine was enhanced in the CyA group (CyA ED50, log -7.66 +/- 0.18 mol/L versus olive oil ED50, log -7.01 +/- 0.11 mol/L; p < 0.01). These experiments suggest that chronic exposure to cyclosporine A could contribute to augmenting vascular tone by (1) decreased release of endothelial relaxing factor mediated by muscarinic receptors, (2) increased production of endothelium-related constricting factor mediated by serotoninergic receptors, and (3) greater vascular smooth muscle sensitivity to circulating catecholamine.

Acetylcholine↗
PubMed1991

Relationships between lymphatic pump flow and total lymph flow in the small intestine.

Response of collecting lymphatics to acute elevations in lymph formation was studied in vivo. Mesentery of 33 rats was prepared for intravital microscopic study, and indexes of lymph propulsion (contraction frequency, stroke volume, and ejection fraction) were monitored. In 14 rats, total lymph flow was measured by cannulating the main intestinal lymph trunk. After a control period, lymph flow was increased by hemodilution with isotonic saline. Right atrial pressure did not significantly increase during the hemodilution period. Total lymph flow increased to approximately 25 times control. Lymph propulsion (the product of stroke volume and contraction frequency) decreased in five lymphangions (group I). In 22 lymphangions, lymph propulsion increased one to five times control (group II). The remaining six lymphangions increased lymph propulsion by greater than five times control (group III). Group I possessed the largest end-diastolic diameter, highest baseline contraction frequency, and did not dilate as lymphatic filling increased. Group III possessed the smallest initial end-diastolic diameter and lowest baseline contraction frequency, and end-diastolic diameter doubled as lymphatic filling increased. The characteristics of group II were between those of groups I and III. Total lymph flow and lymph propulsion by group III lymphangions tended to agree when lymph flow was less than five times control. In more edematous conditions, total lymph flow exceeded lymphatic pump flow. The characteristics of group II were between those of groups I and III. Analysis of the location of various sized lymphangions within the lymphatic network indicated that the smaller group III lymphangions were located nearer the intestinal wall, and the larger group I lymphangions were nearer the outflow from the mesentery.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗