bluuebunny/crossref_metadata_2025 huggingface dataset:
Optimal and actual end systolic pressure‐volume relations in dogs and rabbits. Including new method of Emax determination
Authors: PIENE H. , MYHRE E. S. P. , WINNEM B.
Published: December 2008

Under the assumption that a ventricle and its arterial load are normally matched according to work optimization, a relation between left ventricular (LV) mechanical performance as described by the slope (Emax) of the end systolic pressure‐volume relationship (ESPVR), mean systolic pressure during ejection (mSLVP), and stroke volume (SV), is proposed: optimum Emax=E=mSLVP/SV.

Slope (Emax) was obtained, in 6 dogs and 9 rabbits, by establishing relations among ejected volume and LV diameter squared (D2) in control beats, and among pressure and D2 at end systole (ES) in series of beats of varying load, accomplished either by acute aortic constriction (AOC) or inferior caval occlusion (IVCO). Slope in dogs was also obtained by direct measurements of ventricular volume by a conductance catheter and the results were compared with the above method. A dimensionless index, α= Emsx/E', (optimal value = 1.0) was calculated to indicate how well the ventricle and arterial system were matched. In dogs, E= 10.9 ± 2.1 mmHg ml‐1, Emax= 8.1 ± 2.6 (AOC) and 7.1 ± 2.5 (IVCO), hence α= 0.79 ± 0.23 (AOC) and 0.68 ± 0.15 (IVCO). In rabbits, E= 54.1 ± 20.0 mmHg ml‐1, Emax= 64.8 ± 15.9 (mmHg ml‐1), hence a = 1.23 ± 0.33. α=1.0 fell outside the 95% confidence interval only in experiments of dogs subjected to IVCO.
Somatostatin and methionine‐enkephalin inhibit cholera toxin‐induced jejunal net fluid secretion and release of vasoactive intestinal polypeptide in the cat in vivo
Authors: EKLUND S. , SJÖQVIST A. , FAHRENKRUG J. , JODAL M. , LUNDGREN O.
Published: December 2008

A major part of the net fluid secretion that is elicited by cholera toxin in the small intestine of the cat has been shown to be mediated by intramural nervous reflex(es). The release of vasoactive intestinal polypeptide (VIP) from the small intestine is increased by cholera toxin. We report that close intra‐arterial infusions of methionine‐enkephalin (met‐enk) and somatostatin cause a parallel reduction in cholera toxin‐induced net fluid secretion and in VIP release from the small intestine of the cat. Intestinal blood flow was slightly, but significantly increased by met‐enk and not influenced by somatostatin. These results strengthen the hypothesis that VIP is involved as a neurotransmitter in the nervous reflex mediating cholera toxin‐induced secretion.
Firing patterns of midbrain dopamine neurons: differences between A9 and A10 cells
Authors: GRENHOFF J. , UGEDO L. , SVENSSON T. H.
Published: December 2008

Dopamine neurons of the substantia nigra (A9) and the ventral tegmental area (A 10), giving rise to the nigrostriatal and mesolimbic dopamine pathways, respectively, are commonly supposed to show similar electrophysiological activity. There are, however, instances where the two systems are differently modulated. To assess possible physiological differences in the neuronal activity of A9 and A10 neurons, randomly sampled single cells were extracellularly recorded in the chloral hydrate‐anaesthetized male rat. In addition to firing rate, the degree of burst firing and the regularity of firing were quantitatively analysed. Our results show that although A9 and A10 do not differ in firing rates, A10 neuronal activity is markedly less regular and shows a higher degree of burst firing, as judged from analysis of inter‐spike time interval histograms. Mean burst firing values were 3% for the A9, and 23% for the A10 neurons. Regularity was described by variation coefficients of inter‐spike time interval histograms. The mean variation coefficient was 38.4% in the A9 group and 63.8% in the A10 group, i. e. the AIO neuronal firing was less regular. The difference in regularity is partly, but not fully, dependent on the difference in burst firing. Previous biochemical and physiological studies strongly support the functional significance of modulatory changes in midbrain dopamine‐cell firing patterns. Since the firing pattern of midbrain dopamine cells seems to be controlled by synaptic inputs, our results indicate a higher tonic modulatory influence on the Aro than on the A9 neurons. Thus the present results imply the pharmacological possibility of preferentially affecting AIO versus A9 dopamine cell function.
Oxygen deficit at the onset of submaximal exercise is not due to a delayed oxygen transport
Authors: SAHLIN K. , REN J. M. , BROBERG S.
Published: December 2008

Six subjects cycled on two occasions for 10 min at power output of 188±11 W (x̄± SEM), which corresponded to 70 ± 2% of their maximal oxygen uptake (Vo2 max). The exercise intensity was either increased gradually in a stepwise manner over about 15 min (slow transition ‐ S), or increased directly (direct transition ‐ D) to the predetermined power output. Muscle samples from the quadriceps femoris muscle were taken at rest and immediately after exercise in both trials. During exercise with both D and S muscle lactate increased approximately 10 times (P < 0.0 1), phosphocreatine decreased about 50% (P < 0.01) and ADP increased about 20% (P < 0.05). There were no significant differences between S and D (P > 0.05). Furthermore, blood lactate, O2 deficit, O2 debt, and the calculated increase in muscle content of inorganic phosphate (Pi) were all similar between D and S (P < 0.05). It is concluded that the O2 deficit and the anaerobic energy utilization is not affected by the rate of transition from rest to exercise. Consequently, the O2 deficit at the onset of exercise is not due to a delay in O2 transport, but may be due to a limited peripheral O2 utilization as a result of metabolic adjustments at the cellular level. Increases in ADP and Pi are suggested to be primary metabolic regulators which activate both aerobic and anaerobic energy production resulting in the O2 deficit.
Muscle energy metabolism and electrolyte shifts during low‐level prolonged static contraction in man
Authors: SJØGAARD G.
Published: December 2008

Seven men performed one‐legged isometric knee extension at 5% MVC for I h. Total body oxygen uptake amounted to 451 (42–471) ml min‐1 and oxygen uptake over the contracting leg to 200 (172–216) ml min‐1, with no changes occurring during the in contraction. Venous O2 tension decreased from 29.4 mmHg at rest to 23.1 mmHg with contraction and CO2 tension tended to increase from a resting value of 50.5 mmHg to 57.2 mmHg (ns.). No similar changes occurred in arterial O2 and CO2 tensions. There was a small but continuous glucose uptake at both rest and throughout the contraction, whereas a lactate release occurred only in the early phase (2 min) of contraction. Muscle glycogen content was 312 mmol kg‐1 dry wt at rest, no significant changes had occurred following 30 min or 1 h of contraction. Arterial and venous Hct and Hb values indicated that a flux of water occurred from the vascular bed to the contracting muscle, in which H2O increased from 3.06 I kg‐1 dry wt at rest to 3.30 1 kg‐1 dry wt after 1 h at 5 % MVC. Simultaneously potassium (K), was released from the muscle throughout contraction with a mean venous‐arterial difference of 0.25 mmol I‐1. With a plasma flow of 335 ml min‐1 kg‐1 wet wt the K loss amounted to 5 mmol kg‐1 wet wt or roughly 5% of the total muscle K content. Results from analysis of muscle K content were in line with this, since the mean K content of 460 mmol kg‐1 dry wt at the end of contraction tended to be lower than the mean resting value of 471 mmol kg‐1 dry wt (n.s.). These results indicate that during low‐level contractions, the muscle is able to maintain homeostasis with respect to energy turnover, but not with respect to intra‐/extracellular K concentration. This K imbalance may well play a role in muscle fatigue.
Somatomedin C immunoreactivity in the Achilles tendon varies in a dynamic manner with the mechanical load
Authors: HANSSON H.‐A. , ENGSTRÖM A.M.C. , HOLM S. , ROSENQVIST A.‐I.
Published: December 2008

Distribution of the trophic peptide somatomedin C (Sm‐C; insulin‐like growth factor I; IGF‐I) immunoreactivity was mapped in normal Achilles and tibialis anterior tendons. The spindle‐shaped tendon fibroblasts showed faint perinuclear staining. Fibroblasts in the paratenon mostly had a more intense IGF‐I immunoreactivity, i.e. faint to moderate. When analysing either tendon in detail, areas with more intense IGF‐I immunoreactivity could be recognized and seemed to correlate with areas of high mechanical stress. Increased mechanical load induced over 3 days elevated IGF‐I immunoreactivity throughout the cytoplasm of tendon fibroblasts. Peak intensity was reached in 7 days, and thereafter the IGF‐I immunoreactivity seemed to decrease irrespective of persistent high mechanical load. Training the animals on a treadmill for from 20 up to 60 min per day for 5 days induced after 3–5 days increased IGF‐I immunoreactivity throughout the cytoplasm of the tendon and paratenon fibroblasts. Sudden curtailment of loading the Achilles tendon resulted in a marked reduction of the IGF‐I immunoreactivity in most fibroblasts within 3 days. After a week only a small number of tendon fibroblasts showed any IGF‐I immunoreactivity. The IGF‐I immunoreactivity of tendon fibroblasts thus correlates to mechanical loading of the tendon. It is proposed that IGF‐I may have a trophic influence on tendon and paratenon cells by autocrine and/or paracrine mechanisms.
The release mechanism for atrial natriuretic factor during blood volume expansion and tachycardia in dogs
Authors: CHRISTENSEN G. , ILEBEKK A. , AAKESON I. , KIIL F.
Published: December 2008

Atrial natriuretic factor (ANF) is released during blood volume expansion and tachycardia, but only blood volumer expansion causes atrial distension, which presumably promotes ANF release. Our study was undertaken to search for a common release mechanism. In five anaesthetized, closed‐chest dogs, plasma immunoreactive (IR) ANF was measured at three levels of blood volume, which were obtained by infusing a Ringer's solution. At each level of blood volume, plasma IR‐ANF was measured at three pacing frequencies. Plasma IR‐ANF increased as mean right atrial pressure (mRAP) was raised from 2 to 10 mmHg by volume expansion, whereas pacing tachycardia (at heart rates (HR) 50 ± 3 and 98 ± 1 beats min‐1 above control) at each level of blood volume expansion increased plasma IR‐ANF and systolic RAP (sRAP) at constant mRAP. Plasma IR‐ANF was more strongly correlated to sRAP (r= 0.83) than to mRAP (r = 0.69), but the product sRAP x HR had the highest correlation coefficient (Y= 0.86). According to the multiple regression equation:

plasma IR‐ANF = k1+ k2 mRAP + k3 sRAP + k4 sRAP × HR, the product sRAP × HR had the highest coefficient of determination (r2= 0.75) and was the only significant determinant. We conclude that atrial tension or stress, developing during each atrial systole, is an important determinant of ANF release. Since atrial diastolic and systolic dimensions do not increase during pacing tachycardia, ANF release is not dependent on atrial distension.
Strength of two‐ and one‐leg extension in man
Authors: SECHER N. H. , RUBE N. , ELERS J.
Published: December 2008

Two‐ and one‐leg extension strengths were compared in 155 female and male, untrained and trained (eight bicyclists, 38 weight‐lifters) subjects and in a polio patient with almost no strength in one leg. On average two‐leg strength was 82±1.3% (SE) of the sum of the strength of the right and left legs (leg‐strength ratio) with no significant difference between the untrained and trained subjects. In the polio patient two‐leg strength was lower than the strength of the strongest leg. A similar leg‐strength ratio was found when measurements were made with a knee angle of 150° (n= 128) and 90° (n= 25). The ratio did not change when re‐determined after 1 year (n= 9). Moderate changes in the subjects' position during measurements did not affect one‐leg strength (n= 13). However, familiarization with the experimental apparatus increased the leg‐strength ratio from 80 ± 2.5% to 97 ± 2.9% (P 0.01) (n= 18). In contrast, two‐arm extension strength was similar to the sum of the strength of the right and left arms (n= 15). The results demonstrate that two‐leg strength in general is lower than the sum of the strength of the right and left legs, and that this phenomenon is found even after intensive endurance or strength training. However, familiarization with the experimental apparatus can increase the relative two‐leg strength which suggests that muscle strength in man may be limited by the central nervous system's ability to activate maximally all synergistic muscles and/or to control antagonistic muscles.
Vasodilator responses to alpha‐human‐atrial natriuretic peptide in isolated omental and pulmonary arteries from rabbit and man
Authors: LINDBERG F. , ANDERSSON K.‐E.
Published: December 2008

In isolated vessels from the pulmonary and mesenteric/omental arterial circulations of rabbit and man, the effects of synthetic α‐human atrial natriuretic peptide (α‐hANP) were investigated. The vessels had an outer diameter of 0.6–1.2 mm and were contracted by noradrenaline (NA) and prostaglandin (PG) F2α, (mesenteric/omental arteries) or by 5–hydroxytryptamine (5–HT) and PGF2α (pulmonary arteries). It was found that in rabbits, mesenteric vessels contracted by NA and PGF2α were not significantly relaxed by α‐hANP. Rabbit pulmonary vessels contracted by PGF2α or 5–HT were concentration‐dependently relaxed by α‐hANP (maximum 70%). Human omental vessels contracted by NA and PGF2α showed a moderate (30%) relaxation after addition of the peptide. Human pulmonary arteries contracted by 5–HT were relaxed by α‐hANP almost to baseline, while PGF2α‐contracted vessels showed a maximum relaxation of 65%. It is concluced that α‐hANP has a relatively selective effect on pulmonary arterial vessels from rabbit as well as man. The results suggest that the peptide may be involved in the regulation of pulmonary vascular tone.
Short‐term effects of stimulus interval changes in guinea‐pig and rat atrial muscle
Authors: JÓHANNSSO M. , ÁSGRIMSSON H.
Published: December 2008

Isometric force and action potentials were recorded in thin atrial strips from guinea‐pigs and rats (32 °C). The restitution of peak force and action potential duration, after a regular contraction, was determined (test interval 0.1–120 s), together with the postextrasystolic potentiation. The mechanical restitution could be described with an exponential function in two phases as: force = A(I–e‐k1 t)+B(I–e‐k2 t). By increasing the basic stimulation rate in guinea‐pig atria from 0.2 to 2 Hz, the size of A was approximately doubled while B was only slightly affected. When [Ca2+] was increased from 0.9 to 3.6 mmol I1‐, the size of A increased approximately 3.4 times while B decreased only slightly. There was a close correlation between steady‐state contractility of the muscle and parameter A but not parameter B. In a similar fashion postextrasystolic potentiation can be described as: force = Ce‐kt+D. This potentiation was greater in guinea‐pig than in rat hearts. In both species the rate of potentiation decay (k) was usually similar to the rate of the first phase of restitution (k1). It seems reasonable to interpret the parameters A and B as reflections of two separate intracellular compartments for activator calcium.
Carbonic anhydrase localization to perivenous hepatocytes
Authors: CARTER N. , WISTRAND P. J. , LÖNNERHOLM G.
Published: December 2008

It was shown by immunohistochemical methods, using antisera against highly purified carbonic anhydrases CA I, II and III, that CA II and CA III are specifically located in hepatocytes around central veins of adult rat livers. CA II was found in these perivenous hepatocytes of both male and female rats. Its physiological role is probably to facilitate the secretion of bicarbonate ions by these cells into canalicular bile. CA III and CA I were found in the same hepatocytes but only in the livers of male rats. The function of CA I and CA II exclusively in these cells of male rats cannot be simply explained.
Basic features of an extracellular recording method to study secretion of a sympathetic co‐transmitter, presumably ATP
Authors: STJÄRNE L. , STJÄRNE E.
Published: December 2008

An extracellular recording method is described which permits in suitable model tissues (e. g.guinea‐pig or mouse vas deferens) study of the nerve impulse in sympathetic terminals and the release of transmitter from sites inside or outside the recording electrode. Negative‐ or positive‐going potentials were assumed to reflect the excitatory junction current (EJC) caused by transmitter released inside or outside the electrode, respectively, and hence termed ‘EJCi’ (i for inside) or ‘EJCo’ (o for outside).The EJCo were shown to be Ca2+‐dependent, blocked by addition of tetrodotoxin or guanethidine, resistant to the α1 adrenoceptor blocking agent prazosin but suppressed by desensitization of P2‐purinoceptors by α,β‐methylene ATP, and hence, presumably, are caused by release of ATP as a sympathetic co‐transmitter. The amplitude of the EJCo was voltage‐dependent and increased with the length and frequency of stimulus trains within the range of 1–50 shocks at 0.1–2.5 Hz.

In conclusion, combined use of EJCi and EJCo provides a useful tool for physiological and pharmacological analysis of pre‐ and post‐junctional events associated with the secretion of a sympathetic co‐transmitter, presumably ATP.
Some pharmacological applications of an extracellular recording method to study secretion of a sympathetic co‐transmitter, presumably ATP
Authors: STJÄRNE L. , STJÄRNE E.
Published: December 2008

Extracellular recording in guinea‐pig or mouse vas deferens or rat tail artery was used to study the effects of some pharmacological agents on the nerve terminal spike (NTS) and the secretion of a sympathetic co‐transmitter (presumably ATP), as reflected in the excitatory junction current (EJC).A negative‐going EJCi (i for inside) was assumed to reflect release from sites inside, and a positive‐going EJCo (o for outside) release from sites outside the recording electrode. Passage into or out of the electrode seemed to be slow. Tetrodotoxin (TTX) in the outer medium blocked the NTS and ECJo as well as EJCi; TTX in the pipette blocked stimulus‐evoked but not spontaneous EJCi. The dihydropyridine Ca2+ channel blocking agent, nifedipine, was without effect, but Cd2+ in the external medium blocked EJCo and also, by an effect apparently ‘upstream’ of varicosities, inhibited EJCi (i. e.release within the patch) but not the NTS.When present in the outer medium the α2‐adrenoceptor agonists, clonidine and xylazine, blocked both EJCo and EJCi, but not the NTS.The effects of clonidine were blocked by yohimbine, which in itself increased the EJCo by about 50%.Neuropeptide Y and met‐enkephalin in the outer medium blocked EJCo; the effect of met‐enkephalin was blocked by naloxone. The K+ channel blocking agents, tetraethylammonium and 4‐aminopyridine, inside or outside the electrode, increased dramatically the size of EJCi or EJCo, respectively.
Spermidine/spermine‐N1‐acetyltransferase activity in isoprenaline‐stimulated rat salivary glands
Authors: EKSTRÖM J. , MÅNSSON B. , NILSSON B.‐O. , ROSENGREN E. , TOBIN G.
Published: December 2008

In parotid, sublingual and submaxillary glands stimulated by continuous intravenous infusion of isoprenaline at various doses for 3 h, the concentrations of the polyamines putrescine, spermidine, spermine and N1‐acetylspermidine as well as the activities of ornithine decarboxylase and spermidine/spermine‐N'‐acetyltransferase were determined. Ornithine decarboxylase is the enzyme that catalyses the formation of putrescine from ornithine. The most striking effect was observed in parotid glands. Here, the β‐adrenergic agonist increased the activity of spermidine/spermine‐N1‐acetyltransferase markedly, but only slightly (if at all) that of ornithine decarboxylase. It also increased the concentrations of N1‐acetylspermidine and putrescine markedly. The result obtained in this gland indicates interconversion of higher polyamines to putrescine.
Influences of the sympatho‐adrenal system on gastric motility and acid secretion and on gastroduodenal bicarbonate secretion in the cat
Authors: FÄNDRIKS L. , JÖNSON C.
Published: December 2008

Experiments were performed on acutely vagotomized cats during chloralose anaesthesia. Gastric H‐ and HCO‐3 secretions were calculated from the pH and Pco2 in a luminal perfusate. Gastric motility was reflected by changes in hydrostatic pressure within the luminal perfusion system (‘intragastric pressure’).Duodenal HCO‐3 secretion was monitored by pH titration in situ.Animals with an intact sympatho‐adrenal system (group 1) were compared with others subjected to splanchnicotomy (group 2), adrenal gland ligation (group 3), and splanchnicotomy plus adrenal gland ligation (group 4).Basal gastric H+ secretion, as well as vagally induced H‐ secretory responses, did not differ significantly between groups. Basal gastric HCO‐3 secretion was lower in all groups with a manipulated sympatho‐adrenal system compared to the intact controls. Vagally induced increases in gastric HCO‐3 secretion were enhanced in the splanchnicotomized groups (groups 2 and 4).Basal as well as vagally induced increases in intragastric pressure and duodenal HCO‐3 secretion were enhanced in animals subjected to splanchnicotomy, with or without simultaneous adrenal gland ligation (groups 2 and 4).Adrenal gland ligation per se had no such effects. The results suggest that the adrenal glands exert a stimulatory action on basal gastric HCO‐3 secretion. Basal intragastric pressure and basal duodenal HCO‐3 secretion are inhibited by post‐ganglionic sympathetic neurons, not involving the adrenal glands. Also, vagal excitatory effects on gastric motility, as well as on gastric and duodenal HCO‐3 secretions, are inhibited by such a direct neural mechanism.
Effect of acute intravenous volume loading on haemodynamics and aortic baroreceptor activity in dogs
Authors: HARTIKAINEN J. , AHONEN E. , NEVALAINEN T. , SIKANEN A. , HAKUMÄKI M.
Published: December 2008

This study evaluates the effect of acute intravenous volume loading on haemodynamics and aortic baroreceptor activity in order to determine the mechanistic factors responsible for divergent heart rate responses to volume loading. Eleven beagles were anaesthetized and instrumented for the recording of aortic pressure, diameter, flow and aortic baroreceptor activity. Isotonic saline, equal to 20% of the estimated blood volume, was infused intravenously within 60–90 s. The animals were divided into tachycardic and bradycardic groups according to their heart rate response to volume loading. In the group developing the tachycardic response, aortic baroreceptor activity increased. Total peripheral resistance was reduced by 31% and variables representing aortic stretch, mean aortic pressure, diameter and tension remained unchanged. In contrast, in the group developing the bradycardic response, aortic baroreceptor activity increased markedly. Also in this group peripheral resistance decreased, but only by 15%, which was significantly less than in the tachycardic group. Factors determining aortic stretch, mean aortic pressure, diameter and tension also increased significantly. Earlier studies show that regardless of the resulting heart rate response, atrial receptor activity increases during volume loading. Thus, we conclude that during cardiac acceleration, marked peripheral vasodilation eliminates the stimulation of baroreceptors and therefore the tachycardic response caused by atrial receptors develops. In the case of cardiac slowing, vasodilation also takes place, but is not sufficient to prevent activation of baroreceptors. In consequence, increased baroreceptor activity overrides the tachycardic drive coming from the atrial receptors and a typical baroreceptor reflex becomes manifested.
Effects of reduced oxygen tension on endothelium‐dependent relaxation induced by acetylcholine differ in rabbit femoral artery and jugular vein
Authors: VEDERNIKOV Y.P. , HELLSTRAND P.
Published: December 2008

In intact rabbit femoral artery rings pre‐contracted with phenylephrine, acetylcholine (ACh; 10‐8–10‐6 M) produces endothelium‐dependent relaxation, abolished after mechanical rubbing to remove the endothelium. The response to ACh was absent at low oxygen tension (≤ 4 kPa) or in the presence of sodium cyanide (I mM).Intact rabbit jugular veins relaxed to ACh in lower concentration than did the femoral artery, to 10‐10 10‐8 M; at sufficient ACh concentration the relaxation was complete. In veins with completely removed endothelium no relaxation to ACh occurred, and at concentrations above 3 X 10‐7 M the response was a contraction. The relaxation response to ACh of intact veins persisted during contraction at lower oxygen tension or in the presence of 1 mM sodium cyanide. In rubbed veins, cyanide consistently induced a transient contraction, which was absent in intact veins. The study demonstrates pronounced endothelium‐dependent relaxation to ACh in a venous preparation, with a markedly lower sensitivity of the relaxation response to hypoxia than in a muscular artery of the same species.
The veteran athlete: an echocardiographic comparison of veteran cyclists, former cyclists and non‐athletic subjects
Authors: VOLLMER‐LARSEN A. , VOLLMER‐LARSEN B. , KELBIEK H. , GODTFREDSEN J.
Published: December 2008

To determine the effects of prolonged endurance training on the heart, a comparison was made of veteran cyclists aged 41–51 years, former cyclists, and non‐athletic subjects, including echocardiography, ECG, systolic and diastolic time intervals, and maximal oxygen uptake. The veterans had significantly larger diastolic diameter, systolic diameter, thickness of septum, posterior wall, and left ventricular mass. The enlargement of the left ventricle was found to be proportionate, as the ratio of diastolic diameter to wall thickness showed no change. In contrast to earlier reports, no indication of reduced cardiac function was found in the veterans, as echocardiographically measured function parameters, systolic, and diastolic time intervals were similar in the three groups. In the former athletes, whose previous training experience was similar to that of the veterans, no significant variation in cardiac structure and function was found in relation to the control group. This indicates that the physiological hypertrophy caused by physical training can be reversible
Evidence for sympathetic regulation of the hydraulic conductance of rat jejunal mucosa in vivo
Authors: HEMLIN M. , SJÖVALL H.
Published: December 2008

The aim of the study was to test the hypothesis that sympathetic nerve stimulation inhibits jejunal fluid secretion by decreasing the hydraulic conductance (Lp)of the mucosa. Jejunal segments of anaesthetized rats were mounted in a specially constructed chamber which makes it possible to measure net fluid transport together with transmural potential difference or short circuit current in vivo. Lp was estimated by measuring the effects on net fluid transport rate elicited by stepwise changes in luminal pressure. Lp was measured in four groups of animals: (1) under control conditions; (2) after hexamethonium administration, to block intramural secretory neurons; (3) during efferent stimulation of the mesenteric nerves, to activate sympathetic neurons, and (4) during mesenteric nerve stimulation (MNS) after pre‐treatment with phentolamine, an a‐adrenergic antagonist, to block the sympathetic effector mechanism.

Lp measured at positive luminal pressures in control animals was approximately 4 μl min‐1 cmH2O‐1 100 cm‐2 serosal surface area. When measured at negative luminal pressures, this value increased approximately threefold. Hexamethonium did not significantly influence Lp. At positive luminal pressures, MNS decreased Lp to a value not significantly different from zero. This effect was abolished by phentolamine. At negative lumina] pressures, MNS decreased Lp by approximately 50% and this effect was partly antagonized by phentolamine. The results suggest that a decrease in mucosal hydraulic conductance may contribute to the antisecretory effect of sympathetic nerve stimulation in vivo.
In‐vitro stimulation of the rat epitrochlearis muscle. II. Effects of catecholamines and nutrients on protein degradation and amino acid metabolism
Authors: NIE Z. T. , LISJÖ S. , ÅSTRAND P.‐O. , HENRIKSSON J.
Published: December 2008

The influence of catecholamines and branched‐chain amino acids (BCAA) plus insulin on protein degradation and amino acid metabolism was investigated in isolated and electrically stimulated rat epitrochlearis muscles. 10‐7m adrenaline significantly increased the total amount of muscle tyrosine during 40 min of stimulation with 50 Hz (1 s min‐1) pulse trains. On the other hand, BCAA + insulin at normal and five times normal plasma concentrations had no effect on muscle tyrosine. Muscle 3‐methylhistidine was not influenced by any of the treatments. Muscle release and content of aspartate, alanine, glutamate and glutamine showed individual response characteristics to catecholamines and BCAA + insulin. The data indicate that adrenaline can induce an increased total protein degradation in rat fast muscle during acute contractions in vitro and, furthermore, that BCAA + insulin does not retard protein breakdown during acute muscle contraction.
Oxygen deficit is not affected by the rate of transition from rest to submaximal exercise
Authors: REN J. M. , BROBERG S. , SAHLIN K.
Published: December 2008

Five subjects cycled on an ergometer at power outputs corresponding to 20, 40, 60 and 80% of their maximal oxygen uptake (Vo2 max). On one occasion the transition from rest to work was direct (D), while on the other occasion the power output was increased slowly (S) in a stepwise manner for 6–15 min prior to exercise at the predetermined intensity. Oxygen uptake (Vo2) was measured, and O2 deficit and O2 debt were calculated. Oxygen deficit increased with the exercise intensities, the peak values being 2.1 ± 0.2 and 1.9 ± 0.1 litres (mean ± SEM) at 80% of Vo2 max after D and S respectively. No significant difference was observed in O2 deficit or O2 debt between D and S at any exercise intensity (P < 0.05). The O2 debt was similar to the O2 deficit at 20, 40 and 60% of Vo2 max but lower than the O2 deficit (P < 0.05) at 80% of Vo2 max. Femoral venous blood lactate remained unchanged at 20% of Vo2 max but increased at the higher exercise intensities, reaching peak values of 7.6 ± 0.6 and 7.4 ± 1.1 mmol 1‐1 at 80% of Vo2 max after D and S respectively. Blood lactate was not significantly different between D and S at any exercise intensity (P > 0.05). It is concluded that O2 deficit, O2 debt and blood lactate are not affected by the rate of transition from rest to submaximal exercise. The data contradict the hypothesis that O2 deficit is caused by an inadequate O2 transport at the onset of exercise.
Action potentials of cultured human oat cells: whole‐cell measurements with the patch‐clamp technique
Authors: JOHANSSON S. , RYDQVIST B. , SWERUP C. , HEILBRONN E. , ÅRHEM P.
Published: December 2008

Oat cells (of the small cell carcinoma of the lung) have been reported to generate calcium action potentials. The calcium channels have further been suggested to play a crucial role in the relation between oat cell carcinoma and the often associated myasthenic syndrome. We have examined cultured human oat cells (U‐1690) under voltage‐clamp conditions, using the patch‐clamp technique. We found, contrary to previous reports, that the action potential was caused by sodium and potassium currents. No calcium current was detected under these conditions, which indicates that calcium channels, if present, are very rare. The findings restrict, but do not rule out, the hypothesis that calcium plays a key role in the carcinoma/myasthenic syndrome relation.
Total calorimetry and temperature regulation in the nine‐banded armadillo
Authors: MERCER J. B. , HAMMEL H. T.
Published: December 2008

Cold exposure in the nine‐banded armadillo causes vigorous shivering and a rise in core temperature (Te). The increase in metabolic rate and Te depends upon exposure temperature, but may be as much as six times and 3 °C respectively (Johansen 1961). These findings might indicate an insensitivity to Te, which is puzzling since internal temperature is thought to be the primary and regulated variable. It is suggested that positive feedback may play a role in temperature regulation in these animals. To investigate this problem two series of experiments were performed in the same species.

Series 1. Measurements of changes in heat loss (direct calorimetry) and heat production (indirect calorimetry) following transferral from a thermoneutral to a cold environment. The difference between these measurements determines whether heat storage is positive due to the increased core temperature or negative due to reduction in the size of the core with the increased temperature.

Series 2. Investigation of core thermosensitivity (body core cooling using colonic thermode) under different environmental conditions.

The results of the first series showed that the rise in Te was accompanied by positive heat storage in the body. The second series demonstrated core thermosensitivities similar to those previously reported for a variety of other homeothermic mammals.
Application of a new technique‐blood pressure clamping‐for analysis of prostaglandin interference with sympathetic neurotransmission in man
Authors: WENNMALM Å.
Published: December 2008

To circumvent baroreceptor reflexes following drug‐induced interference with sympathetic neurotransmission, a new technique ‐ blood pressure clamping ‐ has been developed. This implies that the sympathetic activity in an awake human is ‘clamped’ at a supranormal level by infusion of a vasodilator. In 11 healthy volunteers nitroprusside or saline was randomly infused in two consecutive 2‐h periods. Plasma and urinary catecholamine levels were analysed by liquid chromatography. The experiments were repeated after random administration of the prostaglandin synthesis inhibitor, ibuprofen, or placebo. In the basal state (no ibuprofen, saline infusion) the mean arterial blood pressure was 81.4 ± 2.3 mmHg, the heart rate was 60.9 ± 0.3 beats min‐1and the plasma level of noradrenaline was 1.12 ± 0.15nM. Infusion of nitroprusside at a dose lowering the mean blood pressure by 11.6 ± 1.6 mmHg and increasing the heart rate to 74.6 + 2.9 beats min‐1elevated plasma noradrenaline to 2.86 ± 0.39 nM. After pre‐treatment with ibuprofen (saline infusion), the systemic blood pressure, the heart rate, and the plasma and urinary levels of noradrenaline were unaffected in comparison to before drug (80.1±2.3 mmHg, 58.4 ± 0.3 beats min‐1and 1.13±0.12nM respectively). Infusion of nitroprusside at a rate lowering the blood pressure by 11.2 ± 2.4 mmHg and increasing the heart rate to 74.4 ± 0.5 beats min‐1, elevated the plasma level of noradrenaline to 2.46 ± 0.38 ng ml‐1, which is not different from before ibuprofen. The amount of nitroprusside required to lower the blood pressure was not different in the presence and absence of ibuprofen. These data indicate that ibuprofen does not affect sympathetic neurotransmission during a moderate increase in adrenergic activity and, hence, that locally formed prostaglandins do not modulate such transmission under these conditions.
Effects of nerve compression or ischaemia on conduction properties of myelinated and nonmyelinated nerve fibres. An experimental study in the rabbit common peroneal nerve
Authors: DAHLIN L. B. , SHYU B. C. , DANIELSEN N. , ANDERSSON S. A.
Published: December 2008

Compound action potentials of both myelinated (A) and non‐myelinated (C) fibres in the common peroneal nerve of rabbits were studied during and after acute, graded compression of the nerve at 200 or 400 mmHg applied for 2 h or during ischaemia created by nitrogen inhalation or aortic occlusion. Compression of the nerve at 200 mmHg blocked the Ai component (large myelinated fibres) after about 23 min, while compression at 400 mmHg shortened this time to 11 min. The A2 component (thinner myelinated fibres) had a lower conduction velocity and a higher resistance to compression. There was just a slight decrease in conduction velocity of the nonmyelinated fibres when the nerves were compressed at 200 mmHg for 2 h. However, compression at 400 mmHg for 2 h induced a marked deterioration of amplitude and conduction velocity of the C‐fibres. There was an incomplete restitution of function of A‐ and C‐fibres during 2 h of recovery. The thinner myelinated fibres were more susceptible to deprivation of oxygen than the thicker ones, while non‐myelinated fibres differed in response according to method of ischaemia induction. It is concluded that non‐myelinated fibres are very resistant to compression and a very high pressure (> 400 mmHg) is needed to affect these fibres.
Ca2+ oscillations in pancreatic β‐cells exposed to leucine and arginine
Authors: GRAPENGIESSER E. , GYLFE E. , HELLMAN B.
Published: December 2008

Dual‐wavelength microfluorometry with the fura‐2 indicator was employed for continuous recordings of cytoplasmic Ca2+ (Ca2+) in individual pancreatic β‐cells isolated from ob/ob‐mice. When added to a medium containing 3 mmol l‐1 glucose, both 10 mmol r1 leucine and 20 mmol l“1 arginine induced rises in Cai2+ with periodic fluctuations. In the case of leucine, this increase was preceded by initial lowering followed by high‐amplitude oscillations with a periodicity of 2–0 min. In a glucose‐free medium arginine had no effect, and leucine was unable to induce more than a single peak of Cai2+ increase. When present at a concentration of 1 mmol l‐1, leucine sometimes induced a couple of high‐amplitude oscillations at 3 mmol l‐1 glucose but lowered Cai2+ permanently in a glucose‐free medium. It is likely that the high‐amplitude oscillations of Cai2+ are related to the electrical activity of the β‐cells. Provided that some glucose was present, leucine initiated a similar type of Cai2+ response as obtained during glucose‐induced insulin release. The observed leucine effect is therefore compatible with a role of glycolysis in generating high‐amplitude Cai2+ oscillations and pulsatile insulin release.
Orienting reactions to light tactile stimuli after single and repeated partial spinal cord lesions in the cat
Authors: DANIELSSON I. , NORRSELL U.
Published: December 2008

Cats which had been trained to remain quietly standing were tested for orienting responses to light tactile stimulation (ORLT) of either hindlimb before and after different single, and subsequently increased, low thoracic spinal cord lesions. The individual lesions covered one dorsal column, and/or the dorsal part of one lateral funiculus, and/or the ventral part of the lateral funiculus, and/or one entire lateral funiculus and/or one or both ventral quadrants.

Normal ORLTs were produced from the first post‐operative test after each of the above lesions alone, or in combination with one of the others. Acute and chronic disappearances and/or disturbances of the ORLTs were observed for one hindlimb only after lesions involving at least the dorsal column and the dorsal part of the lateral funiculus of the ipsilateral side, as well as the contralateral lateral funiculus. The amount of disturbance varied with the technique in such a way that the number of operations which had been carried out to cause the actual lesion was inversely correlated to the degree of post‐operative defect.

The findings showed that the severity of the tactile symptoms after spinal cord lesions may depend on the speed with which they had developed. The types of lesions causing defects indicated that cats, under normal conditions, may utilize one of the three ascending spinal pathways for orienting reactions to light tactile stimulation. In relation to the peripheral receptive fields, these pathways are the ipsilateral dorsal column and spinocervical pathways, and a pathway of the contralateral lateral funiculus. The possible spinothalamic character of the crossed pathway has yet to be established.
The effects of tonicity on tension and stiffness of tetanized skeletal muscle fibres of the frog
Authors: MÅNSSON A.
Published: December 2008

Tension and stiffness of tetanically activated skeletal muscle fibres of the frog were studied at varied tonicity of the extracellular medium (1.7–3.2 °C; sarcomere length, 2.13–2.22 μm). The stiffness was measured from the change in peak tension in response to fast (0.2 ms) stretches and releases of small amplitude (0.11–0.15% of the fibre length). The bathing solution was made hypotonic by reduction of NaCl and hypertonic by addition of sucrose. The osmotic strength of the solutions tested varied from 81 to 168% of the isotonic value. Maximum tetanic tension decreased markedly with increased tonicity. The active stiffness, on the other hand, increased as the tonicity was raised, and the tension/stiffness ratio (the total extension of the undamped fibre elasticity) was thus greatly reduced under these conditions. Evidence is presented to show that the change in the tension/stiffness ratio is due neither to the development of rigor cross‐bridges nor to the recruitment of passive parallel‐elastic elements in response to increased tonicity. Neither are viscous‐like components important for explaining the effect. A change in the tension/stiffness ratio, similar to that seen in response to increased tonicity, did not occur as fibre width was reduced by increasing the sarcomere length. This suggests that the changes in the fibre volume affect this ratio mainly by mechanisms that are unrelated to changes in lateral spacing between the myofilaments.
Adrenaline‐mediated glycogenolysis in different skeletal muscle fibre types in the anaesthetized rat
Authors: JENSEN J. , DAHL H. A. , OPSTAD P. K.
Published: December 2008

The effect of adrenaline infusion on glycogen breakdown in different muscle fibres types in resting extensor digitorum longus (EDL) and soleus was investigated with histochemical methods. During adrenaline infusion the glycogen content in type IIB and type HA fibres in EDL, as measured in PAS‐stained sections, decreased 24.5 % and 11.5% respectively. The glycogen content in type I fibres in EDL and in type I, type IIA and T‐fibres in soleus did not change during adrenaline infusion. The present study shows that adrenaline infusion has different effects on glycogen breakdown in the different fibre types in EDL and a different effect on type IIA fibres in EDL and soleus. So far, the reason for these differences is unknown.
Increased duodenal HCO3 output after blood volume expansion in the rat: an effect mediated by atrial natriuretic peptide (ANP)?
Authors: JÖNSON C. , FÄNDRIKS L. , PETTERSSON A.
Published: December 2008

Duodenal HCO3‐ secretion was measured by in‐situ titration in chloralose‐anaesthetized rats. The effects of hypervolaemia, induced by i.v. injections of an albumin infusion, on duodenal HCO3‐ secretion were investigated. A 10% increase in blood volume increased duodenal HCO3‐ secretion by about 50%, and this effect was unaffected by splanchnicotomy. If the splanchnicotomy was combined with cervical vagotomy, the basal HCO3‐ secretion was lower but the increase in secretion after 10% blood volume expansion with albumin was still 50%. If the same increase in blood volume was produced in splanchnicotomized and vagotomized rats in which the right atrial appendix had been removed, a procedure that markedly reduces the ANP (atrial natriuretic peptide)‐producing cells, no increase in secretion could be observed. Intravenous injections of α‐r‐ANP (10 μg kg‐1 and 30 μg kg‐1) increased duodenal HCO3‐ secretion in a dose‐dependent fashion. Based on the present findings, we suggest that hypervolaemia increases duodenal HCO3‐ secretion via release of ANP from the heart.
ATP as a sympathetic co‐transmitter in rat vasomotor nerves‐further evidence that individual release sites respond to nerve impulses by intermittent release of single quanta
Authors: ÅRSTRAND P. , STJÄURNE L.
Published: December 2008

A combination of intra‐ and extracellular recording was used to study neurotransmitter release in sympathetic vasomotor fibres in rat femoral and mesenteric arteries. The results show that neurotransmission in these preparations is similar to that in the ‘short’ sympathetic nerves in guinea‐pig vas deferens and the ‘long’ sympathetic nerves in rat tail artery in the following respects:

 The intracellularly recorded excitatory junction potentials (EJPs) and the extracellularly recorded junction currents (EJCs) presumably are caused by ATP secreted as a sympathetic co‐transmitter.

 The stimulus‐evoked and spontaneous EJCs share the same brief time‐course, which is similar to that of spontaneous EJPs, but much briefer than that of stimulus‐evoked EJPs.

 ‘Successful’ nerve impulses appear to release single transmitter quanta.

 The probability of activation of individual release sites is low (0.002–0.02).

 The low release probability cannot be accounted for by failure of the nerve impulse to invade the terminals.

Moreover, it is also shown that application of tetrodotoxin to the medium within the recording electrode effectively abolishes transmitter secretion in the area enclosed by the tip of the electrode, indicating that the effective length constant for a passively propagating nerve action potential is probably very small and that activation of the release mechanisms in ‘long’ sympathetic nerve fibres seems to require that the varicosities are actively invaded.
Shortening velocity, myosin light chain phosphorylation and Ca2+ dependence of force during metabolic inhibition in smooth muscle of rat portal vein
Authors: EKMEHAG B. L. , HELLSTRAND P.
Published: December 2008

The concentration‐response relation for Ca2+ (0.2–5.0 DIM) of high‐K+ contractures (40 mM) in the rat portal vein during respiratory inhibition by 0.2 mM cyanide was investigated. A reduction of force in the presence of cyanide to about 30% of control was associated with a leftward shift of the normalized concentration‐response relation. When force at the plateau of high‐K+ contractures (at about 2 min) was reduced to 65 ± 2% due to the addition of cyanide, the maximal shortening velocity (Vmax) was 94 ± 5% of control (n = 6). In electrically (AC) stimulated preparations giving short tetanic contractions, a reduction of active force to 58 ± 2 % of control in the presence of cyanide was associated with a reduction of Vmax to 83 ± 5 % (n= 7). Phosphorylation of the 20‐kDa regulatory light chains (LC20) of the myosin molecule was studied in the relaxed state and at the plateau of high‐K+ contractures for comparison with the mechanical data. Both control and cyanide‐treated preparations showed 9% LC20 phosphorylation in nominally Ca2+‐free solution (n= 6). After activation the level of phosphorylation increased to 30 ± 3% (n= 9) in the control veins. In cyanide‐treated veins, where force was reduced to 42 ± 6% compared to a preceding control period, the phosphorylation level was 17 ± 2% (n = 7). The study suggests that the mechanical changes caused by inhibition of cellular respiration may involve the combined effect of several metabolic alterations, including decreased LC20 phosphorylation during contraction, but apparently not decreased intracellular Ca2+ concentration or sensitivity of the contractile system to Ca2+.