bluuebunny/crossref_metadata_2025 huggingface dataset:
Electric muscle stimulation in the hind leg of the spontaneously hypertensive rat induces a long‐lasting fall in blood pressure
Authors: HOFFMANN P. , THORÉN P.
Published: December 2008

The influence of prolonged low‐frequency, low‐intensity electric stimulation of the gastrocnemius muscle or of the biceps femoris muscle on blood pressure and heart rate was investigated in unanaesthetized, spontaneously hypertensive rats (SHR). In both groups, elevations of blood pressure and heart rate were elicited during the 60 min of muscle stimulation. After cessation of the stimulation, a depressor response developed within 60 min. Thirty to sixty minutes post‐stimulation the fall in blood pressure was 19 ± 3 and 17 ± 4 mmHg, respectively (mean ± SE) compared with controls. In both groups, the depressor response lasted for over 5 h. In addition, the gastrocnemius‐stimulated animals also developed a post‐stimulatory bradycardia. In one group of SHR the sciatic nerve was anaesthetized with bupivacaine. The arousal response during stimulation was similar to that in the other groups, but after termination of stimulation blood pressure returned to the control level without any further drop.

To investigate further the neurotransmitters involved, one group of gastrocnemius‐stimulated SHR was given naloxone by infusion during the stimulation. A modest post‐stimulatory blood pressure fall also occurred in this group, but it lasted only 90 min. Another SHR group was pre‐treated with parachlorophenylalanine, a serotonin synthesis blocker, which completely abolished the post‐stimulatory depressor response. These results indicate that prolonged muscle stimulation gives rise to a post‐stimulatory long‐lasting drop in blood pressure and that this response is mediated by somatic nerve afferents. Involvement of the endorphin and serotonin systems is also suggested.
Arterial blood pressure at the onset of dynamic exercise in partially curarized man
Authors: SECHER N. H. , KJÆR M. , GALBO H.
Published: December 2008

In six young men, heart rate and arterial mean blood pressure responses to the onset of light dynamic exercise 99 W (range 59–138) on a stationary bicycle were followed during partial neuromuscular blockade with tubocurarine. Tubocurarine was used in order to accentuate the central nervous (central command) influence on the cardiovascular variables and reduced hand‐grip strength to 42% (36–47) of control. At the onset of exercise heart rate increased immediately and similarly with and without neuromuscular blockade. Mean arterial blood pressure remained constant during the first 6 s of control exercise and then increased. With tubocurarine a decrease of 9 mmHg (3–12) was seen during the first 6 s (P < 0.01) before blood pressure increased. The similar heart rate responses seen with and without neuromuscular blockade indicate that central command has little influence on this variable at the onset of dynamic exercise. The constant blood pressure at the onset of control exercise suggests that the immediate changes in cardiac output and peripheral vascular resistance, respectively, are accurately matched. The decrease in blood pressure at the onset of exercise with tubocurarine suggests that central command stimulates vasodilatating nerves to arterioles in the working muscles.
Low‐affinity uptake of [3H]choline by rat neurointermediate lobein vitro
Authors: VON SPRECKELSEN S. , MØLLER M. , TREIMAN M.
Published: December 2008

Uptake of [3H]choline by rat neurointermediate lobesin vitrowas investigated. The rate of uptake showed saturation with concentration of [3H]choline above 120 μM. Lowering of the incubation temperature from 32 to 4 ±C, or increasing the concentration of K+in the incubation medium from 5 to 100 mM, diminished the rate of uptake by 83.8% (SEM6.9%,n= 3) or 43.1 % (SEM 13.5%,n= 3), respectively. Following preloading with [3H]choline, a slow efflux (1 % of the content every 20 min) of [3H]radioactivity was observed from the perifused glands. This efflux was enhanced 10‐fold by increasing the concentration of K+in the perifusion medium to 100 mM. Neither the uptake of [3H]choline, nor the subsequent basal or potassium‐enhanced efflux of [3H]radioactivity were affected by reducing the concentration of Na+from 125 to 19 mM, or by including 10 μM hemicholinium‐3 in the medium during preincubation and perifusion. Replacing Ca2+by 0.5 mM EGTA during perifusion resulted in a minor decrease (28%, SEM 7‐3%>n= 7) in the potassium‐enhanced [3H]radioactivity efflux. This decrease occurred only in one of the two high‐potassium periods during the perifusion. In conclusion, uptake of [3H]choline by rat neurointermediate lobes was due to a low‐affinity, saturable mechanism, with the efflux of [3H]radioactivity most likely representing the depolarization‐facilitated outflow of [3H]choline. Autoradiography of the tissue sections showed this uptake to be localized to both neuronal and glial elements of the neural lobe, in contrast to sparse labelling of pars intermedia.
Decreased passage of the nonapeptide dDAVP over the intestinal epithelium during development in the young rat
Authors: FOLKESSON H. G. , WESTROM B. R. , LUNDIN S. , KARLSSON B. W.
Published: December 2008

The nonapeptide i‐deamino‐cysteine‐8‐D‐arginine vasopressin (dDAVP) was gavage‐fed together with cow's milk whey protein to young, developing rats. The transepithelial passage of dDAVP in the gastrointestinal (GI) tract was assessed by a specific RIA as immunoreactive levels in blood serum extracts and as urinary excretion of dDAVP 0.5–8 h after feeding. In 14‐day‐old rats the passage of dDAVP was higher than in 30‐day‐old rats, since the 14‐day‐old rats had significantly higher serum levels (5–10 times) 0.5‐2 h after feeding and a urinary excretion approaching 0.15% of the administered amount after 8 h. In the 30‐day‐old rats urinary excretion increased up to 0.05 % after 2 h and then levelled off. It was also clear that 30‐day‐old rats had a slower transfer to and faster elimination from serum than 14‐day‐old rats. dDAVP appeared to be passed over the GI tract mucosa independently of intestinal proteolysis since feeding it to 30‐day‐old rats together with the proteinase inhibitors, soya‐bean trypsin inhibitor and pepstatin did not influence the serum or urinary levels. Thus, dDAVP was taken up from the GI tract into the blood circulation and excreted in the urine of young rats. The decrease in the passage of dDAVP found around weaning appears to be related to developmental processes affecting the permeability of the intestinal epithelium rather than intestinal proteolysis.
Anabolic steroids alter the haemodynamic effects of endurance training and deconditioning in rats
Authors: KARHUNEN M. K. , RÄMÖ M. P. , KETTUNEN R.
Published: December 2008

The haemodynamic effects of endurance training with or without anabolic steroid treatment (nandrolone decanoate, 5.0 mg kg‐1 week‐1) were studied before and after a six‐week sedentary period in anaesthetized, open‐chest rats during isoproterenol and CaCl2 loads. In comparison to the control group (CG I, n= 13) endurance training (TG I, n= 10) increased the resting stroke index significantly, end‐diastolic pressure and during CaCl2 infusion the end‐diastolic and end‐systolic volumes. Peripheral resistance decreased in TG I during both inotropic loads but increased in CG I (P < 0.01 between the groups). After combined endurance training and anabolic steroid treatment (TSG I, n= 16) the haemodynamic state was similar to that in CG I except peripheral resistance which was even higher than in CG I. The heart weight to body weight ratio was significantly greater both in TG I and TSG I than in CG I. After a six‐week deconditioning period the haemodynamic values were essentially similar in endurance trained (TG II, n= 10) and in control rats (CG II, n= 12). After the sedentary period, in the simultaneously trained and anabolic steroid‐treated group (TSG II, n= 13) stroke index and end‐diastolic volume decreased more during isoproterenol load when compared with TG II or CG II (P < 0.05 between the groups). Peripheral resistance was higher in the TSG II than in the two other groups. In conclusion, the enhanced pumping performance of the heart by increased left ventricular diastolic filling after endurance training is attenuated by simultaneous anabolic steroid treatment which further increases the peripheral resistance. Detraining reversed the main training effects in six weeks and simultaneous anabolic steroid treatment led to a decreased left ventricular filling and to elevated peripheral resistance after the sedentary period.
Myocardial oxygen consumption during atrial pacing at various inotropic levels
Authors: ANDERSEN F. R. , ILEBEKK A. , KIIL F.
Published: December 2008

In anaesthetized open‐chest pigs (n= 15) we examined whether myocardial oxygen consumption (M Vo2) per min increased in proportion to heart rate during right atrial pacing at control, high and low inotropy. By modulating aortic constriction and the circulating blood volume, left ventricular (LV) systolic blood pressure, stroke volume and LV dimensions were kept constant. Examinations at control inotropy (n= 7) showed a linear relationship between increments in MVo2 beat‐1 and LV dP/dt when heart rate was increased in four steps, each of 10 beats min‐1 from 130 ± 3 beats min‐1 (r = 0.76 ± 0.08). In a second series (n= 8) heart rate was increased by 36–37 beats min‐1 in control experiments, during intracoronary isoproterenol infusion (high inotropy) and after propranolol administration (low inotropy). The increments in MVo2 min‐1 during pacing tachycardia were not significantly different at control, high or low inotropy. At high inotropy MVo2 beat‐1 and LVdP/dt did not rise significantly during pacing tachycardia. Myocardial oxygen consumption beat‐1 increased more at control (6.3 ± 2.0%) than at high inotropy (diflf: P < 0.02). At low inotropy MVo2 beat‐1 increased even more (17.4 ± 2.8%) than at control inotropy (diff: P < 0.05). Thus, the increase in MVo2 beat‐1 during pacing tachycardia is related to the increase in LVdP/ dt and is dependent on the level of inotropy; great increments during tachycardia after propranolol administration and no changes during intracoronary isoproterenol infusion.
Transmural distribution of biochemical markers of total protein and collagen synthesis, myocardial contraction speed and capillary density in the rat left ventricle in angiotensin ll‐induced hypertension
Authors: LEIPÄLÄ J. A. , TAKALA T. E. S. , RUSKOAHO H. , MYLLYLÄ R. , KAINULAINEN H. , HASSINEN I. E. , ANTTINEN H. , VIHKO V.
Published: December 2008

The effect of angiotensin II‐induced hypertension on selected biochemical parameters was studied in Sprague‐Dawley rats. Angiotensin II infusion at rates of 41.7 μg h‐1 kg‐1 and 12.5 μg h‐1 kg‐1 for 2, 5, 10 and 15 days elevated the systolic blood pressure from 143 ± 7 mmHg to 215–230 mmHg (P < 0.001) and 185–195 mmHg (P < 0.001), respectively. The left ventricular weight/body weight ratio increased 10–14% (P < 0.05) and 23–32% (P < 0.001) after 2–15 days in rats treated at the lower and higher infusion rates, respectively. Prolyl 4‐hydroxylase (PH) activity, a marker of collagen synthesis, was evenly distributed in the left ventricle. PH activity increased by about 100% in both subendocardial and subepicardial layers of the left ventricular wall after angiotensin II infusion for 10 days at 41.7 γ h‐1 kg‐1, but remained unaltered at 12.5 μg h‐1 kg‐1. No change was observed in hydroxyproline concentration. Myosin isoenzymes (V1‐V3), which reflect myocardial contractility, were unevenly distributed in the left ventricular wall: the proportion of the fast‐turnover isoenzyme (V1) was smaller in the subendocardial layer than in the subepicardial layer. The proportion of Vl decreased after treatment in both layers. Alkaline phosphatase activity, a marker of capillary density, was evenly distributed transmurally in the left ventricular wall. Angiotensin II caused a slight decrease in this activity in both myocardial layers. The results suggest that the elevation of blood pressure leads to transmurally evenly distributed changes in biochemical parameters reflecting collagen synthesis, capillary density and contractile properties of the myocardium.
Muscle capillary permeability for [14C]inulin and [51Cr]EDTA in human forearm
Authors: KEIDING S. , HENRIKSEN O. , SEJRSEN P.
Published: December 2008

Capillary permeability of [14C]inulin and [51Cr]EDTA was examined in human forearm in five healthy, subjects by indicator diffusion technique. Injections of, initially [125I]albumin and [14C]inulin, and after 30 min resting, of [125I]albumin and [51Cr]EDTA, were given in a brachial artery. During light exercise of the forearm, blood was sampled in 2‐s periods from a deep cubital vein primarily draining muscles. The plasma flow rate, calculated as the dose of [125I]albumin in the injectate divided by the area under the curve for the venous concentration of 125I, was, on average, 8.5 ml min‐1 100 g‐1 forearm. Assuming [125I]albumin is a partially permeable tracer, a correction for extraction of albumin was performed. This gave extraction fractions of 0.107 ± 0.015 (mean ± SEM) for [14C]inulin and 0.377 ± 0.033 for [51Cr]EDTA, respectively. The capillary permeability surface area product per 100 g tissue (CDC) was for [14C]inulin 0.90 ± 0.19, and for [51Cr]EDTA 3.31 ± 0.38 ml min‐1 100 g‐1 forearm. The average of the ratios of the CDC values of [51Cr]EDTA to those of [14C]inulin, 4.0 ± 0.5, is significantly higher than the corresponding ratio between the measured free diffusion coefficients in water at 37 ±C, 3.07 ± 0.002 (N= 36 and 17, respectively). This indicates that there is some degree of restriction for [14C]inulin (MW 5200) relative to [51Cr]EDTA (MW 340.2) and it points to an ‘equivalent pore radius estimate’ of about 160 Å in human muscle capillaries.
Lumbar back muscle activity during locomotion: effects of voluntary modifications of normal trunk movements
Authors: CARLSON H. , THORSTENSSON A. , NILSSON J.
Published: December 2008

The mechanisms of adaptation of the trunk to changed mechanical conditions were studied during locomotion in man. The myoelectrical (EMG) activity in lumbar back muscles and the movements of the trunk were recorded in nine healthy subjects during walking and running on a motor‐driven treadmill. Two different types of voluntary modifications of the movement pattern were used: (1) The trunk was kept in an extreme forward or backward tilted position. In both these situations the basic EMG pattern with two periods of activity per stride cycle was maintained during walking, whereas a major shift relative to the stride cycle (25 % of the stride cycle duration) occurred in running with the trunk tilted backwards. The synchrony of the back muscle activation at both sides increased when locomotion was performed with the trunk tilted forwards. The relative duration of the EMG bursts was similar to normal locomotion and corresponded to 15–26% of the stride cycle duration in walking and 23–37% in running. (2) In the other type of modification the subjects were instructed to exaggerate the angular trunk movements either in the sagittal or in the frontal plane. The basic EMG pattern and phase relationships remained in most cases unchanged. One exception was running with exaggerated lateral movements, in which only one period of back muscle activity per stride cycle was observed. The relative duration of the bursts was longer in trials with exaggerated trunk movements as compared to normal locomotion. In walking and running with the trunk tilted forwards or backwards the lumbar back muscles were not always involved as prime movers of the trunk. This was in contrast to the more dynamic situations, in which the back muscle activity appeared to be directly involved in braking and reversing the exaggerated trunk movements.
Separate resistive loading of the respiratory phases during mild hypercapnia in man
Authors: BARNETT T. B. , RASMUSSEN B.
Published: December 2008

Eleven human subjects were studied during steady state, controlled mild hypercapnia with resistive loading of either inspiration (R1) or expiration (RE). Minute ventilation and frequency were significantly reduced by R1 (P ‐ < 0.01) and even more so by RE (P= < 0.001). Tidal volume was unchanged. Both R1 and RE reduced mean flow in the loaded phase ‐ an effect relatively greater with RE. Neither Rt nor RE altered mean flow in the unloaded phase. Although mean inspiratory flow was unchanged with RE, mouth occlusion pressure (P0.1) was increased (P= < 0.01). Functional residual capacity (seven subjects) was increased with RE, but not with R1 (P= < 0.05). Five additional subjects were similarly studied with and without RE in whom transdiaphragmatic pressure (PDI) and peak diaphragmatic EMG (EMGDI) were examined. Changes in ventilation, breathing pattern and P0.1 were similar to those described above. Neither PDI nor EMGDI were significantly altered by RE, but with RE, diaphragmatic EMG activity began 50–190 ms before inspiratory flow. In conclusion, ventilation is reduced more by RE than by R1 due to greater respiratory phase time. Moderately heavy RE does not augment inspiratory drive as reflected by mean flow, PDI or EMGDI. With RE and increased FRC, P0.1 does not accurately reflect inspiratory drive because of dissociation between EMG and flow.
Effects of some calcium antagonists on aggregation by adrenalin and serotonin and on α‐adrenoceptor radioligand binding in human platelets
Authors: VINGE E. , ANDERSSON T. L. G. , LARSSON B.
Published: December 2008

The inhibitory effects of verapamil, nifedipine and diltiazem, representatives of different classes of calcium antagonists, were studied on aggregation of human platelets induced by adrenalin and serotonin (5‐HT). For references, the α‐adrenoceptor‐antagonists phentolamine (α1 and α2) and rauwolscine (α2), and the s‐HT2‐receptor‐antagonist ketanserin were included. Verapamil in the concentration range 10‐6‐ 10‐4 M inhibited both adrenalin‐ and serotonin‐induced aggregation in a concentration‐dependent manner, whereas nifedipine and diltiazem had little or no effect. Phentolamine and rauwolscine were clearly weaker than verapamil as antagonists of serotonin, and ketanserin lacked effect on adrenalin‐induced aggregation. Binding studies with [3H]dihydro‐α‐ergocryptine and [3H]rauwolscine on human platelet membranes showed equal numbers of binding sites, suggesting that only α2‐adrenoceptors were present. In the same concentration range as inhibition of aggregation was obtained, verapamil inhibited binding of either radioligand. Nifedipine, diltiazem and 5‐HT were all poor inhibitors of radioligand binding. The results suggest that verapamil at high concentrations not only has α‐adrenoceptor antagonistic properties but also exerts 5‐HT‐receptor blocking effects. This was not found with the other calcium channel blockers examined (nifedipine, diltiazem).
Increase in proximal tubular fluid reabsorption by renal nerve stimulation. A split oil droplet study
Authors: GÖRANSSON A. , ULFENDAHL H. R.
Published: December 2008

The influence of renal sympathetic nerve stimulation on fluid reabsorption in the proximal tubules was studied in anaesthetized male Sprague‐Dawley rats. Direct stimulation with a frequency of 2 Hz was applied, and a modification of the split oil droplet technique was used. The fluid reabsorption was determined as the half‐time (t1/2) of the shrinking droplet. In the control situation t1/2 was 30.7 ± 3.4 s. On stimulation at 2 Hz, t1/2 decreased in all nine rats studied by an average of 25 ± 5%, to 22.4 ± 2.6 s (P < 0.01). The decrease in t1/2 indicates an increased rate of proximal tubular fluid reabsorption. The results support the concept that the anatomically established adrenergic innervation of renal proximal tubules participates in the direct regulation of tubular fluid reabsorption, a role which might be important in the control of the extracellular volume.
Contractile and metabolic characteristics of creatine‐depleted vascular smooth muscle of the rat portal vein
Authors: EKMEHAG B. L. , HELLSTRAND P.
Published: December 2008

The functional consequences of phosphocreatine (PCr) depletion for mechanical properties, O2 consumption, and lactate production of the rat portal vein were investigated. After feeding rats for 8–9 weeks on a diet containing 2%β‐guanidino propionic acid (BGPA), PCr of the portal vein was reduced to 14% of control, whereas ATP was unchanged. No significant change was found in the level of spontaneous contractile activity or the force developed in a high‐K+ contracture. Lactate production and the relationship between contractile force and O2 consumption were uninfluenced by BGPA treatment. The force‐velocity relation of electrically stimulated portal veins showed no influence of BGPA treatment on Vmax. To investigate whether decrease in PCr influenced the response to metabolic stress, portal veins were exposed to graded concentrations (0.1‐0.5 mM) of cyanide to depress cellular respiration. Veins from control and BGPA‐treated rats showed the same relative decrease of contractile activity and O2 consumption, and the same increase in lactate production. Cyanide treatment resulting in a reduction of electrically stimulated force to 70–80% of the original gave a reduction of Vmax to 85–90%. The relative degree of reduction was uninfluenced by BGPA treatment. Reduction of PCr content thus does not affect the functional properties of metabolism or contractility under normoxic conditions. Furthermore, it can be inferred that the PCr reduction known to occur in smooth muscle exposed to hypoxia (Lövgren & Hellstrand 1985) is not in itself the major factor causing hypoxic inhibition of mechanical activity.
Afferent electrical stimulation of mesenteric nerves inhibits duodenal HCO3 secretion via a spinal reflex activation of the splanchnic nerves in the rat
Authors: JÖNSON C. , FÄNDRIKS L.
Published: December 2008

The experiments were performed on male Sprague‐Dawley rats anaesthetized with chloralose. Duodenal HGO‐ 3 secretion was measured in situ by pH‐stat titration. The nerves bundles surrounding two randomly chosen mesenteric vessels were electrically stimulated (3 Hz, supramaximal intensity) in the afferent direction. This was done in order to mimic the intestino‐intestinal spinal reflex activation of the splanchnic sympathetic fibres. The procedure reduced duodenal HCO‐ 3 secretion by 20% together with an increase in mean arterial pressure and heart rate. Duodenal HGO‐ 3 secretion decreased similarly in control rats and in those subjected to a cervical cord transection, whereas animals with bilaterally cut splanchnic nerves did not respond to such mesenteric nerve stimulation. Pharmacological pretreatment with guanethidine or yohimbine, but not prazosin, inhibited the reduction in duodenal HCO‐ 3 secretion. Thus the data suggest that electrical stimulation of mesenteric afferent nerves inhibits duodenal HCO‐ 3 secretion via a spinal reflex activation of splanchnic sympathetic nerve fibres to the duodenum, and that the response is mediated via alpha2 adrenoceptors.
Involvement of opioid and nicotinic receptors in rectal and anal reflex inhibition of urinary bladder motility in cats
Authors: HELLSTRÖM P. M. , SJÖQVIST A.
Published: December 2008

The present study was performed to investigate mechanisms involved in urinary bladder relaxation during reflex activation of the pelvic nerves in the cat. Electrical stimulation of the pelvic nerves produced a contraction of the urinary bladder (P < 0.05) and colon (P < 0.05). Reflex activation of the pelvic nerves by rectal distension or mechanical stimulation of the anus induced relaxation of the bladder (P < 0.05), while a colonic contraction was elicited (P < 0.05). Naloxone (1.5 mg kg‐1, i.v.) abolished the reflex inhibition of bladder motility elicited by rectal distension or mechanical stimulation of the anus (P < 0.05). However, the urinary bladder and colonic contraction produced by electrical stimulation of the pelvic nerves were not affected. Hexamethonium (10 mg kg‐1, i.v.) or severing of the pelvic nerves completely abolished the responses of the urinary bladder and colon to electrical stimulation or reflex activation of the pelvic nerves. The results indicate that inhibitory reflexes from the rectum and anal canal to the urinary bladder are conveyed via efferents of the pelvic nerves, and involve both nicotinic and opioid receptor mechanisms.
Adsorption of coagulation proteins and adhesion and activation of platelets at the blood‐solid interface. An experimental study of human whole blood
Authors: NYGREN H. , ELAM J.‐H. , STENBERG M.
Published: December 2008

A procedure is presented allowing detailed studies of the adsorption of coagulation factors from whole blood on to surface. Anticoagulant (citrate or hirudin) was added to fresh venous blood. The blood was incubated in hydrophilic or hydrophobic glass tubes without contact with air. The adsorption of fibrinogen, fibronectin and factor IX was measured with an enzyme immunoassay using specific antibodies directed against these proteins. Adsorption of enzymically active kallikrein was measured using a chromogenic peptide substrate. Adhesion and activation of platelets was measured by direct examination in a scanning electron microscope and by measurement of release of beta‐thromboglobulin. The results show that the adsorption of plasma proteins at the blood‐solid interface is dependent on the anticoagulant used, surface energy of the test surface and incubation time. In experiments using hirudin a specific inactivator of thrombin, as anticoagulant, we found dynamic changes of the adsorbed protein film which could not be studied using citrated blood.
The calcium entry blocker verapamil increases red cell flux in the vasa recta of the exposed renal papilla
Authors: HANSELL P. , SJÖQUIST M. , ULFENDAHL H. R.
Published: December 2008

To investigate the vasoreactivity of the vessels of the juxtamedullary vasculature, measurements were made of the red blood cell flux (Qrbe) in the vasa recta of the exposed renal papilla of anaesthetized rats by means of fluorescently labelled erythrocytes. The flux was measured before and after intravenous administration of the calcium entry blocker verapamil, which was infused in two different doses. A control group receiving vehicle was studied in parallel. The lower dose of verapamil (0.6 mg h‐lkg‐1body wt) increasedQrbeby 30 ± 6% (n =9,P <0.05, mean ± I SEM) and reduced the systemic blood pressure by 6% (P <0.05). The osmolality of urine samples from the papillary tip remained statistically unchanged (1199 ± 60vs. 1186 ± 102 mosm kg‐1H2O). In the animals receiving the higher dose of verapamil (2.4 mg h‐1kg‐1body wt), Qrbcincreased by 39 ± 7% (n =10,P0.05) and the blood pressure was reduced by 9% (P <0.05), while urine osmolality was unchanged (1104 ± 110vs. 1264 ± 123 mosm kg‐1H2O). In the time control group there was no statistically significant change in Qrbe(+ 6 ± 8%,n= 10), blood pressure or urine osmolality (1006 ± 61vs. 1091 ± 70 mosm kg‐1H2O).

The verapamil‐induced increase inQrbcis probably mainly mediated by a relaxation of the afferent arteriole of the juxtamedullary nephrons. The results confirm our previous indication of a high vasoreactivity in the vessels of the juxtamedullary vasculature. This vasoreactivity is a prerequisite for the large regulatory span of the renal medullary blood flow and consequently for the medullary function.
Reflex activation of renal nerves in humans: differential effects on noradrenaline, dopamine and renin overflow to renal venous plasma
Authors: TIDGREN B. , HJEMDAHL P.
Published: December 2008

Using a thermodilution technique for renal venous blood flow measurements, renal sympathetic nerve activity was evaluated in 10 healthy volunteers by measurements of noradrenaline (NA) and dopamine (DA) overflow to renal venous plasma. Renin release was measured simultaneously. At rest, arterial adrenaline (ADR) levels were 0.24 ± 0.03 nmol l‐1and NA and DA levels were higher in renal venous than in arterial plasma (12.4vs. 0.98 and 0.14vs. 0.09 nmol l‐1, respectively,P <0.01 for both). The renal extraction of ADR from arterial plasma was 40 ± 4%. ADR extractions were used to correct for the renal removal of NA or DA from arterial plasma when calculating the renal overflow of NA or DA to renal venous plasma. At rest, the thus corrected renal venous overflows of NA and DA were 228 ± 34 and 29 ± 3 pmol min‐1, respectively. Isometric handgrip exercise (IHG) increased renal vascular resistance (RVR) by 20% and NA overflow by 123 %, without altering renin release or DA overflow. Vasodilatation induced by dihydralazine (HYDR) increased NA overflow by 63% (P <0.05) and elevated DA overflow by 107 ± 59%. The renal DA/NA overflow ratio was reduced from 0.15 to 0.06 (P <0.01) during IHG, but was not altered by HYDR. Renin release increased by 377% after HYDR (P <0.001) and was correlated to the reduction of mean arterial pressure but not to changes in NA overflow. Thus, both IHG and HYDR increased renal sympathetic nerve activity, although differential effects on renin release and DA overflow were observed. The dissociation of renal NA and DA responses suggests that the human kidney may have a subset of dopaminergic nerves.
Trifluoperazine stimulated sodium transport through the apical surface of isolated frog skin
Authors: BJERREGAARD H. F. , NIELSEN R.
Published: December 2008

When added to the apical solution of isolated frog skin, the calmodulin antagonist trifluoperazine (TFP)* stimulated the short‐circuit current (SCC) in a dose‐dependent manner. The increase in SCC was due to an enhanced active transepithelial Na transport. After addition of TFP (15 ,μm) the intracellular voltage depolarized, showing that TFP acts by increasing the sodium (Na) permeability of the apical membrane. The TFP‐induced increase in SCC was not accompanied by an increase in prostaglandin E2, release from the skins as observed by basolateral addition of TFP. When the apical Na concentration in fast‐flow experiments was changed from o to 50 mM, the SCC increased promptly and then reclined. The presence of TFP in the apical solution abolished this recline. The apparent inhibition constant for amiloride changed in the presence of TFP from 1.42 ± 0.12 μM to 0.38 ± 0.05 μM (n = 11) and TFP abolished the inhibition of SCC caused by high apical Na concentrations. These observations indicate that TFP acts by abolishing the Na self‐inhibition of the Na channels. Calmidazolium and chlorpromazine stimulated the SCC to the same degree and in the same concentration range as TFP, suggesting that the effect of TFP was not mediated by the Ca2+calmodulin complex.
Comparative potency of carbachol, sham feeding, fundic distension and 16,16‐dimethyl prostaglandin E2 as stimulants of human gastric bicarbonate secretion
Authors: FORSSELL H. , LIND T. , OLBE L.
Published: December 2008

Six healthy subjects in random order underwent gastric bicarbonate secretion investigations, including stimulation with increasing doses of the cholinergic agonist carbachol, sham feeding, fundic distension and gastric instillation of 16, 16‐dimethyl prostaglandin E2. Bicarbonate secretion was measured by a computer‐based system which continuously recorded pH and PCO2 of the effluent in a high‐volume gastric perfusion system. The peak 30 min gastric bicarbonate output in response to carbachol, 150 mg subcutaneously, was 114% (P < 0.05). Vagal stimulation by sham feeding resulted in a corresponding increase of 112% (P < 0.05), while fundic distension to a volume of 600 ml gave an increase of 114% (P < 0.05). In comparison, the response to 80 μg 16, 16‐dimethyl prostaglandin E, was much greater, the peak bicarbonate output being increased by 245 % (P < 0.05). Both sham feeding and fundic distension appear to be either submaximal stimuli of gastric bicarbonate secretion in man or may possess both stimulatory and inhibitory actions.
The importance of the subepithelial resistance for the electrical properties of the rat jejunum in vitro
Authors: HEMLIN M. , JODAL M. , LUNDGREN O. , SJÖVALL H. , STAGE L.
Published: December 2008

The aim of the study was to evaluate full‐thickness and partially stripped jejunum as a model for neurogenic control of electrogenic ion transport. The electrical properties of full‐thickness and partially stripped segments were studied in Ussing chambers. Using square‐pulse analysis, subepithelial and epithelial resistances (Rs and Rp) were determined, and by compensating for the potential fall across Rs, the current generated by the epithelium could be measured.

In full‐thickness tissue, Rs was approximately 80% of total tissue resistance, and the current measured during short‐circuiting of the whole tissue (SCC) was therefore only 20–25 % of the current generated by the epithelium (Im). Surgical stripping of the tissue decreased Rs by 10–20%. This means that in full thickness as well as in stripped tissue, 70–80% of the potential difference across the epithelial layer remains after traditional ‘short circuiting’.

Over a 25‐min period, none of the electrical parameters changed significantly in the full‐thickness tissues. In the stripped group PD, SCC and Im fell significantly, and in parallel during the same period of time. Neither glucose, noradrenaline, met‐enkephaline or karbachol had any significant effect on Rs, Rp or the Rs/Rp ratio. The relative effects of these agents on Im and SCC were therefore similar. Substance P and VIP increased the Rs/Rp ratio significantly and, therefore, the effect of these drugs on Im, was significantly more pronounced than the effect on SCC. The results show that the subepithelial resistance must be taken into account when the electrogenic activity in the epithelium is to be determined correctly. Conventionally measured SCC reflects the electrogenic effect of the tested putative neurotransmitters, but the magnitude of the responses is grossly underestimated, particularly for substance P and VIP.
Transcutaneous electrical nerve stimulation (TENS) increases survival of ischaemic musculocutaneous flaps
Authors: KJARTANSSON J. , LUNDEBERG T. , SAMUELSON U. E. , DALSGAARD C.‐J.
Published: December 2008

The effect of transcutaneous electrical nerve stimulation (TENS) on the survival of a dorsal musculocutaneous flap was studied in the rat. Postoperative TENS treatment significantly increased the flap survival area in groups of rats receiving different modes of TENS. The flap survival area was up to 95% in the TENS‐treated groups compared with 33–45 % in the control groups. Repeated (3 days) high intensity (20 mA), high‐frequency (80 Hz) TENS applied segmentally at the base of the flap was shown to be the most effective treatment in increasing the flap survival. Preoperative TENS did not increase flap survival area compared with untreated controls. It is concluded that postoperative TENS treatment markedly increases the experimental flap survival area and may be of clinical value for treatment of local ischaemia.
Effects of hypovolaemia or isoprenaline infusion on the sympathetic reflex response to PEEP ventilation in rats
Authors: SELLDÉN H. , RICKSTEN S.‐E.
Published: December 2008

The aim of this investigation was to study vagally mediated sympathetic reflex responses to mechanical ventilation with positive end‐expiratory pressure (PEEP), during hypovolaemia or during high inotropic stimulation of the heart by isoprenaline infusion. Renal sympathetic nerve activity (RSNA), heart rate and mean arterial pressure were studied during mechanical ventilation with zero end‐expiratory pressure (ZEEP) and 5 and 10 cmH2O PEEP in chloralose anaesthetized Wistar rats.

Experiments were performed on two groups of rats: eight animals were subjected to 10% blood volume depletion, and seven animals to infusion of isoprenaline. PEEP ventilation was applied during control conditions and during hypovolaemia or isoprenaline infusion before and after vagotomy. In the intact (control) situation, there was a significant increase in RSNA from ZEEP to 10 PEEP in both groups (+ 75%, + 51%). During hypovolaemia or isoprenaline infusion, PEEP ventilation did not induce any significant increase in RSNA in both groups after vagotomy, 10 PEEP induced a significant increase in both groups (+ 56%, +54%).

These results indicated that under conditions of hypovolaemia or increased cardiac inotropism, PEEP ventilation may elicit a vagally mediated reflex with an inhibitory action on sympathetic activity, in turn probably caused by an activation of left ventricular receptors.
Studies of the luteinization process in the rat: development of catecholamine response on progesterone production during the peri‐ovulatory period
Authors: ÅGREN P. L. , SELSTAM G. , NORJAVAARA E. , KINNANDER G. , KNUTSSON A.
Published: December 2008

The present study was undertaken to investigate whether pre‐ovulatory follicles have an adrenergic response in terms of progesterone production. Extirpated pre‐ovulatory follicles obtained both before and after the endogenous gonadotropin surge and newly formed corpora lutea were obtained from the PMSG rat ovulatory model. Follicles and corpora lutea were incubated for IZO min in MEM with Earle's salt and 10 mM Hepes, 37 °C, pH 7.4 and 100% oxygen, with 30 μMnoradrenaline or 10 μg ml‐1 LH‐B9). Pre‐ovulatory follicles were barely stimulable by noradrenaline, while newly formed corpora lutea responded markedly. Luteinizing hormone (LH) levels significantly increased progesterone accumulation in all groups. In order to determine whether pre‐ovulatory follicles need intact surrounding tissue for an adrenergic response on progesterone production, pieces of ovaries containing pre‐ovulatory follicles were incubated. No significant effect of noradrenaline or adrenaline was seen, while LH had a substantial effect. The results show that catecholamines acutely exert a selective effect on steroidogenesis in the ovary with a marked stimulatory effect on corpora lutea and a marginal effect on the pre‐ovulatory follicle.
Intracerebroventricular and systemic saralasin used to investigate angiotensin‐elicited activation of the pituitary‐adrenocortical axis in the goat
Authors: JUNKERGÅRD J. , JÓNASSON H.
Published: December 2008

Intracerebroventricular (ICV) infusion of the competitive inhibitor for angiotensin II (AII), saralasin, (13 pmol kg‐1 min‐1), preceding and outlasting the intravenous (i.v.) infusion of AII (40 pmol kg‐1 min‐1) extinguished the elevation in plasma cortisol (PC) obtained in response to just the i.v. AII infusion. The corresponding i.v. infusion of saralasin did not visibly influence the AII‐induced elevation of PC, whereas bilateral intracarotid infusions of the inhibitor tended to reduce the response. The ICV administration of the inhibitor also significantly reduced the rise in plasma aldosterone (PA) seen as an effect of the i.v. AII. Paradoxically, however, the intravascular infusions of saralasin conspicuously augmented the rise in PA obtained after the simultaneous i.v. infusion of AII. It is concluded that cerebral mediation of the ACTH‐cortisol response to systemic AII occurs at sites accessible to inhibition from both sides of the blood‐brain barrier, and that also the PA response to blood‐borne AII may be to some extent cerebrally mediated.
Increased behavioural response to intrathecal serotonin after lesion of serotonergic pathways with 5,7‐dihydroxytryptamine seems not to be due to depletion of serotonin
Authors: EIDE P. K. , HOLE K.
Published: December 2008

The hehavioural response to intrarhecal i.th. serotonin (5‐HT) was examined in mice pretreated with the neurotoxin 5,7‐dihydroxytryptamine (5,7‐DIIT) or the 5‐HT synthesis inhibitorp‐chlorophenylalanine (PCPA) which produce similar extensive depletion of central 5‐HT levels. Intrathecal 5‐HT (0.4 γg) elicited a hehavioural response consisting of reciprocal hindlimb scratching and biting or licking of the hindquarters indicative of nociceptive stimulation. The response to i.th. 5‐HT was markedly increased 5 days after intracerebroventricular (i.c.v.) injection of 5,7‐DHT (80 γgbase per mouse). On the other hand, 24 h after the last pretreatment injection of PCPA (400 mg kg‐1for 6 consecutive days), the response to i.th. 5‐HT was unaltered. These results indicate that i.c.v. 5,7‐DHT produces supersensitivity to 5‐HT. Since PCPA failed to alter the effect of 5‐HT, the supersensitivity seems not to be due to depletion of 5‐HT levels after the lesion.
Physiological aspects of freezing behaviour in willow ptarmigan hens
Authors: STEEN J. B. , GABRIELSEN G. W. , KANWISHER J. W.
Published: December 2008

When threatened, wild willow ptarmigan (Lagopus lagopus lagopus) hens displayed freezing behaviour, i.e. motionless, crouched with head down and eyes open. But while non‐incubating hens showed increased heart (HR) (from 229±18 to 254 ± 33 beats min‐1) and ventilation rates (VR) (from 25 ± 2 to 31± 4 breaths min ‐1), incubating hens showed bradycardia (from 208 ± 40 to 102 ± 13 beats min‐1) and reduced VR (from 25 ± 2 to 10 ± 2 breaths min‐1), which could be maintained for as long as 20 min. The bradycardia response became stronger as hatching approached. The bradycardia period was interspersed by short bursts of tachycardia and hyperventilation which presumably supplied oxygen to blood and muscles. The bradycardia period was typically followed by a period of increased HR (276 ± 104 beats min‐1) and VR (32 ± 3 breaths min‐1). Atropine abolished the bradycardia response, which was thus apparently due to parasympathetic stimulation. The bradycardia response observed in incubating ptarmigan hens, during forced diving of birds and mammals and during death feigning in other animals are all examples of how emotional stimuli trigger a basic bradycardia reflex.
Effect of naloxone on tooth pulp‐evoked jaw‐opening reflex in the barbiturate‐anaesthetized cat
Authors: HUOPANIEMI T. , PERTOVAARA A. , JYVÄSJÄRVI E. , CARLSON S.
Published: December 2008

The threshold of the tooth pulp‐evoked jaw‐opening reflex was uninfluenced by administration of 0.5 or 5.0 mg kg‐1, i.v. naloxone, a specific opioid antagonist, in the barbiturate‐anaesthetized cat. Furthermore, facilitatory or inhibitory interactions between two successive tooth pulp‐evoked jaw reflex responses were not influenced by naloxone. It is concluded that naloxone‐sensitive opioid receptor‐mediated mechanisms do not contribute to the modulation of tooth pulp‐evoked reflexes by conditioning dental stimuli. Also they do not exert a tonic inhibition on the sensory or motor part of the tooth pulp‐driven reflexes. Experiments performed for comparison showed that the non‐nociceptive polysynaptic reflex discharge in the flexo‐motor neurons of the limb was not influenced by naloxone either.
Do the fibre‐type proportion and the angular velocity influence the mean power frequency of the electromyogram?
Authors: GERDLE B. , WRETLING M.‐L. , HENRIKSSON‐LARSÉN K.
Published: December 2008

The dependence of the mean‐power frequency and the signal amplitude of the electromyogram (EMG) on the angular velocity and the fibre‐type proportion were investigated in nine female volunteers. The subjects were required to perform maximum knee extensions using an isokinetic dynamometer at different angular velocities; 0.57, 1.05, 1.57, 2.09 and 3.14 rad S‐1. Electromyographic signals were obtained from the vastus lateralis, vastus medialis and the rectus femoris muscles. The angle and the torque signals were recorded simultaneously with the three EMG signals on a tape‐recorder. From the EMG recordings the mean power frequency (MPF) and the signal amplitude were determined. Muscle biopsies were later obtained from the right vastus lateralis and stained for alkaline and acid mATPase for the determination of fibre‐type proportions and areas.

Neither the signal amplitude nor the MPF of the EMG of the three muscles were dependent on the angular velocity. The MPF of the vastus lateralis correlated significantly (r = ‐0.93) with the type 1 fibre proportion at 1.57 rad s‐1. However, there was no significant correlation between the areas of the fibre types, alone or together, and the MPF. In conclusion the fibre‐type proportion was the major factor behind the MPF irrespective of angular velocity.
Epidermal growth factor and insulin‐like growth factor I are localized in different compartments of salivary gland duct cells. lmmunohistochemical evidence
Authors: HANSSON H.‐A. , TUNHALL S.
Published: December 2008

Immunohistochemical methods were used to map EGF (epidermal growth factor) and IGF‐I (insulin‐like growth factor I; somatomedin C) immunoreactivities in salivary glands of adult rodents. Epidermal growth factor is, as is NGF (nerve growth factor), limited in distribution to the granules in granular duct cells in the submandibular gland. Insulin‐like growth factor I is, in contrast, cytoplasmic and has a much more widespread distribution. It is seen in intercalated, striated and granulated duct cells as well as in apical parts of excretory duct cells. The parotid and the palatine salivary glands, lacking EGF immunoreactivity, have their IGF‐I immunoreactivity similarly distributed as the submandibular gland. Isoproterenol treatment of adult male rats results in rapid and extensive growth of the submandibular and the parotid glands, which double their weights in just a few days. Isoproterenol causes release of granules from the submandibular granular duct cells and decrease in frequency of EGF immunoreactive cells. However, there is no or only minor concomitant changes in the distribution and intensity of the IGF‐I immunoreactivity in these duct cells. Our results indicate that the trophic peptides EGF (and NGF) and IGF‐I are localized in different compartments in salivary gland duct cells and that divergent pathways control their release.
Vasomotor changes in isolated coronary arteries from diabetic rats
Authors: SJÖGREN A. , EDVINSSON L.
Published: December 2008

Contractile responses to prostaglandin F2α, serotonin, noradrenaline, and potassium were examined in isolated intramyocardial arteries of Wistar rats 8 weeks after the induction of diabetes mellitus by administration of streptozotocin (STZ). The concentration‐response curves obtained were compared with those noted in vessels both from age‐ and from weight‐matched control rats. Light and electron microscopy did not reveal any major change in coronary artery wall thickness or morphology. There was no difference in the pattern of vasomotor responses between the two control groups. Contractile responses to prostaglandin F2αand potassium were significantly reduced, while contractile responses to serotonin and noradrenaline were unaltered in coronary arteries from diabetic rats. The vasomotor responses to noradrenaline and potassium showed a biphasic pattern in control vessels, i.e. contraction noted at high agonist concentrations was preceded by slight, but reproducible relaxation at lower concentrations. In diabetic vessels these relaxant responses were absent. The contraction produced by noradrenaline was markedly enhanced by the presence of propranolol in both diabetic and control vessels. Dilator responses to verapamil, diltiazem, nifedipine, papverine and magnesium were studied in serotonin‐precontracted coronary arteries; the concentration‐response curves obtained by verapamil and diltiazem were shifted to the right in diabetic vessels. It appears justified to use vessels from age‐matched rats as controls when vasomotor reactivity in coronary arteries from STZ‐diabetic rats is investigated. The reduction in contractile responses to prostaglandin F2αand potassium, and the reduction or lack of relaxant responses to noradrenaline, potassium, verapamil and diltiazem, in diabetic coronary arteries, indicate a selective modification of the coronary circulation by the diabetic disease.