Microtip Pressure Transducer Research Articles

Monoamine oxidase-A is an important source of oxidative stress and promotes cardiac dysfunction, apoptosis, and fibrosis in diabetic cardiomyopathy

Oxidative stress is closely associated with the pathophysiology of diabetic cardiomyopathy (DCM). The mitochondrial flavoenzyme monoamine oxidase A (MAO-A) is an important source of oxidative stress in the myocardium. We sought to determine whether MAO-A plays a major role in modulating DCM. Diabetes was induced in Wistar rats by single intraperitoneal injection of streptozotocin (STZ). To investigate the role of MAO-A in the development of pathophysiological features of DCM, hyperglycemic and age-matched control rats were treated with or without the MAO-A-specific inhibitor clorgyline (CLG) at 1mg/kg/day for 8 weeks. Diabetes upregulated MAO-A activity; elevated markers of oxidative stress such as cardiac lipid peroxidation, superoxide dismutase activity, and UCP3 protein expression; enhanced apoptotic cell death; and increased fibrosis. All these parameters were significantly attenuated by CLG treatment. In addition, treatment with CLG substantially prevented diabetes-induced cardiac contractile dysfunction as evidenced by decreased QRS, QT, and corrected QT intervals, measured by ECG, and LV systolic and LV end-diastolic pressure measured by microtip pressure transducer. These beneficial effects of CLG were seen despite the persistent hyperglycemic and hyperlipidemic environments in STZ-induced experimental diabetes. In summary, this study provides strong evidence that MAO-A is an important source of oxidative stress in the heart and that MAO-A-derived reactive oxygen species contribute to DCM.

Murine study of portal hypertension associated endothelin-1 hypo-response.

To investigate endothelin-1 hypo-responsive associated with portal hypertension in order to improve patient treatment outcomes. Wild type, eNOS(-/-) and iNOS(-/-) mice received partial portal vein ligation surgery to induce portal hypertension or sham surgery. Development of portal hypertension was determined by measuring the splenic pulp pressure, abdominal aortic flow and portal systemic shunting. To measure splenic pulp pressure, a microtip pressure transducer was inserted into the spleen pulp. Abdominal aortic flow was measured by placing an ultrasonic Doppler flow probe around the abdominal aorta between the diaphragm and celiac artery. Portal systemic shunting was calculated by injection of fluorescent microspheres in to the splenic vein and determining the percentage accumulation of spheres in liver and pulmonary beds. Endothelin-1 hypo-response was evaluated by measuring the change in abdominal aortic flow in response to endothelin-1 intravenous administration. In addition, thoracic aorta endothelin-1 contraction was measured in 5 mm isolated thoracic aorta rings ex-vivo using an ADI small vessel myograph. In wild type and iNOS(-/-) mice splenic pulp pressure increased from 7.5 ± 1.1 mmHg and 7.2 ± 1 mmHg to 25.4 ± 3.1 mmHg and 22 ± 4 mmHg respectively. In eNOS(-/-) mice splenic pulp pressure was increased after 1 d (P = NS), after which it decreased and by 7 d was not significantly elevated when compared to 7 d sham operated controls (6.9 ± 0.6 mmHg and 7.3 ± 0.8 mmHg respectively, P = 0.3). Abdominal aortic flow was increased by 80% and 73% in 7 d portal vein ligated wild type and iNOS when compared to shams, whereas there was no significant difference in 7 d portal vein ligated eNOS(-/-) mice when compared to shams. Endothelin-1 induced a rapid reduction in abdominal aortic blood flow in wild type, eNOS(-/-) and iNOS(-/-) sham mice (50% ± 8%, 73% ± 9% and 47% ± 9% respectively). Following portal vein ligation endothelin-1 reduction in blood flow was significantly diminished in each mouse group. Abdominal aortic flow was reduced by 19% ± 9%, 32% ± 10% and 9% ± 9% in wild type, eNOS(-/-) and iNOS(-/-) mice respectively. Aberrant endothelin-1 response in murine portal hypertension is NOS isoform independent. Moreover, portal hypertension in the portal vein ligation model is independent of ET-1 function.

Use of a vessel sealant device for cystic duct ligation in the dog.

To compare a vessel sealant device to hemostatic clips for cystic duct ligation in a canine cadaveric model. Experimental. Hepatobiliary systems were collected from normal dogs. A microtip pressure transducer was inserted into the common bile duct and a 20-24 g intravenous catheter was placed in a hepatic duct. The cystic duct was ligated with 1 of 3 techniques: vessel sealant device (VSD), 10 mm medium Endoclips™, or 10 mm large Endoclips™ with 6 specimens in each group. Methylene blue was infused until failure, which was recorded as seal/clip failure or retrograde movement of methylene blue into the liver. Mean failure pressure of the medium endoclip group was significantly lower than the large endoclip group (P = .014). There was no difference between the failure pressure of the VSD group and the medium and large endoclip groups (P = .097, P = .34, respectively). Failure by leakage at the cut surface of the cystic duct occurred in 2 specimens in the medium endoclip group while all others failed by retrograde flow of the methylene blue through the hepatic ducts. The vessel sealant device appears comparable to large endoclips for closure of the cystic duct in an acute cadaveric model, while medium endoclips may not fully compress or span the diameter of a cystic duct in large breed dogs and leak at lower pressures.

Peroxynitrite Is a Key Mediator of the Cardioprotection Afforded by Ischemic Postconditioning In Vivo

Myocardial ischemic postconditioning (PosC) describes an acquired resistance to lethal ischemia-reperfusion (I/R) injury afforded by brief episodes of I/R applied immediately after the ischemic insult. Cardioprotection is conveyed by parallel signaling pathways converging to prevent mitochondria permeability transition. Recent observations indicated that PostC is associated with free radicals generation, including nitric oxide (NO.) and superoxide (O2 .-), and that cardioprotection is abrogated by antioxidants. Since NO. And O2 . - react to form peroxynitrite, we hypothesized that postC might trigger the formation of peroxyntrite to promote cardioprotection in vivo. Rats were exposed to 45 min of myocardial ischemia followed by 3h reperfusion. PostC (3 cycles of 30 seconds ischemia/30 seconds reperfusion) was applied at the end of index ischemia. In a subgroup of rats, the peroxynitrite decomposition catalyst 5,10,15,20-tetrakis(4-sulphonatophenyl) porphyrinato iron (FeTPPS) was given intravenously (10 mg/kg-1) 5 minutes before PostC. Myocardial nitrotyrosine was determined as an index of peroxynitrite formation. Infarct size (colorimetric technique and plasma creatine kinase-CK-levels) and left ventricle (LV) function (micro-tip pressure transducer), were determined. A significant generation of 3-nitrotyrosine was detected just after the PostC manoeuvre. PostC resulted in a marked reduction of infarct size, CK release and LV systolic dysfunction. Treatment with FeTPPS before PostC abrogated the beneficial effects of PostC on myocardial infarct size and LV function. Thus, peroxynitrite formed in the myocardium during PostC induces cardioprotective mechanisms improving both structural and functional integrity of the left ventricle exposed to ischemia and reperfusion in vivo.

Multiple Antioxidants Improve Cardiac Complications and Inhibit Cardiac Cell Death in Streptozotocin-Induced Diabetic Rats

Diabetic cardiomyopathy, a disorder of the heart muscle in diabetic patients, is one of the major causes of heart failure. Since diabetic cardiomyopathy is now known to have a high prevalence in the asymptomatic diabetic patient, prevention at the earliest stage of development by existing molecules would be appropriate in order to prevent the progression of heart failure. In this study, we investigated the protective role of multiple antioxidants (MA), on cardiac dysfunction and cardiac cell apoptosis in streptozotocin (STZ)-induced diabetic rat. Diabetic cardiomyopathy in STZ-treated animals was characterized by declined systolic, diastolic myocardial performance, oxidative stress and apoptosis in cardiac cells. Diabetic rats on supplementation with MA showed decreased oxidative stress evaluated by the content of reduced levels of lipid per-oxidation and decreased activity of catalase with down-regulation of heme-oxygenase-1 mRNA. Supplementation with MA also resulted in a normalized lipid profile and decreased levels of pro-inflammatory transcription factor NF-kappaB as well as cytokines such as TNF-α, IFN-γ, TGF-β, and IL-10. MA was found to decrease the expression of ROS-generating enzymes like xanthine oxidase, monoamine oxidase-A along with 5-Lipoxygenase mRNA and/or protein expression. Further, left ventricular function, measured by a microtip pressure transducer, was re-established as evidenced by increase in ±dp/dtmax, heart rate, decreased blood pressure, systolic and diastolic pressure as well as decrease in the TUNEL positive cardiac cells with increased Bcl-2/Bax ratio. In addition, MA supplementation decreased cell death and activation of NF-kappaB in cardiac H9c2 cells. Based on our results, we conclude that MA supplementation significantly attenuated cardiac dysfunction in diabetic rats; hence MA supplementation may have important clinical implications in terms of prevention and management of diabetic cardiomyopathy.

Tramadol enhances urethral continence function through µ‐opioid receptors in rats

(±)-Tramadol hydrochloride (tramadol) is a widely used analgesic that stimulates the µ-opioid receptor and inhibits the reuptake of serotonin and noradrenalin. Although tramadol is also known to inhibit the micturition reflex in rats, its effects on urethral continence function have not been reported. We therefore examined whether intravenous tramadol (1, 3, and 10 mg/kg) affects intraurethral pressure, bladder leak point pressure, and leak volume in urethane-anesthetized female rats. (1) The intraurethral pressure was recorded with a microtip pressure transducer placed at the maximum pressure zone of the intrinsic urethral sphincter. (2) Gentle pressure was directly applied to the saline-filled bladder with a cotton bud until leakage occurred, and the bladder pressure at the moment of leakage was taken as the bladder leak point pressure. (3) The leak volume was measured as the amount of fluid leakage from the urethral orifice after electrical stimulation of abdominal muscles. Tramadol significantly increased the intraurethral pressure. Both tramadol and morphine increased the bladder leak point pressure and decreased the leak volume. These changes were reversed by subcutaneous pretreatment with naloxone. Tramadol improved urethral function and inhibited urinary incontinence through µ-opioid receptors.

Keeping the heart empty and beating improves preservation of hypertrophied hearts for valve surgery

This study was designed to determine whether keeping the heart empty and beating improved myocardial fluid homeostasis and energy metabolism of hypertrophied pig hearts in comparison with cardioplegic arrest. Twenty piglets underwent a 8-weeks (corrected) ascending aortic banding to induce left ventricular hypertrophy. Isolated hypertrophied hearts were divided into 4 groups (n = 5 in each group). Two groups underwent normothermic normokalemic simultaneous perfusion. The other 2 groups were subjected to normothermic hyperkalemic simultaneous perfusion and used as controls. Intramyocardial hydrostatic pressure was monitored with a microtip pressure transducer. Volumes of intracellular and extracellular compartments and myocardial energy metabolism were monitored by using phosphorus 31 magnetic resonance spectroscopy. Normothermic normokalemic simultaneous perfusion (NNSP) maintained intramyocardial hydrostatic pressure at a significantly lower level (13.0 +/- 0.6 mm Hg) compared with normothermic hyperkalemic simultaneous perfusion (NHSP) (23.3 +/- 1.2 mm Hg) during a 90-minute preservation. NNSP maintained the normal volume of the intracellular compartment throughout the preservation period, whereas NHSP caused significant enlargement (to 123% +/- 6% of its normal volume) of the intracellular compartment. Expansion of the extracellular compartment during preservation was significantly less in the NNSP group (124% +/- 6%) than in the NHSP group (152% +/- 7%). NNSP maintained normal levels of phosphocreatine and adenosine triphosphate until coronary perfusion flow was reduced to 50% of the initial control level. No decrease in energy metabolites was observed in the NHSP group even when coronary perfusion flow was reduced to 10% of the initial control level. Keeping the heart empty and beating improves myocardial fluid homeostasis for hypertrophied hearts relative to cardioplegic arrest. Its ability to maintain energy metabolism depends on the degree of coronary stenosis. This technique may be a promising protective strategy for hypertrophied hearts.

Motor evoked potentials (MEP) and evoked pressure curves (EPC) from the urethral compressive musculature (UCM) by functional magnetic stimulation in healthy volunteers and patients with neurogenic incontinence

The aim of this study is to assess neurogenic lesions of the somatomotor efferent nervous pathway to the urethral compressive musculature (UCM) by means of motor evoked potentials (MEP) and simultaneously recorded evoked pressure curves (EPC). Nine healthy subjects and 33 patients (15 spinal cord injury, 14 cauda equina lesion, and 4 multiple sclerosis (MS)) with neurogenic urinary incontinence were prospectively examined by means of urodynamics and electrophysiology. MEP responses from the UCM were evoked after transcranial (tc) and lumbosacral (ls) single pulse magnetic stimulation. A ratio out of tx/ls latencies was calculated to distinguish between central (i.e., spinal) and peripheral lesions. The mechanical UCM pressure responses (=EPC) were recorded simultaneously with electromyographic (EMG) recordings using a microtip pressure transducer catheter with integrated bipolar surface electrodes. In nine healthy subjects the central latency was 19.0 msec, the peripheral latency was 4.25 msec, and the ratio was 4.4. In patients with incomplete spinal cord lesion the central latency was significantly delayed (22.7 msec), whereas the peripheral responses were normal. The ratio (5.5) was increased. Thirteen of these 15 patients suffered from neurogenic incontinence. Patients with a complete spinal lesion showed no UCM reaction after tc stimulation, whereas peripheral responses were normal. Patients with MS showed significantly prolonged central latencies (25.5 msec). The increased ratio of 6.0 indicated a spinal lesion. Ten patients with incomplete cauda equina lesions and urinary incontinence had normal central latencies but prolonged peripheral latencies of 6.7 msec. The ratio of 3.4 indicated a lesion of the sacral caudal roots. In patients with complete cauda injury neither central nor peripheral responses could be evoked. Tc evoked mechanical pressure responses (i.e., contractions) from the UCM could only be recorded in intact or incompletely injured spinal and peripheral motor nervous pathways, whereas they could be evoked after ls stimulation only in cases with partially preserved sacral caudal roots independent of a spinal lesion. MEP and EPC from the UCM proved to be a well tolerated disgnostic tool in patients with neurogenic incontinence that distinguished central and peripheral lesions of the motor efferent pathways to the UCM.

The effect of tamsulosin on the resting tone and the contractile behaviour of the female urethra: a functional urodynamic study in healthy women.

The aim of this functional urodynamic experiment was to study the effect of the selective alpha1(A)-blocker tamsulosin on the urethral pressure in healthy human females and assessed first the resting urethral pressure and second the urethral contractility in response to magnetic stimulation of the sacral roots. 11 healthy female subjects gave their written informed consent and were included. A microtip pressure transducer catheter was inserted into the bladder and three baseline urethral pressure profiles were obtained. Another three urethral pressure profiles were recorded while magnetic single pulse stimulation of the sacral roots was performed above the motor threshold of the pelvic floor to evoke reproducible urethral contractions. Then the subjects received 0.4 mg of tamsulosin and the entire protocol was repeated 6 hours after drug administration. Cardiovascular monitoring was obtained during the baseline and follow-up measurements. Mean and maximal urethral pressure values calculated over the entire urethra, mean pressure values calculated over the proximal, middle and distal third of the urethra and the pressure amplitudes to magnetic stimulation at baseline were statistically compared to the follow-up measurements with tamsulosin. The oral administration of tamsulosin did not change the systemic blood pressure, but did significantly reduce the mean and maximal urethral pressure acquired over the entire urethra. When the proximal, middle and distal third of the urethra were analysed separately, there was a significant pressure reduction in all three segments. Amplitudes of the urethral contractions evoked by sacral magnetic stimulation remained unchanged after tamsulosin. These data show a significant relaxing effect of tamsulosin on the resting urethral tone in healthy females in vivo. These results may suggest tamsulosin as a new pharmacological approach to treat urinary retention due to overactive or non-relaxing urethra in women.

The effects of breath control on intra-abdominal pressure during lifting tasks.

This was a repeated measures study examining 11 asymptomatic subjects while performing dynamic lifting using various postures, loads, and breath control methods. To examine the effects of breath control on magnitude and timing of intra-abdominal pressure during dynamic lifting. Intra-abdominal pressure has been shown to increase consistently during static and dynamic lifting tasks. The relationship between breath control and intra-abdominal pressure during lifting is not clear. Eleven healthy subjects were tested using lifting trials consisting of two levels of posture and load and four levels of breath control (natural breathing, inhalation-hold, exhalation-hold, inhalation-exhalation). Intra-abdominal pressure was measured using a microtip pressure transducer placed within the stomach through the nose. Timing of intra-abdominal pressure was determined relative to lift-off of the weights. Repeated measures analysis of variance was used to determine the effect of breath control, posture, and load on intra-abdominal pressure magnitude and timing. There was a significant effect of breath control (P < 0.018) and load (P < 0.002), but not of posture (P < 0.434), on intra-abdominal pressure magnitude. The inhalation-hold form of breath control produced significantly greater peak intra-abdominal pressure than all other forms of breath control (P < 0.000 for all comparisons). No other comparisons among levels of breath were significantly different. No significant main effects of breath control were found relative to intra-abdominal pressure timing. Breath control is a significant factor in the generation of intra-abdominal pressure magnitude during lifting tasks. The effects of respiration should be controlled in studies analyzing intra-abdominal pressure during lifting.

Functional magnetic stimulation of the spinal cord--a urodynamic study in healthy humans.

To study the effects of functional magnetic stimulation of the spinal cord in healthy subjects on somatic and autonomic pathways innervating the anal and the external urethral sphincter, bladder, bladder neck, and rectum. Eight healthy male volunteers gave their written informed consent and underwent functional magnetic stimulation of the thoracolumbar and sacral spinal cord. A two-channel microtip pressure transducer catheter was placed rectally measuring the abdominal and anal sphincter pressure. A three-channel microtip pressure transducer catheter was inserted into the urethra measuring the bladder, the bladder neck, and the external urethral sphincter pressure. A comprehensive protocol of single and repetitive magnetic stimulations was performed. Frequency, location, and duration of stimulation were varied while the intensity of stimulation was adapted to the maximum the subjects could tolerate. In four subjects, the degree of bladder filling was changed and the protocol was repeated when the subjects reported a full bladder and desire to void. Continuous magnetic stimulation of the thoracolumbar spinal cord and the sacral roots applied with different frequencies (5, 15, 30, 60, 100 Hz) and different duration of stimulation (10, 30, 120 sec) evoked sphincter contraction of both anal and urethral sphincters. The stimulation could not evoke contractions of the bladder, the bladder neck, or the rectum. Also with filled bladder and present desire to void, the magnetic stimulation could not activate autonomic pathways innervating these structures. Considering our results, we suggest that in individuals with preserved sensibility magnetic stimulation of the spinal cord with intensities below the pain threshold is ineffective in activating autonomic nerve fibres innervating bladder, bladder neck, and rectum.

The effect of nitric oxide on the resting tone and the contractile behaviour of the external urethral sphincter: a functional urodynamic study in healthy humans.

This functional urodynamic study assessed the effect of the nitric oxide donor isosorbide dinitrate on the external urethral sphincter and hypothesised first that nitric oxide could lower the resting sphincter pressure, second that nitric oxide could influence the sphincter contractility during magnetic stimulation, and third that nitric oxide could induce a faster external urethral sphincter fatigue during continuous magnetic stimulation. Eight healthy males gave their written informed consent and were included. A 2-channel microtip pressure transducer catheter was inserted into the urethra measuring the bladder and the external urethral sphincter pressure. Magnetic stimulation of the sacral roots was performed to evoke reproducible contractions of the external urethral sphincter. The baseline protocol included six single pulse stimulations and three stimulations 10sec in duration each for two frequencies 5Hz and 50Hz with intensities at the motor threshold of the pelvic floor. Then the subjects received 10 mg of isosorbide nitrate sublingually and the protocol was repeated 5min, 20min, 40min and 60min after drug administration. The sublingual administration of isosorbide dinitrate could significantly reduce the resting pressure of the external urethral sphincter for at least one hour. The maximal contractile strength measured as the maximal urethral pressure during single pulse and continuous magnetic stimulation of the sacral roots also decreased significantly. Nitric oxide did not induce a significantly faster fatigue of the external urethral sphincter during continuous magnetic stimulation of the sacral roots. This study shows a functionally relevant effect of nitric oxide on the resting tone and the contractile behaviour of the human external urethral sphincter in vivo while the fatigue properties did not changed significantly. Nitric oxide donors could offer a new pharmacological approach to treat urinary retention due to overactive or non-relaxing external urethral sphincter.

Comparison of measurements obtained with microtip and external water pressure transducers

The aim of this study was to compare pressure readings obtained with catheter-mounted microtip and external water pressure transducers using a mechanical model for vesical pressure during Valsalva straining and coughing. The two catheter-mounted pressure transducers were simultaneously placed in a vinyl i.v. bag designed to mimic the parameters of the human bladder to allow comparison of simultaneous readings from both transducers. Simulated cough and Valsalva maneuvers of various strengths at different volumes (100 ml, 200 ml, 300 ml) were performed and the pressure readings generated by the two systems compared. The Pearson correlation coefficient between the systems was 0.998 for coughs and 0.998 for Valsalva efforts. Data were also analyzed by volume and strength of simulated cough and Valsalva effort, and correlations were found to be high (> or = 0.940) for all subgroup analyses. Mean absolute differences between events recorded by the two systems were small, as indicated by the y-intercept of 3.76 cmH2O pressure. Neither transducer recorded consistently higher pressures than the other. We concluded that there is a high correlation between pressure measurements obtained from microtip and external water pressure transducers during simulated cough and Valsalva efforts in this model. As similar correlation should exist in vivo, urodynamic data generated by the two transducer types should be comparable.

Respiratory responses of mature horses to intravenous lobeline bolus.

The respiratory stimulant lobeline has been used in equine clinical practice to increase inspiratory and expiratory airflow rates at rest in order to facilitate investigation of both lower and upper airway function. Some of the responses to lobeline in the pony have been reported, but the detailed time course, effect of dose, possible side effects and reproducibility associated with lobeline administration have not been described in the horse. Respiratory airflow rates and oesophageal pressure were measured with a Fleisch No. 5 pneumotachometer and lightweight facemask and a microtip pressure transducer catheter, respectively. The output of the Fleisch pneumotachometer was calibrated for flow rates up to +/- 70 l/s. Seven mature horses with no clinical signs of respiratory disease were studied. Investigations were conducted to determine: (1) the responses to different doses of lobeline (0.15, 0.20, 0.25 and 0.30 mg/kg bwt) as a rapid i.v. bolus (6 horses); (2) arterial blood gases during and after lobeline administration (0.20 mg/kg bwt; 3 horses); and (3) the reproducibility of lobeline-stimulated hyperpnoea (5 horses; 2 doses of 0.20 mg/kg bwt lobeline, 15 min apart). All horses tolerated the lobeline-stimulated hyperpnoea well, although one always coughed or snorted at the onset. Mild tremor was noted following the highest dose in several horses. Apnoea of approximately 40 s was common after the hyperpnoea. Both tidal volume (VT) and frequency (fR) increased with lobeline dose. During peak hyperpnoea at a dose of 0.30 mg/kg bwt, peak inspired flow rate (PIF), peak expired flow rate (PEF) and minute ventilation (VE) were mean +/- s.e. 41+/-5 l/s, 61+/-10 l/s and 920+/-99 l/min, respectively. The hyperpnoea also caused marked changes in arterial PaO2, PaCO2 and pHa at 90 s after lobeline (0.20 mg/kg bwt) administration (mean +/- s.e. 146.0+/-6.9 mmHg, 20.6+/-0.8 mmHg and 7.707+/-0.020, respectively) compared to at rest (mean +/- s.e. 104.0+/-4.0 mmHg, 50.6+/-2.8 mmHg and 7.432+/-0.012). Dynamic lung compliance (Cdyn) was unaltered by lobeline administration. The lobeline-induced hyperpnoea was highly reproducible, with no significant difference in any of the parameters during 2 stimulations 15 min apart. Lobeline induced highly reproducible responses without any apparent adverse effects and may be useful in the investigation of pulmonary function in healthy horses and those with airway disease.

Intramuscular Pressure in the Erector Spinae and Intra-abdominal Pressure Related to Posture and Load

Intramuscular pressures in both Erectors Spinae and intra-abdominal pressures were measured during different holding tasks. To investigate the potential for using intramuscular pressure measurements in both Erectors Spinae to better quantitate the role of muscles during different lifting tasks in vivo. Intramuscular pressure and intra-abdominal pressure were measured previously under isometric and dynamic conditions. However, no previous study systematically has addressed the relation between intramuscular and intra-abdominal pressures and different loads, tasks, and postures. Intramuscular and intra-abdominal were measured simultaneously with microtip pressure transducers in 10 healthy volunteers performing 24 different static holding tasks. Tasks included different weights (10 kg and 20 kg), postures (squat or back lift), and positions of the weight. Intramuscular pressures were dependent on posture. Kyphotic back posture produced intramuscular pressures of 120-130 mm Hg, compared with the 10-25 mm Hg produced when volunteers were in the erect position (P < 0.001). Holding a 10-kg weight at the thighs close to the body produced significantly (P < 0.001) lower intramuscular pressures (25-32 mm Hg) than that produced by holding it 25 cm in front of the body (47-56 mm Hg). In all tasks, intramuscular pressures were significantly higher with the 20-kg weight than with the 10-kg weight (P < 0.001). Highest values (> 300 mm Hg) were measured when the 20-kg weight was held in the kyphotic posture above the floor and 25 cm away from the body. Intramuscular pressure measurements in the erector spinae seem to be a valuable tool for quantitating the role of back muscles during different lifting tasks.

Feasibility of Implant Driven Micturition in Paraplegic Dogs

This study evaluates the feasibility of using existing technology for implant driven micturition in paralyzed dogs (part I) and also examines a less invasive technique for implant driven micturition (part II). Part I. Sacral nerve root dimensions and bladder and urethral pressure responses to intradural and extradural sacral nerve root stimulation were measured to determine the optimal location and size for sacral nerve root electrodes. Part II. Sacral nerve roots were stimulated via wire electrodes introduced into the S2 foramina. Ten dogs (five dogs in part I and five dogs in part II). Part I. Microtip pressure transducers were used to monitor bladder and urethral pressure responses to sacral nerve root stimulation with tripolar hook electrodes. After euthanasia, sacral nerve root, and spinal canal dimensions were measured. Part II. Bipolar electrical stimulation of the sacral nerve roots was performed by introducing wire electrodes into the S2 foramina. Bladder and urethral pressures were recorded as in part I. Part I. Stimulation of SI produced an increase in urethral, but not bladder, pressure. Stimulation of S2 or S3 produced increases in bladder pressure and decreases in urethral pressure. Intradural and extradural nerve roots were not significantly different with respect to nerve dimensions or effects on nerve stimulation. Part II. High bladder pressures were achieved, but effective voiding could not be produced, primarily because of urethral resistance. Part I. Extradural implantation was determined to be the most appropriate site based on ease of dissection, nerve root dimensions, and decreased risk of iatrogenic trauma. Enough space is available to implant two to four tripolar spiral nerve cuffs. Part II. Transforaminal sacral nerve root stimulation did not effectively empty the bladder. Clinical trials in paraplegic dogs are necessary to evaluate the number of sacral nerve cuff electrodes necessary to produce effective bladder emptying.

Human gallbladder pressure and volume: validation of a new direct method for measurements of gallbladder pressure in patients with acute cholecystitis.

Increased gallbladder (GB) pressure is probably a part of the pathogenesis of acute cholecystitis, and measurements of GB pressure might therefore be of interest. The aim of this study was to validate a microtip pressure transducer for intraluminal GB pressure measurements. In vitro precision and accuracy was within 0.2 mmHg, (SD) and 0.6 +/- 0.1 mmHg (mean +/- SD), respectively. Pressure rise rate was 24.8 +/- 5.5 mmHg s-1. Zero drift was in the range 0.3 +/- 0.4 to 0.8 +/- 0.9 mmHg (mean +/- SD). GB pressure was investigated in 16 patients with acute cholecystitis treated with percutaneous ultrasonically guided cholecystostomy. Basal intraluminal GB pressure was 8.9 mmHg (2.1-12.2 mmHg; n = 9, open cystic duct) and 1.8 and 5.8 mmHg (n = 2, closed cystic duct). There was no significant difference between two different measurements in the same patients (n = 5). The pressure was significantly influenced by respiration (n = 8) and the pressure seems to be higher in the sitting position than in the supine position (n = 5). Cystic duct opening pressure was 10.4, 11.2 and 16.8 mmHg (n = 3). Pressure-volume responses showed that the GB up to a certain volume could accommodate increases in intraluminal volume with only slight changes in intraluminal pressure (n = 4). Except for the zero drift, this piece of equipment seemed to fulfil the requirements of being able to measure pressure in the GB. In vivo measurements showed a good clinical reproducibility of the method, and also that respiration and patient posture influenced the pressure measurements. Further, a GB pressure-volume relationship was demonstrated, and the possibility of a cystic duct opening pressure was described.

Lusitropic effects of a Ca2+ sensitization with a new cardiotonic agent, MCI-154, on diseased human hearts

Recognition of the problems of conventional cardiotonic agents has led to an interest in drugs that produce a positive inotropic action by altering the responsiveness of myofilament to Ca2+ (i.e., Ca2+ sensitizing agents). The importance of the effects of these compounds on left ventricular (LV) systolic function has been emphasized, whereas the effect of them on LV diastolic function is still problematic. To investigate the lusitropic action of a novel Ca2+ sensitizing agent, MCI-154, we compared the effects of MCI-154 on LV relaxation and filling dynamics with those of dobutamine in diseased human hearts. We assessed the slope of the end-systolic pressure-volume relation (Emax), the time constant of LV pressure decay (Tw) and the maximum rate of LV early filling (dV/dtmax) before and after the infusion of dobutamine (n = 10) or MCI-154 (n = 9). LV volume and pressure were measured by a conductance catheter and a micro-tip catheter pressure transducer. When both agents increased Emax comparably, dobutamine decreased Tw from 51 to 37 ms and MCI-154 decreased Tw from 54 to 44 ms. The decrease of Tw with MCI-154 was less than that with dobutamine (17 vs. 29%, P < 0.05). At the same time, dobutamine increased dV/dtmax per end-diastolic volume (dV/dtmax/V) from 2.84 to 3.88 s-1, whereas MCI-154 did not. Diastolic properties were not compromised by MCI-154, though the alteration in them with MCI-154 was less than that with dobutamine when MCI-154 increased LV contractile state to the same extent as dobutamine. The present results suggest that MCI-154 would be an ideal Ca2+ sensitizing agent that enhances force during systole without impairing diastolic function.

Mechanical effects of respiration and stepping on systolic arterial pressure variability during treadmill exercise

To evaluate the changes produced by maximal dynamic exercise in the rhythmic components of systolic arterial pressure variability. We studied seven normotensive subjects during different levels of a modified treadmill test (Bruce protocol, up to stage 4). Arterial pressure was measured directly by a high-fidelity microtip pressure transducer. Spectral analysis provided two main oscillatory components of systolic arterial pressure variability, a low-frequency component related to the sympathetic-mediated neural control of vasomotion and a high-frequency component reflecting the mechanical effects of respiration on blood pressure. The low-frequency component increased at the beginning of exercise and remained stable thereafter, while the high-frequency component increased progressively. A third rhythmic component (very high frequency) with a frequency higher than respiration and synchronous with the rate of the subjects' footsteps, which was undetectable on a visual inspection of analog tracings, became progressively more apparent, reaching its maximum at exercise stage 4. These findings emphasize the importance of high-fidelity techniques and computer analysis for the evaluation of arterial pressure variability in dynamic conditions.

Effects of endurance training on left ventricular performance: a study in anaesthetized rabbits.

Endurance training is known to increase ventricular performance during exercise and to decrease resting heart rate. The aim of this study was to evaluate a model for endurance training in rabbits and to study the effects of endurance training on local myocardial performance in the left ventricle during resting conditions. One group of rabbits underwent a 10-week exercise training programme. The rabbits trained 5 days a week on a treadmill. Training periods increased gradually from 15 min to 1 h with increments in speed from 0.5 to 1.2 km h-1. After the training programme the rabbits were anaesthetized and studied as acute open-chest preparations. A micro-tip pressure transducer was introduced via apex to the left ventricle and two pairs of ultrasonic crystals were implanted in the left anterior wall to measure segment lengths. One pair measured shortening in the circumferential direction whereas the other pair measured shortening in the longitudinal direction. Heart rate was lower in the trained group (n = 5), 172 +/- 9 beats min-1 (mean +/- SEM), compared with 235 +/- 19 beats min-1 in the control group (n = 8) (P < 0.02). Stroke volume, measured by radio-nuclidelabelled microspheres, was greater in the trained rabbits compared with controls (P < 0.03). Shortening in both segments was of similar magnitude for the trained and control groups. End-systolic pressure-length relations (ESPLR) obtained by occlusion of the descending aorta (balloon catheter) showed reduced slopes for longitudinal segments in the trained group compared with the control group (P < 0.05). We conclude that this endurance training programme in rabbits can be used to study myocardial effects of endurance training. Furthermore, the less steep slope of ESPLRs for the longitudinal segment in the trained animals might indicate a structural myocardial remodelling and increased contractile reserve that might be recruited during adrenergic stimulation in the trained group.