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Biomedical subjects

R S Reneman

Publications and source records attributed to R S Reneman.

At least 73 records · Page 4Linked to original sources
PubMed1997

Heat stress protects aged hypertrophied and nonhypertrophied rat hearts against ischemic damage.

To explore the effects of heat stress (HS) in aged hypertrophied and nonhypertrophied rat hearts, postischemic recovery was investigated 15 mo after aortic constriction (AoB) or sham operation (Sham). Twenty-four hours after HS (42 degrees C; 15 min) or control treatment (normothermia), global ischemia was induced for 20 min in isolated AoB hearts and for 20 or 30 min in Sham hearts. After HS, postischemic recovery after 20-min ischemia in AoB hearts and 30-min ischemia in Sham hearts, respectively, was significantly better than in corresponding controls. In AoB hearts, cardiac output (CO), left ventricular developed pressure (LVDP), and the positive maximal first derivative of left ventricular pressure (+dP/dtmax) recovered to 33 +/- 26 (means +/- SD), 87 +/- 5, and 72 +/- 12%, respectively, after HS and to 5 +/- 8, 22 +/- 39, and 17 +/- 29% of preischemic values, respectively, in controls. Postischemic arrhythmias were significantly reduced in HS hypertrophied hearts, but creatine kinase (CK) loss was not reduced. In Sham hearts subjected to 30 min ischemia, CO, LVDP, and +dP/dtmax recovered to 20 +/- 20, 75 +/- 8, and 59 +/- 15%, respectively, after HS and to 3 +/- 8, 21 +/- 32, and 16 +/- 32% of preischemic values, respectively, in controls. Duration of arrhythmias and CK loss were not reduced in the heated hearts. When Sham hearts were subjected to only 20-min ischemia, functional recovery was not different in HS and control hearts, indicating that HS pretreatment extends the ischemic interval before irreversible injury occurs in the heart. In all HS Sham hearts, the myocardial 72-kDa HS protein (HSP 70) content was significantly increased. However, in HS AoB hearts, HSP 70 levels were not significantly different from the values in the control hearts. These results indicate that HS pretreatment induces cardioprotection in aged hypertrophied and nonhypertrophied rat hearts, which, however, cannot be unequivocally related to increased HSP 70 tissue contents.

Animals↗
PubMed1997

Venous myogenic tone and its regulation through K+ channels depends on chronic intravascular pressure.

In this study, we compared the level of myogenic tone and its negative-feedback control through specific K+ channels in two types of human veins (saphenous [SV] and cephalic [CV] veins), which experience different ranges of pressure in vivo. We also investigated whether an experimental model of increased venous pressure in rats exposed to head-up tilt for 2 weeks produced changes similar to those observed in the human veins. Cylindrical vein segments were cannulated, their diameters were measured, and the intraluminal pressure was set at different levels (2 to 30 mm Hg) in vitro. Acetylcholine test showed that during the regular harvesting process 76% of the human SVs exposed for coronary bypass grafts had no functional endothelium. We found significant myogenic tone in the human SV, where the in vivo pressure is high, but it was not present in the human CV, where the in vivo pressure is low. The nonspecific K+ channel antagonist, tetraethylammonium (TEA), decreased the diameter of the human SV but not the CV. Iberiotoxin and 4-aminopyridine, blockers of the Ca(2+)-sensitive (KCa) and voltage-gated K+ (KV) channels, also decreased the diameter of the human SV by 10.2 +/- 4.8% and 19.5 +/- 4.7%, respectively. In the rat SV, significant myogenic tone was found, but TEA had no effect, even after 2 weeks of in vivo pressure increase in the hindlimb by head-up tilt. We conclude that (1) an increased venous myogenic tone correlates with higher chronic intraluminal pressure loads, (2) KCa and KV channels counterregulate the myogenic tone in human, but not in rat, saphenous vein, (3) the counterregulatory effect is more effective at high than at low intraluminal in vitro pressure levels, and (4) its development is probably a long-term process.

Acetylcholine↗
PubMed1996

The spinal component to skin blood flow abnormalities in reflex sympathetic dystrophy.

OBJECTIVE: To determine whether the mechanisms of reflex sympathetic dystrophy, a neuropathic pain syndrome characterized by skin blood flow abnormalities associated with sympathetic vasoconstrictor and antidromic vasodilator mechanisms, are solely of peripheral origin or have an additional spinal component and act exclusively through neural or also involve humoral pathways. PATIENTS: The 54 patients with unilateral reflex sympathetic dystrophy were divided into the following three stages according to their perception of skin temperature in the clinically affected hand: stage I, stationary warmth sensation; stage II, intermittent warmth and cold sensation; and stage III, stationary cold sensation. METHODS: Investigation of basal skin blood flow and vasoconstrictive response to dependency of skin microvessels in the clinically unaffected hand and the clinically affected hand of patients with reflex sympathetic dystrophy and the left hand of 16 control subjects. Microcirculation was investigated at the predominantly neurally controlled thermoregulatory level (Doppler laser flowmetry) and at the predominantly humorally controlled nutritive level (capillary microscopy). RESULTS: In the clinically unaffected hand, at the thermoregulatory level of the microcirculation: (1) basal skin blood flow was increased at stage I compared with the control subjects, whereas no differences could be observed at this stage compared with the clinically affected hand; (2) the vasoconstrictive response to dependency (defined as skin blood flow at heart level divided by skin blood flow in the dependent position) was attenuated at stage I compared with the control subjects, whereas no differences could be observed at this stage compared with the clinically affected hand; and (3) basal skin blood flow and the vasoconstrictive response to dependency did not differ from the control subjects at stages II and III. In the clinically unaffected hand, at the nutritive level, no differences could be observed at any stage of the syndrome compared with the control subjects. CONCLUSIONS: This study indicates that there is a spinal component to microcirculatory abnormalities at stage I of the reflex sympathetic dystrophy syndrome that most likely acts through neural (antidromic vasodilator) mechanisms and that may be initiated by traumatic excitation of a peripheral nerve on the clinically affected side.

Adult↗
PubMed1996

Inability of the heat-shocked heart to adjust its pre-ischemic and post-ischemic performance to variable loading conditions.

The aim of the present study was to investigate whether the pre-ischemic and post-ischemic hemodynamic function of the heat-shocked rat heart is affected by changes in afterload and extracellular calcium concentrations ([Ca2+]e). Experiments were performed on isolated, ejecting Lewis rat hearts 24h after in vivo heat shock (LewHS) or anesthesia alone (Lewc). In vitro hearts were subjected to 60 min normoxic perfusion, 45 min global ischemia, and 60 min of reperfusion. Pre-ischemic and post-ischemic left ventricular performance was evaluated at [Ca2+]e ranging between 0.65 and 3.0 mM at afterloads of 8.0 kPa and 16.0 kPa. At 8.0 kPa, pre-ischemic function was comparable in LewHS and Lewc at [Ca2+]e equal to or above 2.25 mM. At lower [Ca2+]e, i.e., 0.65 and 1.25 mM, cardiac output (CO) was significantly lower in LewHS than in Lewc hearts. At 16.0 kPa, significantly lower CO values were found in LewHS than Lewc hearts at all [Ca2+]e levels. During post-ischemic reperfusion under basal conditions (8.0 kPa; [Ca2+]e = 2.25 mM) a significantly better recovery was observed in LewHS than Lewc hearts, persisting at [Ca2+]e equal to 1.25 mM. However, either by lowering [Ca2+]e to 0.65 mM or increasing afterload to 16.0 kPa (at all [Ca2+]e), heat shock-associated improvement of post-ischemic performance disappeared. In conclusion, pre-ischemic left ventricular performance of the isolated heat-shocked heart is depressed when it performs at low [Ca2+]e or against a relatively high afterload. The heat shock-mediated improvement of post-ischemic function is only present at relatively low afterload levels in combination with normal extracellular calcium concentrations.

Adaptation, Physiological↗
PubMed1996

A noninvasive method to estimate arterial impedance by means of assessment of local diameter change and the local center-line blood flow velocity using ultrasound.

Vascular impedance is defined as the ratio between the frequency components of the local blood pressure waveform and those of the local blood volume flow waveform. Assessment of vascular impedance is, for example, important to study heart load and distal vascular bed vasomotricity. However, only a few studies on vascular impedance have been performed in humans because pulsatile pressure and volume flow waveforms, simultaneously recorded at the same location, are difficult to obtain noninvasively. The noninvasive assessment of arterial impedance as described in this study is based on the replacement of the pressure waveform by the distension (change in diameter) waveform and the volume flow waveform by the center-line blood flow velocity waveform. Both waveforms can simultaneously and accurately be assessed by means of pulsed ultrasound. It will be shown that, depending on the Womersley number, the volume flow waveform may be replaced by the center-line blood flow velocity waveform for a given frequency range and that the pressure waveform may be replaced by the distension waveform for a wide frequency range. The validation of the proposed ultrasound method was performed through an in vitro study in a flow model with a distensible tube terminated with a hydraulic load (modified windkessel model). It is shown that, in vitro, the proposed method gives the same results as the local spectral pressure-flow relationship.

Arteries↗
PubMed1996

Skin blood flow disturbances in the contralateral limb in a peripheral mononeuropathy in the rat.

Electrical excitation of nociceptive afferents in an extremity has been demonstrated to increase skin blood flow in the contralateral extremity. Hence, one would expect that loose sciatic nerve ligation, which induces an experimental painful peripheral neuropathy, may also provoke a vasodilator response in the contralateral hindpaw. On the non-ligated side, such a response may involve inhibited skin vasoconstrictor activity as well as neurogenically mediated active vasodilation. We studied skin blood flow changes in the rat hindpaw consequent to contralateral loose sciatic nerve ligation. After ligation, we also investigated whether blockade of afferent input from the ligated sciatic nerve to the spinal cord, by means of lidocaine, overrules the vasodilator response in the non-ligated paw. On the non-ligated side, we assessed the vasoconstrictor response of skin microvessels to cooling of the rat abdomen as a measure of skin vasoconstrictor activity in this paw. In order to investigate the involvement of sensory and/or non-sensory nerve fibers in the non-ligated sciatic nerve on skin blood flow abnormalities in the non-ligated paw, we studied the influence of blockade of these fibers through successive capsaicin and lidocaine application. We show that loose ligation of the sciatic nerve induces a vasodilator response in the contralateral hindpaw, which is completely abolished by blockade of afferent input from the ligated sciatic nerve. From day 1 after ligation, skin vasoconstrictor activity in the non-ligated paw was reduced, as indicated by an impaired vasoconstrictor response to cooling of the rat abdomen. Besides, blockade of sensory but not of non-sensory nerve fibers on the non-ligated side attenuated the vasodilator response in this paw. The data presented here indicate that loose ligation of the rat sciatic nerve induces a vasodilator response in the contralateral hindpaw. On the non-ligated side, this vasodilator response may involve inhibition of skin vasoconstrictor activity, as well as antidromically acting sensory nerve fibers.

Animals↗
PubMed1996

Reflex sympathetic dystrophy: does sympathetic dysfunction originate from peripheral neuropathy?

BACKGROUND: Sympathetic dysfunction in reflex sympathetic dystrophy (RSD) has been purported to consist of an afferently-induced increase in efferent sympathetic nerve impulses (somato-sympathetic reflex) and/or denervation-induced supersensitivity to catecholamines. In addition, both the central and peripheral nervous systems have been claimed to be involved. It was the aim of this study to obtain more insights into these underlying mechanisms. METHODS: In the affected extremeties of 42 patients with RSD we investigated as indirect measures of sympathetic (dys)function: (1) skin blood flow and the vasoconstrictive response to dependency of skin microvessels by means of laser Doppler flowmetry (distal to the site of trauma), (2) relative distention of the brachial artery and changes in relative distention consequent to a cold pressor test by means of ultrasonic vessel wall tracking (proximal to the site of trauma), and (3) arterial blood pressures by means of the Finapres technique. Both provocation tests induce a sympathetically mediated response. Patients were divided into three categories according to their perception of skin temperature in their injured limb (stage I, stationary warmth sensation; stage II, intermittent warmth and cold sensation; or stage III, stationary cold sensation). RESULTS: Distal to the site of trauma, when compared with controls, skin blood flow was increased at stage I and decreased at stages II and III, whereas the vasoconstrictive response to dependency was impaired at all three stages. Proximally, when compared with controls, relative distention of the brachial artery and its response to the cold pressor test were decreased at all three stages. No differences were observed in pulse pressure between patient groups and controls. CONCLUSIONS: These results suggest that sympathetic dysfunction in extremities of patients with RSD distal to the site of trauma consists of hypersensitivity to catecholamines at stages II and III as a result of autonomic denervation at stage I, whereas proximal to the site of trauma sympathetic nerve impulses may be increased at all three stages.

Adult↗
PubMed1996

Influence of partial nerve injury in the rat on efferent function of sympathetic and antidromically acting sensory nerve fibers.

OBJECTIVE: To investigate how partial injury of a large peripheral nerve affects efferent (vasomotor) function of sympathetic and antidromically acting sensory nerve fibers. DESIGN: Randomized animal study. MATERIALS AND METHODS: We assessed, by laser Doppler flowmetry, skin blood flow (SBF) in the hindpaw of male Lewis rats before partial injury of the ipsilateral sciatic nerve (through loose ligation) as well as at an early stage (day 4) and at a later stage (day 21) after this procedure. This procedure has been reported to induce signs and symptoms like those observed in patients with causalgia. At the two time points after nerve injury, SBF was assessed before and after (chemical) blockade of sensory and nonsensory (sympathetic) sciatic nerve fibers. Furthermore, at day 21 we measured the density of sympathetic nerve fibers in footpad arteries. MEASUREMENTS AND MAIN RESULTS: At day 4, compared with preligation values, we observed an increase in SBF that was reduced by blockade of sensory nerve fibers. Subsequent blockade of nonsensory nerve fibers further reduced SBF. At day 21, SBF was decreased compared with preligation values. Blockade of sensory nerve fibers further reduced SBF, and subsequent blockade of nonsensory nerve fibers did so as well. The density of sympathetic nerve fibers was lower on the ligated side than on the nonligated side. CONCLUSIONS: Partial injury of the rat sciatic nerve causes an ipsilateral increase in SBF at an early stage, which is followed by a decrease at a later stage. At both stages, antidromically acting sensory and orthodromically acting nonsensory (sympathetic) nerve fibers are involved in the vasodilator response. At a later stage, however, neurogenic vasodilator mechanisms are overruled by a nonneurogenic vasoconstrictor mechanism. The latter may consist of supersensitivity of skin microvessels to catecholamines consequent to reduced neurogenic disposition of catecholamines.

Animals↗
PubMed1996

Regional wall mechanics in the ischemic left ventricle: numerical modeling and dog experiments.

The mechanics of the ischemic left ventricle during a complete cardiac cycle were simulated using a finite-element model accounting for the thick-walled ventricular geometry, the fibrous nature of the myocardial tissue, and the dependency of active muscle fiber stress on time, strain, and strain rate. Ischemia was modeled by disabling the generation of active stress in a region comprising approximately 12% of total wall volume. In the model simulations, the approximately 12% reduction in the amount of normally contracting tissue resulted in an approximately 25% reduction in stroke work compared with the normal situation. The more-than-proportional loss of stroke work may partly be attributed to storage of elastic energy in the bulging ischemic region. Furthermore the mechanical performance in the nonischemic border zone deteriorated because of reduced systolic fiber stress (if fibers were in series with those in the ischemic region) or reduced fiber shortening (if fibers were parallel). The deformation pattern of the ventricle was asymmetric with respect to the ischemic region because of the anisotropy of the myocardial tissue. Epicardial fiber shortening in and around the ischemic region, as predicted from the model simulations, was in qualitative agreement with shortening, as measured in four dogs in which ischemia was induced by occlusion of the distal part of the left anterior interventricular coronary artery.

Animals↗
PubMed1996

A technique to assess aortic distensibility and compliance in anesthetized and awake rats.

A noninvasive ultrasonic technique, based on tracking arterial wall displacements with a vessel wall-tracking device attached to a conventional B-mode imager, to assess end-diastolic aortic diameter (d) and aortic diameter changes during the cardiac cycle (delta d) in anesthetized and awake rats is presented. From these parameters and invasively measured aortic pulse pressure (delta P), aortic distensibility and compliance, the relative and absolute increases in lumen cross-sectional area for a given increase in delta P, respectively, can be calculated. d, delta d, and delta P could be determined with good intra-session (variations per day) and inter-session (variations between days) coefficients of variation (CV). The CVs for delta d were smaller in awake (4.6-6.0%) than in anesthetized rats (7.9-11.0%), probably due to variations in delta P during anesthesia (CV: 9.0-12.3%). The CVs for d in awake (3.3-6.5%) and anesthetized rats (2.6-5.0%) were comparable. In awake rats the CV for delta d, but not for d, increased after implantation of the aortic catheter. It is concluded that d, delta d, and delta P of the aorta can be reliably measured noninvasively in anesthetized and awake rats, allowing the in vivo assessment of aortic distensibility and compliance. The technique is sensitive enough to detect effects of agents on aortic wall properties.

Adrenergic alpha-Agonists↗
PubMed1996

Calcium homeostasis in cardiomyocytes isolated from heat-shocked rats.

The cellular mechanism of heat shock-mediated cardioprotection is still under debate. Because heat pretreatment negatively affects the normoxic left ventricular contractile performance in vitro when the extracellular Ca2+ concentration ([Ca2+]o) is relatively low (0.65-1.25 mM), the intracellular Ca2+ homeostasis was studied in more detail in cardiomyocytes isolated from adult rats 24 h after heat stress (42 degrees C for 15 min) or anesthesia (control). Sensitivity to Ca2+ overload was assessed by exposure to veratridine (quiescent cells) or to [Ca2+]o ranging from 0.125 to 20 mM in quiescent and paced cardiomyocytes. The fraction of irreversibly hypercontracted cells was not different between groups. The fura-2 fluorescence ratio (I340/I380), which was used as a measure for cytoplasmic Ca2+ concentration ([Ca2+]i) in quiescent cells after exposure to [Ca2+]o (0.5-10 mM), was also not different between groups. Myofilament Ca2+ sensitivity was assessed in paced (0.5 Hz) cells by simultaneous measurement of [Ca2+]i transients and cell shortening. At stepwise increases of [Ca2+]o from 1 to 10 mM, these parameters were comparable between groups. The diastolic cell length shortened progressively and equally in both groups after increasing [Ca2+]o. However, within 2 min of return from 10 to 1 mM [Ca2+]o, cells from heat-shocked rats retained the same length, whereas cells from control rats contracted further (P = 0.05). These data suggest that heat stress improves relaxation after challenge with high [Ca2+]o.

Animals↗
PubMed1996

Regional electrical activation and mechanical function in the partially ischemic left ventricle of dogs.

During normoxia, asynchronous electrical activation of the left ventricle significantly affects regional mechanical performance. Regional fiber strain and external work during the ejection phase are found to be lower in early-activated than in late-activated regions. Because electrical activation is known to be delayed during ischemia, the present study was designed to investigate the influence of this electrical asynchrony on regional fiber strain, if any, during moderate and severe myocardial ischemia. Regional electrical activation time (t(ea)) and fiber strain during the ejection phase (ef,e) were measured in the epicardial layers of the left ventricular anterior wall during normoxia and after 15 min of total occlusion (n = 5) or 30, 60, 120, and 180 min of partial occlusion of the left anterior interventricular coronary artery (LAICA; n = 11). Myocardial blood flow (MBF) was assessed with radioactive microspheres. Blood gases, pH, and lactate and Pi contents were determined in arterial, local venous, and coronary sinus blood. During normoxia, t(ea) and ef,e were similar in various epicardial regions of the left ventricular anterior wall. During total LAICA occlusion, in the ischemic area, subepicardial MBF decreased from 0.86 +/- 0.36 (SD) to 0.18 +/- 0.09 ml.g-1.min-1 and subepicardial ef,e decreased from -0.11 +/- 0.02 to -0.01 +/- 0.01, whereas the delay in t(ea) between the normoxic basal-lateral and ischemic apical-medial areas increased slightly but significantly from 1.9 +/- 8.0 to 7.5 +/- 8.0 ms. After a 180-min partial occlusion of the LAICA, in the ischemic area, subepicardial MBF decreased from 0.62 +/- 0.17 to 0.49 +/- 0.18 ml.g-1.min-1 and ef,e decreased from -0.08 +/- 0.01 to -0.03 +/- 0.01. No significant change in the difference in t(ea) between the normoxic and ischemic areas could be detected (5.1 +/- 4.8 and 5.2 +/- 5.8 ms in the control situation and after 180-min partial occlusion, respectively). These findings indicate that in the ischemic epicardium 1) mechanical function is more affected than electrical impulse conduction and 2) delayed activation, if any, is accompanied by decreased instead of increased fiber strain, as found in the normoxic left ventricle.

Animals↗
PubMed1995

Biophysical principles of vascular diagnosis.

Visual inspection of the spectral composition of the Doppler signal as a function of time (sonogram) has been very helpful in detecting the presence of stenoses with substantial lumen narrowing causing abnormal flow patterns. Attempts to grade a stenosis based on the spectral width at peak systole were less successful because of the obscuring effects of the ultrasound beam width with respect to lumen diameter, dimensions of the sample volume, angle of observation, and spectral broadening due to vessel branching and bends. The introduction of color flow imaging has put emphasis on the width of the velocity distribution and the consistency of flow patterns within the region of interest. This technique requires a high resolution in space, velocity, and time necessitating the development of new velocity estimation algorithms. The observed flow patterns can be related to the echogenicity and local wall thickness of peripheral vessels. In addition, the displacement behavior of arterial walls over time provides information about the elasticity of the wall. Knowing the instantaneous velocity of arterial walls, it becomes possible to suppress selectively and adaptively the arterial wall contribution, allowing for the assessment of low blood flow velocities close to the wall and, hence, of wall shear rate. The latter development enables the study of the interaction of blood velocities and the metabolism and structure of the walls, providing possible clues for atherogenesis.

Algorithms↗