Biomedical subjects

S Magder

Publications and source records attributed to S Magder.

At least 55 records · Page 3Linked to original sources

PubMed1995

Pressure-flow relationships in in vitro model of compartment syndrome.

Compartment syndrome is a condition in which an increase in intramuscular pressure decreases blood flow to skeletal muscle. According to the Starling resistor (i.e., vascular waterfall) model of blood flow, the decrease in flow could occur through an increase in arterial resistance (Rart) or an increase in the critical closing pressure (Pcrit). To determine which explains the decrease in flow, we pump perfused a canine gastrocnemius muscle placed within an airtight box, controlled box pressures (Pbox) so that flow ranged from 100 to 50%, and measured Pcrit, Rart, arterial compliance, small venular pressure (measured by the double-occlusion technique), and venous pressure. An increase in Pbox limited flow mainly through an increase in Pcrit (75-85%), with only small changes in Rart (15-25%) and no change in arterial compliance. Increases in Pbox also produced a vascular waterfall in the venous circulation, but small venular transmural pressure always remained less than control levels. We conclude that increases in Pbox mostly limit blood flow through increases in Pcrit and that Rart plays a minor role. Transmural pressure across the small venules decreases with increases in intramuscular pressure, which contradicts the currently held belief that compartment syndrome is due to a cycle of swelling-ischemia-swelling.

Animals↗

PubMed1995

Maximal vasodilation does not eliminate the vascular waterfall in the canine hindlimb.

Previous studies have shown that blood flow through skeletal muscle is regulated by changes in an arteriolar vascular waterfall [critical pressure (Pcrit)] and a proximal (arterial) resistance (Ra) element. To determine whether Pcrit still exists during maximal vasodilation, we pump perfused vascularly isolated canine hindlimbs. We set outflow pressure to zero and measured Pcrit, perfusion pressure (Pper), and regional elastic recoil pressure (Pcl; by a stop-flow technique) and calculated both Ra and venous resistance before and after maximal vasodilation with adenosine and nitroprusside. Pcrit was 56.4 +/- 5.1 mmHg before vasodilation and decreased to 11.0 +/- 0.6 mmHg after vasodilation, which was less than the downstream pressure in the venous compliant region (Pel). Therefore, Pcrit should not have affected flow at normal Pper levels under vasodilated conditions. However, we could still measure Pcrit because our technique allowed Pel to decline and Pcrit becomes apparent once Pel < Pcrit. With vasodilation, Ra decreased to < 8.1 +/- 2.6% and Rv decreased to 41 +/- 6% of control values. In contrast to the nonvasodilated vasculature, increases in venous pressure during maximal vasodilation caused immediate increases in Pper. This also suggests that the vascular waterfall is inactive under conditions of maximal vasodilation. We conclude that a small arteriolar Pcrit is still present in the maximally vasodilated hindlimb but is less than the downstream pressure and does not affect flow under these conditions.

Adenosine↗

PubMed1995

Venous mechanics of contracting gastrocnemius muscle and the muscle pump theory.

The time constant of venous drainage (tau v) is an important determinant of the return of blood to the heart. The lower the tau v, the higher the flow for a given volume. To determine whether the tau v of muscle decreases during muscle contraction, we anesthetized dogs with pentobarbital sodium and mechanically ventilated them. We isolated the vasculature of the gastrocnemius muscle and attached the muscle to a force transducer. The muscle was pump perfused, and flows were measured with electromagnetic flow probes on the artery and vein. Pressure in the venous compliant region (Pel) was obtained by simultaneously occluding the artery and vein. Changes in volume (delta V) were produced by changing inflow and obtaining the integral of the difference between inflow and outflow. The tau v was obtained from delta V divided by change in flow. Compliance was calculated from delta V divided by change in Pel from before to after a change in flow. The venous resistance was calculated from tau v divided by venous compliance. The muscle was set at the optimal length, and contractions were produced by stimulating the nerve to the muscle with supramaximal voltage at either 1- or 5-Hz trains with stimulations at 20 Hz, 0.2-ms duration, and duty cycle of 0.25. The tau v at rest was 4.06 +/- 2.16 s and decreased to 2.44 +/- 1.07 s (P < 0.05) at 1 Hz and to 1.81 +/- 0.4 s at 5 Hz. There were no significant changes in venous compliance or venous resistance. In conclusion, muscle contractions can reduce the time constant of venous drainage of muscle and could thereby contribute to the increased venous return and cardiac output during exercise.

Animals↗

PubMed1994

Phrenic afferent stimulation by bradykinin and the distribution of the inspiratory motor drive.

Activation of thin-fiber (groups III and IV) afferents from the diaphragm using capsaicin or ischemia increases the respiratory muscle activity. To assess whether bradykinin causes similar effects, we injected boluses of bradykinin into the phrenic artery of in situ, isolated and innervated left hemi-diaphragm preparations in 8 alpha-chloralose anesthetized, vagotomized, mechanically ventilated dogs. Inspiratory motor drive during spontaneous breathing attempts was assessed from the integrated EMG activity of several inspiratory muscles. Fifty micrograms of bradykinin increased peak integrated EMG activities of alae nasi to 110%, genioglossus to 189%, left diaphragm to 115% (P < 0.05) and parasternal to 109% (P < 0.01) of baseline activity 60 sec after the injection. Inspiratory time decreased by 10% (P < 0.01). The mean arterial blood pressure increased by about 10 mmHg. Responses were similar with 10, 25 and 100 micrograms of bradykinin. After left phrenicotomy, bradykinin did not affect inspiratory muscle EMG or respiratory timing. In conclusion, thin-fiber phrenic afferent activation by bradykinin exerts an excitatory but disproportionate influence on the inspiratory motor drive.

Animals↗

PubMed1994

Influence of neuropeptide Y on regional vascular capacitance in dogs.

To determine the effect of neuropeptide Y (NPY) on regional vascular capacitances, we measured the regional blood volume (Vb), unstressed volume (V0), blood flow distribution, venous compliance (Cv), venous resistance (Rv), and the time constant of venous drainage (tau v) in the splanchnic and extrasplanchnic circulation of 13 dogs anesthetized with chloralose. Cardiac output was kept constant with circulatory bypass. The extrasplanchnic region was further divided into superior vena caval (SVC) and inferior vena caval (IVC) regions. Vb was measured in the splanchnic and SVC regions using indicator dilution curves and the mean transit times. Changes in venous outflow pressures were used to change regional volumes, and a stop-flow procedure was used to obtain the regional venous filling pressures. This allowed construction of pressure-volume (P-V) curves and the calculation of Cv, Rv, and tau v. Hexamethonium chloride was infused throughout the experiment to prevent autonomic reflexes. Sham injections had no effects on four dogs. In nine dogs, NPY (bolus of 7.4 x 10(-8) or 14.8 x 10(-8) mol and 0.37 mol/min infusion) increased arterial blood pressure from 98.4 +/- 4.2 to 121.3 +/- 6.9 mmHg (P < 0.001), decreased splanchnic Vb from 31.6 +/- 2.1 to 24.9 +/- 1.8 ml/kg (P < 0.01), and decreased splanchnic V0 from 21.8 +/- 2.6 to 12.1 +/- 2.2 ml/kg (P < 0.001). SVC volumes were not affected by NPY. Extrasplanchnic Cv increased with NPY, but splanchnic Cv did not change. Thus exogenous NPY infusion decreases splanchnic capacitance, which could potentially increase venous return and cardiac output.

Animals↗

PubMed1994

Effects of heat stress on vascular capacitance.

In dogs and humans, heat stress is associated with an increase in cardiac output that sustains blood flow to heat-dissipating organs. Because cardiac output and venous return are equal in the steady state, the circulation must also adjust in heat stress to allow the venous return to increase. To analyze these adjustments, we measured blood volumes, unstressed volumes, blood flow distribution, venous compliance, venous resistance, and the time constant of venous drainage of the splanchnic and extrasplanchnic vascular beds in dogs anesthetized with alpha-chloralose at normal and at high core temperatures. We repeated the measurements at high core temperatures with ganglionic blockade, alpha-adrenergic receptor blockade, or beta-adrenergic receptor blockade to determine the efferent neurohumoral pathway. When core temperature was increased from 37.8 +/- 0.2 to 41.9 +/- 0.1 degrees C, total splanchnic blood volume decreased 23% (4.6 +/- 1.4 ml/kg) and splanchnic unstressed volume decreased 38.5%. None of the other determinants of venous return changed. Ganglionic blockade shifted the total and unstressed splanchnic blood volume during heat stress back to normothermic values. However, beta- and alpha-blockade did not affect splanchnic volumes. We conclude that a decrease in splanchnic unstressed volume is an important factor for the increased venous return during heat stress. Although mediated through sympathetic ganglions, this decrease is not abolished by alpha- or beta-receptor blockade.

Animals↗

PubMed1993

A physical chemical approach to the analysis of acid-base balance in the clinical setting.

We evaluated the clinical application of a model of acid-base balance, which is based on quantitative physical chemical principles (Stewart model). This model postulates that acid-base balance is normally determined by the difference in concentration between strong cations and anions (strong ion difference [SID]), PCO2, and weak acids (primarily proteins). We measured electrolytes and blood gases in arterial blood samples from 21 patients in a medical or surgical intensive care unit or emergency room of a tertiary care hospital. The measured SID frequently differed from SID calculated from the measured blood components, which indicates that unmeasured cations or anions are present; these could not be accounted for by lactate, ketones, or other readily identifiable ions. We used an approach to acid-base analysis that is based on changes in base excess or deficit due to changes in: (1) free water as assessed by [Na+]; (2) in [Cl-]; (3) protein concentration; and (4) "other species" (ie, anion and cations other than [Na+], [K+], and [Cl-]). The contribution of "other species" was obtained from the difference between the SID measured and that predicted from Stewart's equation. It could also be calculated from the difference between the standard Siggaard-Anderson calculation of base excess and base excess attributable to free water, [Cl-], and proteins (ie, base-excess gap). Our results indicate that the SID gap, base excess gap, and anion gap reflect the presence of unmeasured ions, and both the anion-gap and base-excess gap provide readily available estimates of the SID gap. This provides a simple bedside approach for using the Stewart model to analyze the nonrespiratory component of clinical acid-base disorders and indicates that, in addition to unmeasured anions, unmeasured cations can be present.

Acid-Base Equilibrium↗

PubMed1993

Effect of carotid sinus stimulation on resistance and critical closing pressure of the canine hindlimb.

Sympathetically mediated changes in blood pressure are thought to occur through changes in arterial resistance (Ra). To test whether the critical closing pressure (Pcrit) could also play a role, we pump-perfused the vascularly isolated canine hindlimb at constant flow. Carotid sinuses were isolated and both vagus nerves cut. Carotid sinus (Pcar), arterial, perfusion (Pper), and venous (Pv) pressures and flow to the hindlimb (Q, electromagnetic flow probe) were measured. By decreasing pump flow to zero over time periods of 1-10 s and measuring the pressure at zero-flow, it was possible to estimate arterial compliance and Pcrit. Ra was calculated as (Pper - Pcrit)/Q. Venous resistance was calculated as (Pel - Pv)/Q, where Pel is the pressure in the compliant region obtained by the double-occlusion technique. Raising Pcar from 115 +/- 7 to 203 +/- 10 mmHg (n = 6) decreased Pcrit from 49.7 +/- 4.3 to 25.9 +/- 2.6 mmHg and Ra from 10.7 +/- 1.2 to 6.8 +/- 0.9 mmHg.min.100 g-1.ml-1 (P < 0.05). Lowering Pcar from 119 +/- 6 to 71 +/- 6 mmHg (n = 6) increased Pcrit from 37.0 +/- 3.3 to 61.0 +/- 8.5 mmHg and Ra from 10.0 +/- 1.6 to 14.0 +/- 2.4 mmHg.min.100 g.ml-1 (P < 0.05). Arterial compliance increased when Pcar was raised (P < 0.05) and decreased when Pcar was decreased (P < 0.1). Venous resistance did not change when Pcar was altered. In conclusion, changes in carotid sinus stimulation alters blood flow to the hindlimb through changes in both Pcrit and Ra.

Animals↗

PubMed1993

Response of arterial resistance and critical pressure to changes in perfusion pressure in canine hindlimb.

The dynamic pressure-flow relationship in the canine hindlimb at normal arterial pressure is best explained by modeling a Starling resistor (critical pressure, Pcrit) at the level of the arterioles. Regulation of flow can therefore occur at the Starling resistor through changes in Pcrit or along the length of the vessel through changes in arterial resistance (Ra). We hypothesized that increasing perfusion pressure (Pper) would increase Pcrit due to the myogenic response but would decrease Ra because of flow-mediated vasodilation and passive effects. We pump-perfused vascularly isolated hindlimbs of anesthetized dogs and then measured Pcrit and calculated Ra over Pper range of 75-175 mmHg. When Pper was increased from 75 to 175 mmHg, Pcrit increased from 33 +/- 2 to 48 +/- 6 (means +/- SE) mmHg, whereas Ra decreased from 10.1 +/- 1.2 to 7.86 +/- 0.7 mmHg.min.100 g.ml-1 (P < 0.01). Thus the responses of Pcrit and Ra to an increase in Pper were dissociated. In a second part of the study, we lowered carotid sinus pressure to determine the effects of central factors on local autoregulation. A decrease in carotid sinus pressure increased Pcrit and Ra at each Pper (P < 0.05). We conclude that an increase in Pper causes the arterial vasculature to constrict at the level of the Starling resistor and dilate more proximally. The carotid baroreflex causes an increase in tone throughout the arterial vasculature but does not alter the local response to increases in Pper.

Animals↗

PubMed1993

Effect of selective diaphragmatic paralysis on the inspiratory motor drive.

Using alpha-chloralose-anesthetized mechanically ventilated vagotomized dogs, we assessed the effects of selective diaphragmatic paralysis on the inspiratory motor drive. Diaphragmatic paralysis was accomplished by a bolus injection of vecuronium, a neuromuscular junction blocker, into the left phrenic artery of an in situ vascularly isolated and innervated left diaphragm. The inspiratory motor drive during spontaneous breathing attempts was assessed by measuring peak integrated electromyographic (EMG) activities of the left and right diaphragms and parasternal and alae nasi muscles. Respiratory timing parameters were measured from the integrated EMG signals of the diaphragm. Three groups of dogs were studied. In group 1 (n = 9), vecuronium was injected into the phrenic artery with the left diaphragmatic length adjusted at the functional residual capacity. Vecuronium injection (0.2 mg) resulted in a significant decline in left diaphragmatic tension and integrated EMG. Breathing frequency increased by 24% of the baseline value, whereas right diaphragm, parasternal, and alae nasi EMG activities rose to 136, 227, and 165% of their respective baseline values a few seconds after the vecuronium injection. In group 2 (n = 6), vecuronium injection in left phrenectomized animals did not alter the EMG activities of the inspiratory muscles (left EMG signal was abolished) nor did it alter respiratory timing. In group 3 (n = 4), the left diaphragm was placed in a flaccid position. Vecuronium injection in this group did not produce any changes in the EMG activities or respiratory timing. We conclude that selective diaphragmatic paralysis elicits a significant rise in the inspiratory motor drive. This effect is likely to be mediated through the inhibition of diaphragmatic Golgi tendon organ activity.

Animals↗

PubMed1992

Baroreflex control of regional capacitance and blood flow distribution with or without alpha-adrenergic blockade.

Regional blood volumes (Vb), unstressed volumes (V0), blood flow distribution, venous compliances (Cv), venous resistances (Rv), and time constants of drainage (tau v) were determined in dogs anesthetized with alpha-chloralose at carotid sinus pressures (Pcs) of 50 and 200 mmHg and dosed with alpha-adrenergic or ganglionic blockade at a Pcs of 50 mmHg. Vb was measured in each region from indicator dilution curves and mean transit times. V0 was extrapolated from the pressure-volume curves. Pcs of 50 and 200 mmHg were maintained in random order. With a decrease in Pcs, arterial pressure increased from 58.7 +/- 4.1 to 104.6 +/- 6.4 mmHg (P < 0.01), peripheral fractional blood flow decreased from 69.8 +/- 3.8 to 55.8 +/- 3.9% (P < 0.001), splanchnic Vb decreased from 28.3 +/- 1.9 to 19.3 +/- 1.2 ml/kg (P < 0.01), and splanchnic V0 decreased from 19.6 +/- 1.4 to 6.3 +/- 2.1 ml/kg (P < 0.001). Splanchnic Rv and tau v also decreased, whereas splanchnic Cv increased. Phentolamine at low Pcs only partially reversed the decrease in splanchnic capacitance, whereas hexamethonium completely abolished it. In conclusion, changes in splanchnic Rv and blood flow distribution are important components of the carotid sinus reflex, and alpha-adrenergic receptor activation is only partially responsible for the changes in vascular capacitance by the baroreceptor reflex.

Adrenergic alpha-Antagonists↗

PubMed1992

Role of endothelium-derived relaxing factor in active hyperemia of the canine diaphragm.

To assess the effect of endothelium-derived relaxing factor (EDRF) on diaphragmatic vascular resistance at rest and during contractions, we studied an in situ isolated diaphragm preparation in anesthetized and mechanically ventilated dogs. The arterial supply of the left diaphragm (phrenic artery) was catheterized and perfused with arterial blood at a fixed flow rate. Drugs were infused through a side port of the arterial catheter at 1/100th of the phrenic arterial flow. The inferior phrenic vein was catheterized to complete the isolation from the systemic circulation. Three sets of experiments were performed. In set 1 (n = 3), we infused endothelium-dependent (acetylcholine, ACh) and endothelium-independent (sodium nitroprusside, SNP) dilators at increasing concentrations. ACh and SNP infusion elicited a dose-dependent decline in phrenic vascular resistance (Rphr) at concentrations greater than 10(-8) M and 0.50 micrograms/ml, respectively. In set 2 (n = 15), we infused an inhibitor of EDRF synthesis and release, L-argininosuccinic acid (ArgSA), at increasing concentrations (10(-4), 3 x 10(-4), and 6 x 10(-4) M). ArgSA produced a dose-dependent increase in Rphr. Infusion of another EDRF inhibitor (NG-nitro-L-arginine, LNA, 6 x 10(-4) M) elicited increase in Rphr similar to that induced by ArgSA. In set 3 (n = 25), we infused ArgSA or LNA (6 x 10(-4) M) simultaneously with ACh and SNP and during sustained (2-Hz) contractions of the diaphragm. Both ArgSA and LNA completely reversed ACh vasodilation, whereas SNP vasodilation was reversed by 26 and 11%, respectively. ArgSA or LNA infusion during contractions reversed vasodilation by 48 and 52%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗

PubMed1992

Adaptations of the peripheral circulation to PEEP.

The purpose of this study was to determine the role of changes in the parameters of venous return on the homeostatic adaption to the application of PEEP. We studied 13 dogs anesthetized with alpha-chloralose, intubated, and ventilated. We measured central venous pressure (CVP), arterial pressure (Pao) and cardiac output by thermal dilution. The cardiac output was transiently stopped by inflating a balloon in the right atrium, and the subsequent plateau in the CVP was used to obtain mean circulatory filling pressure (MCFP). Total blood volume was measured with Evans blue. To measure vascular capacitance and compliance, we rapidly infused 4 ml/kg or 8 ml/kg of blood and repeated the MCFP measurement. The same volume was withdrawn after the measurement. The volume and MCFP were used to construct pressure-volume (P-V) lines, and the unstressed volume was calculated by extrapolating the P-V to zero pressure. The P-V appeared linear in the range studied. PEEP produced a left shift of the curves and, thus, a decrease in unstressed volume. The shift with 20 cm H2O of PEEP was greater than with 10 cm H2O of PEEP. The rise in MCFP matched the rise in CVP so that the pressure gradient for venous return did not change. However, there was also an increase in the resistance to venous return, which resulted in a lower cardiac output than expected for the rise in MCFP. In conclusion, homeostatic adjustments to PEEP included a decrease in vascular capacitance, which is partially offset by a rise in the resistance to venous return.

Adaptation, Physiological↗

PubMed1991

Failure of oxygen radical scavengers to modify fatigue in electrically stimulated muscle.

We used in situ gastrocnemius muscle of anaesthetized dogs to test the hypothesis that O2 radical production during muscle contraction contributes to fatigue. Muscle tension was measured with a force transducer and blood flow was monitored with an electromagnetic flow probe. Muscle contractions were produced by stimulating the nerve for 15 min at 20 Hz, 12 trains/min, and a duty cycle of 0.25. Three groups of seven animals were given an infusion of 0.2 mL.min-1 of either saline, low-dose oxygen radical scavengers (250 IU.mL-1 superoxide dismutase, 640 IU.mL-1 polyethylene glycol (PEG)-catalase, 0.25 mg.mL-1 deferoxamine, and 0.1 mg.mL-1 oxypurinol), or high-dose oxygen radical scavengers (3300 IU.mL-1 superoxide dismutase, 6600 IU.mL-1 PEG-catalase, 2.5 mg.mL-1 deferoxamine, and 0.1 mg.mL-1 oxypurinol). Blood flow and vascular resistance of the gastrocnemius muscle during stimulation did not differ among groups. After 15 min of stimulation, the developed tension (represented as a percentage of initial tension developed) was 66 +/- 7% in the saline treated group, 70 +/- 6% in the low-dose group, and 70 +/- 4% in the high-dose group. The change in tension during recovery was not significant in the control or low-dose groups. However, there was partial recovery in the high-dose group. In conclusion, in this preparation, oxygen radical scavengers did not delay the development of decreased muscle tension.

Animals↗

PubMed1991

Chemical activation of thin-fiber phrenic afferents. 2. Cardiovascular responses.

To assess the effects of groups III and IV (thin-fiber) phrenic afferents on arterial pressure, heart rate, and distribution of cardiac output, we injected capsaicin into phrenic arteries of in situ isolated and innervated left diaphragms of dogs anesthetized with chloralose, vagotomized, and mechanically ventilated. Blood flow in the ascending aorta, common carotid, renal, superior mesenteric, and femoral arteries was measured by electromagnetic and Doppler flow probes. Injection of 1 mg capsaicin into the left phrenic artery produced congruent to 15% increase in mean arterial pressure and congruent to 7% increase in heart rate with no change in aortic flow. Phrenic arterial flow decreased by 64%, renal arterial flow by 16%, and superior mesenteric arterial flow by 10%, whereas carotid flow increased by 13% and flow to the right gastrocnemius muscle did not change. Mean arterial pressure, heart rate, and blood flow distribution (with the exception of the decline in phrenic blood flow) returned to baseline within 60 s of the injection. Injection of 1.5 mg capsaicin into the right isolated and innervated gastrocnemius produced congruent to 35% increase in mean arterial pressure, 17% rise in heart rate, and no change in aortic blood flow. Phrenic and carotid arterial flow rose by 240 and 41%, respectively, whereas renal and superior mesenteric flow declined by 50 and 20%, respectively. In conclusion, thin-fiber phrenic afferents have an excitatory effect on arterial pressure and heart rate. They redistribute blood flow away from the renal and intestinal vascular beds and toward the carotid vascular bed. On the other hand, the cardiovascular reflex from thin-fiber phrenic afferents seems less potent than that from limb muscle afferents.

Afferent Pathways↗

PubMed1991

Diaphragmatic intramuscular pressure in relation to tension, shortening, and blood flow.

We used an in situ isolated diaphragmatic preparation in anesthetized dogs to relate intramuscular pressure (IMP) to the blood flow, tension, and shortening of the diaphragm. In this preparation, the diaphragm shortens in a fashion similar to the intact diaphragm. Tension was measured by transducers attached to the left costal margin, which was detached from the rib cage and abdomen; IMP was measured by a miniature transducer placed between muscle fibers; length was measured by sonomicrometry; and diaphragmatic blood flow was monitored by measuring left phrenic arterial flow. In protocol 1, the relationships between tension, shortening, and IMP were assessed by stimulating the diaphragm for 2 s at various frequencies. Tension and shortening increased with increasing stimulation frequency up to 50 Hz with no change thereafter. Tension was linearly related to IMP. Similarly, there was a linear relationship between the degree of shortening and IMP; however, the slopes varied considerably between dogs. In protocol 2, the diaphragm was paced intermittently (12 trains/min, duty cycle of 0.5) with a gradual increase in stimulation frequency. Blood flow during contraction phase rose slightly at low tension and then declined significantly when tension exceeded 30% of maximum, whereas relaxation-phase flow increased with the increase in tension. IMP rose linearly with the increase in tension, and the IMP, at the point where contraction-phase flow became severely limited, was 50 +/- 14 mmHg (mean +/- SE). We conclude the following. 1) IMP is linearly related to tension and shortening; however, because tension and shortening changed simultaneously during contractions, the independent relationship of either tension or shortening and IMP remained untested.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1991

Subclinical cardiac dysfunction in sarcoidosis.

Clinically apparent myocardial disease is infrequent in sarcoidosis. However, autopsy data show myocardial involvement in up to 30 percent of patients. Unexplained exertional symptomatology is a common complaint in patients with sarcoidosis. In this study, we investigated whether abnormal cardiac function might limit exercise performance in patients with sarcoidosis without overt cardiac involvement. We studied exercise responses in 35 patients with sarcoidosis and compared them with 28 untrained controls. Seventy-seven percent of the patients were symptomatic. Pulmonary function test results were lower in the group with sarcoidosis than normal controls, but they were within normal range. Only one patient had evidence of ventilatory limitation to exercise. Sixteen (46 percent) patients had abnormally increased heart rates (HRs) at rest prior to exercise testing and/or with exercise. Rapid HRs were confirmed during daily activities by continuous ambulatory electrocardiographic (ECG) monitoring. Left ventricular ejection fraction (LVEF) was measured to determine if systolic dysfunction could account for abnormal HR responses. Of patients with abnormally increased HRs, five had LVEFs less than 50 percent, and eight had normal LVEFs, of whom 75 percent had tachycardia at rest. Retrospective comparison of HR responses and LVEF between patients who did or did not receive corticosteroids revealed no significant differences between groups. We conclude that abnormal HR responses in patients without evident cardiac sarcoidosis are common and exertional symptoms in this population are often associated with chronotropic abnormalities. The exact mechanisms underlying the chronotropic abnormalities are unclear, but they likely include ventricular systolic dysfunction, sinus node dysfunction from granulomatous infiltration, or combinations of the two.

Adult↗

PubMed1990

Vascular mechanics of venous drainage in dog hindlimbs.

The time constant of venous drainage (tau v) of a vascular bed is an important determinant of the change in regional volume that will occur with a change in blood flow or venous pressure (Pv). Therefore, to measure tau v of the dog hindlimb, the vasculature was isolated and perfused with a pump. Inflow and outflow were measured with electromagnetic flow probes. Blood volume was changed (delta V) by changing flow (delta Q), and a double-occlusion procedure was used to obtain the venous elastic recoil pressure (Pel) from the plateau of Pv. Venous resistance (Rv), compliance (Cv), and tau v could then be calculated. Rv was 7.7 +/- 1.4 mmHg.ml-1.min.100 g-1 and Cv was 0.59 +/- 0.25 ml/mmHg, tau v calculated from the product of Rv and Cv was 4.20 +/- 1.58 s and from the ratio of delta V to delta Q was 4.95 +/- 1.53 s (P = NS) at a mean Pel of 17.6 +/- 3.7 mmHg. delta V was also produced by changing Pv; the average tau v (1.95 +/- 0.37 s), was shorter than that with changes in flow. Finally, a ramp increase in flow was used to calculate tau v from the time delay between inflow and outflow. tau v by this method was longer (6.06 +/- 1.70 s) and was probably influenced by the change in Pv. In conclusion, the hindlimb has a short tau v of venous drainage and would not be expected to store large volumes of blood even with large increases in blood flow.

Animals↗