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Biomedical subjects

S Magder

Publications and source records attributed to S Magder.

At least 73 records · Page 4Linked to original sources
PubMed1990

Skin vascular bed is a potential blood reservoir during heat stress.

To determine the potential role of the skin vasculature as a blood reservoir, we measured venous compliance (Cv), resistance (Rv), and their product, the time constant of venous drainage (tau sk = RvCv), in skin flaps from the hindlimbs of 15 dogs anesthetized with pentobarbital sodium at different core temperatures (Tc, 37-42 degrees C), skin temperature (Ts, 25.3-50.0 degrees C), and during an infusion of papaverine (5%). The vasculature of the flap was isolated, and a double-occlusion technique was used to measure the static pressure in the venous compartment. The blood volume of the flap was altered by changing either flow or outflow pressure (Pv). The change in volume was estimated from the change in weight of the flap with a force transducer. At Tc = 37 degrees C, Rv was 2.27 +/- 0.81 mmHg.min.ml-1.100 g-1 (means +/- SD), Cv was 0.17 +/- 0.06 ml.mmHg-1.100 g-1, and tau sk was 28.0 +/- 8.8 s. Rv decreased with elevated Tc, Ts, and with papaverine. Cv increased with a rise in Tc and Ts. Increasing Tc and Ts did not change tau sk, but the papaverine infusion shortened it. The lowest tau sk (20 s) occurred during maximal vasodilatation. This long tau sk indicates that the skin could serve as a blood reservoir during heat stress.

Animals↗
PubMed1990

Chemical activation of thin-fiber phrenic afferents: respiratory responses.

In supine chloralose-anesthetized and mechanically ventilated dogs, we assessed the effects of group III and IV thin-fiber phrenic afferents on cardiorespiratory control by injecting capsaicin into the phrenic artery of an in situ isolated and innervated left diaphragm. Inspiratory motor drive was assessed by measuring the electromyogram of left and right diaphragm, left parasternal, and mylohyoid muscles in five protocols. 1) Three boluses (2 ml) of capsaicin (1, 10, and 50 micrograms/ml) were injected 30 min apart. Only the 50-micrograms/ml injection elicited a significant increase in arterial pressure, heart rate, and inspiratory motor drive. 2) Repeated doses of capsaicin were tested. The pressor and hyperpneic responses were weakened. 3) High doses of capsaicin (100 and 500 micrograms/ml) were given. Hyperpneic and pressor responses were similar to those elicited by the 50-micrograms/ml dose. 4) When the left phrenic nerve was sectioned, the pressor and hyperpneic responses to the 50-micrograms/ml injection were abolished. 5) Capsaicin (50 micrograms/ml) was infused into the arterial supply of the in situ vascularly isolated and innervated gastrocnemius. Arterial pressure, breathing frequency, and inspiratory motor drive to all inspiratory muscles increased significantly and to a greater degree than in the diaphragm. In conclusion, diaphragmatic thin-fiber afferents have an excitatory effect on the inspiratory motor drive and arterial pressure that is similar to that seen in limb muscles.

Animals↗
PubMed1990

Starling resistor versus compliance. Which explains the zero-flow pressure of a dynamic arterial pressure-flow relation?

Arterial pressure at zero flow (Pz = 0) that is higher than venous pressure (Pv) in dynamic pressure-flow relations has been explained by the presence of an arteriolar Starling resistor (SR) mechanism (i.e., vascular waterfall) or the discharge of vascular capacitance. To determine which was predominant, I studied in vivo hind limbs of 18 anesthetized dogs in which femoral arteries were cannulated with in-line electromagnetic flow probes to measure inflow (Qin), Pv was controlled, and collateral flow was eliminated with a tourniquet. Pz = 0 was obtained by turning flow to zero. Three tests were applied: 1) Pv was raised in steps with either constant Qin or constant arterial pressure (Pa) to determine the pressure at which upstream vascular characteristics were affected by a change in Pv, 2) the time to reach Pz = 0 was varied to determine compliance effects, and 3) an equation was developed to determine if experimentally derived parameters could explain Pz = 0 without invoking an SR. With constant Qin and a Pz = 0 of 56.9 +/- 11.7 mm Hg (time to Pz = 0, 3 seconds), Pv could be raised by 9.6 +/- 6.2 to 16.3 +/- 6.0 mm Hg before Pa increased, and with constant Pa, Pv could be raised by 6.8 +/- 7.3 to 14.0 +/- 8.0 mm Hg before Qin decreased. With increasing times to reach Pz = 0, Pz = 0 initially dropped precipitously, but then decreased by only a small amount over the next 5-10 seconds even though arterial pressure was much above Pv. This could be explained by an SR mechanism with a critical pressure of 42.3 +/- 11.4 mm Hg and an arterial compliance of 0.0104 +/- 0.0023 ml.mm Hg-1 (n = 6). There was no value for the compliance that described the results when the arterial outflow pressure was Pv. Thus, this study supports the hypothesis that an SR mechanism is present in the vascular system. It is most likely precapillary, and in the resting limb, it has a value of 40-50 mm Hg. However, Pz = 0 in dynamic pressure-flow studies of less than 4 seconds is also greatly influenced by capacitance effects and the initial Pa.

Animals↗
PubMed1990

Cardiac arrhythmias during exercise in severe chronic obstructive pulmonary disease.

We studied the effect of maximal exercise on the prevalence of arrhythmias in 122 subjects with severe COPD. At rest, ten subjects had supraventricular arrhythmias while 13 had unifocal VPB greater than or equal to 6/min or ventricular bigeminy. At peak exercise, six subjects had supraventricular arrhythmias while 24 had VAs. Univariate and multivariate analysis with logistic regression did not show relationships between exercise-related cardiac arrhythmias and the severity of pulmonary disease, oxyhemoglobin desaturation or ECG evidence of chronic lung disease. Exercise-related arrhythmias were significantly associated with the presence of arrhythmias at rest and 87 percent of subjects who had no arrhythmias at rest did not have any during exercise. In patients with COPD, the development of potentially serious arrhythmias during exercise is uncommon without clinically apparent CAD or arrhythmias at rest. However, routine cardiac monitoring during exercise testing should not be abandoned in this population since VAs can occur despite their absence at rest.

Aged↗
PubMed1989

Blood volume after coronary artery bypass grafting.

Patients with stable angina pectoris are reported to have a markedly reduced blood volume (BV). In the present study, average BV was still 19% less than that predicted in 77 men examined 5 years after coronary artery bypass grafting. Beneficial effects of the operation such as relieved angina, absence of medication, complete revascularization status at repeat angiography, and restored physical fitness were not found to be associated with a normalization of the BV. No significant correlation was found between BV and body weight, heart volume, exercise capacity, ejection fraction or left ventricular end-diastolic pressure. The reduced BV in patients with angina pectoris after successful revascularization and the absence of correlation with physiological variables indicate a persisting disturbed regulation mechanism.

Adult↗
PubMed1989

Effects of tension, duty cycle, and arterial pressure on diaphragmatic blood flow in dogs.

We investigated the selective effects of changes in transdiaphragmatic pressure (Pdi) and duty cycle on diaphragmatic blood flow in supine dogs at normal arterial pressure (N), moderate hypotension (MH), and severe hypotension (SH) [mean arterial pressure (Part) of 116, 75, and 50 mmHg, respectively]. The diaphragm was paced at a rate of 12/min by bilateral phrenic nerve stimulation. Left phrenic (Qphr-T) and left internal mammary (Qim-T) arterial flows were measured by electromagnetic flow probes. Changes in Pdi and duty cycle were achieved by changing the stimulation frequencies and the duration of contraction, whereas Part changes were produced by bleeding. With N and at a duty cycle of 0.5, incremental increases in Pdi produced peaks in Qphr-T and Qim-T at 30% maximum diaphragmatic pressure (Pdimax) with a gradual decline at higher Pdi. With MH and SH, blood flow peaked at 10% Pdimax. At any given Pdi, blood flow was lower with MH and SH in comparison to N. The effect of duty cycle was tested at two levels of Pdi. With N and at low Pdi (25% Pdimax), blood flow rose progressively with increases in duty cycle, whereas at moderate Pdi level (50% Pdimax) blood flow peaked at a duty cycle of 0.3, with no increase thereafter. With MH, blood flow at low Pdi rose linearly with increasing duty cycle but to a lesser extent than with N, and at a moderate Pdi flow peaked at a duty cycle of 0.3. With SH, blood flow at low and moderate Pdi was limited at duty cycles greater than 0.3 and 0.1, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Effect of saline infusion on body temperature and endurance during heavy exercise.

We tested the hypothesis that volume infusion during strenuous exercise, by expanding blood volume, would allow better skin blood flow and better temperature homeostasis and thereby improve endurance time. Nine males exercised to exhaustion at 84.0 +/- 3.14% (SE) of maximum O2 consumption on a cycle ergometer in a double-blind randomized protocol with either no infusion (control) or an infusion of 0.9% NaCl (mean vol 1,280.3 +/- 107.3 ml). Blood samples and expired gases (breath-by-breath), as well as core and skin temperatures, were analyzed. Plasma volume decreased less during exercise with the infusion at 15 min (-13.7 +/- 1.4% control vs. -5.3 +/- 1.7% infusion, P less than 0.05) and at exhaustion (-13.6 +/- 1.2% vs. -1.3 +/- 2.2%, P less than 0.01). The improved fluid homeostasis was associated with a lower core temperature during exercise (39.0 +/- 0.2 degrees C for control and 38.5 +/- 0.2 degrees C for infusion at exhaustion, P less than 0.01) and lower heart rate (194.1 +/- 3.9 beats/min for control and 186.0 +/- 5.1 beats/min for infusion at exhaustion, P less than 0.05). However, endurance time did not differ between control and infusion (21.96 +/- 3.56 and 20.82 +/- 2.63 min, respectively), and neither did [H+], peak O2 uptake, and CO2 production, end-tidal partial pressure of CO2, blood lactate, or blood pressure. In conclusion, saline infusion increases heat dissipation and lowers core temperature during strenuous exercise but does not influence endurance time.

Adolescent↗
PubMed1989

In situ isolated perfused and innervated left hemidiaphragm preparation.

We developed a vascularly isolated in situ preparation of the left hemidiaphragm in which arterial blood was only provided through the left phrenic artery and the venous blood only drained through the phrenic vein. The costal margins were secured and connected to three force transducers. Muscle shortening was measured by sonomicrometry. The presence of arterial collaterals between the left hemidiaphragm and the systemic circulation was excluded by the systemic injection of a vital dye (Lissamine Green), a neuromuscular blocking agent (succinylcholine), and by the injection of epinephrine. Left phrenic nerve stimulation produced homogeneous shortening and tension. The degree of shortening in the isolated and intact left diaphragm at the same resting length was similar. The preparation was stable for 2 h with less than 10% decline in maximum tension. Two advantages of this preparation are particularly important. 1) Diaphragmatic energetics can be studied independently of systemic factors, and 2) the role of phrenic nerve afferents in the control of breathing and systemic circulation can easily be assessed without activating nonphrenic nerve afferents.

Animals↗
PubMed1988

Autoregulation of diaphragmatic blood flow in dogs.

In eight anesthetized spontaneously breathing dogs, we determined whether diaphragmatic blood flow is dependent on arterial blood pressure (Pa) or whether it is autoregulated. We also determined whether diaphragmatic muscular activity affects the degree of autoregulation. We measured blood flow through the left phrenic artery (Qphr) with an electromagnetic flow probe and decreased Pa in steps by controlled hemorrhage. Phrenic venous blood was sampled to allow the calculation of diaphragmatic O2 consumption (VO2phr). Diaphragmatic energy demands were varied by using three inspiratory resistances (R1, R2, and R3), which increased peak transdiaphragmatic pressure two-, three-, and fourfold, respectively. During quiet breathing, Qphr was independent of Pa between Pa of 90 and 120 mmHg (i.e., plateau of pressure-flow relation), but at lower Pa, Qphr was directly related to Pa. During inspiratory loading, the Qphr plateau ended at a higher Pa than with quiet breathing, but within the normal ranges of Pa there still was a plateau. VO2phr at a given work load was constant between Pa of 70 and 120 mmHg, but at Pa of 50-55 mmHg, VO2phr declined with all work loads. We conclude that in spontaneously breathing dogs 1) Qphr is autoregulated over the normal range of blood pressures and 2) VO2phr is maintained over wider ranges of Pa than Qphr.

Animals↗
PubMed1988

Diaphragmatic energetics and blood flow during pulmonary edema and hypotension.

We studied the role of O2 supply and demand factors for producing diaphragmatic failure in a canine model of cardiogenic shock with pulmonary edema. We produced pulmonary edema with oleic acid and then hypotension with cardiac tamponade and followed the animals until respiratory failure began, which was defined by a 50% fall in frequency of breathing and diaphragmatic pressure-time index (PTI; cmH2O.s-1.min-1) with no decrease in the diaphragmatic electromyogram. Regional blood flows were measured with radiolabeled microspheres. Diaphragmatic O2 consumption (VO2 di) (ml.min-1.100 g-1) was determined from the diaphragmatic blood flow (Qdi) and the arterial and phrenic venous O2 contents. With oleic acid-induced pulmonary edema, PTI Qdi, and VO2 di increased from control of 101.7 +/- 31.7, 17 +/- 1.8, and 0.81 +/- 0.11, respectively, to 187.2 +/- 27.6, 42.2 +/- 7.2, and 3.32 +/- 0.35 (P less than 0.05). With tamponade, PTI did not change (186.7 +/- 60.0), whereas VO2 di increased further to 3.98 +/- 0.98 (P less than 0.05) due to increased O2 extraction and no significant change in Qdi (32.8 +/- 4.0). As fatigue developed, VO2 di decreased to 2.30 +/- 0.23 due to the combined effects of small declines in Qdi and the arterial O2 content but remained higher than control even though the energy demands returned to control values. In conclusion, when cardiogenic shock is added to pulmonary edema VO2 di and energy output do not increase further and eventually fall.

Animals↗
PubMed1988

Interposed abdominal compressions and carotid blood flow during cardiopulmonary resuscitation. Support for a thoracoabdominal unit.

To determine if the timing of interposed abdominal compressions (IAC) affects the augmented blood flow during this form of cardiopulmonary resuscitation (CPR), we performed early-onset or late-onset abdominal compressions at three vascular volumes in nine dogs. Early-onset IAC began immediately following chest compression; we predicted that this would act primarily by emptying the aorta and sustaining the elevated intrathoracic pressure. Late-onset IAC began one-fourth to one-third of the time into diastole; this would have primarily increased venous return. We measured carotid blood flow (electromagnetic flow probe) and right atrial (Pra), thoracic aortic (Pta), abdominal aortic (Paa), and intra-abdominal pressures. The IAC-CPR increased carotid blood flow compared with conventional CPR (22.8 +/- 13.1 percent vs 8.7 +/- 5.8 percent of control; p less than 0.003), but there was no difference between the early and late modes of IAC (22.7 +/- 11.6 percent vs 22.9 +/- 14.7 percent of control). The increase in carotid blood flow was present with the first abdominal compression and was constant over the 40 to 60 seconds of CPR. Peak Pra, Pta, and Paa were similar during abdominal compression (91.8 +/- 16.9 mm Hg, 96.1 +/- 16.0 mm Hg, and 102.4 +/- 15.2 mm Hg, respectively; p less than 0.001). The Pta-Pra diastolic gradient was 18.0 +/- 8.2 mm Hg for early-onset and 20.6 +/- 7.5 mm Hg for late-onset compression (not significant). We conclude that increased carotid blood flow in IAC-CPR in the dog is principally due to the increased pressure in a common thoracoabdominal unit.

Abdomen↗
PubMed1987

Comparison of the effects of pindolol and propranolol on exercise performance in patients with angina pectoris.

The effects of pindolol (mean dose 17 +/- 8 mg/day), a beta-blocking drug with intrinsic sympathomimetic activity (ISA), and propranolol (130 +/- 40 mg/day) on exercise performance in 11 patients with stable angina pectoris were compared. Doses were titrated to symptoms. The design was a randomized, double-blind, crossover protocol with 8 weeks of treatment with each drug. At the end of each drug period, subjects performed 3 exercise tests: a symptom-limited test on a cycle ergometer with measurement of gas exchange parameters; a steady-state exercise test to measure cardiac output by the CO2 rebreathing method; and a supine exercise test with radionuclide angiography. The ISA effect of pindolol was evident at rest in that the heart rate of 82 +/- 4 beats/min was higher than with propranolol (70 +/- 3). At low levels of exercise heart rate, cardiac output and O2 consumption (VO2) were still higher. However, there was no difference in cardiac output or VO2 at higher levels of exercise and no difference in the VO2 at the anaerobic threshold and peak exercise. Peak VO2 was 1,344 +/- 108 ml/min with propranolol and 1,350 +/- 116 with pindolol therapy. There were also no differences in ejection fraction or cardiac volumes at rest or during exercise. The incidence of side effects was similar with both drugs and there was no significant preference for either medication. In conclusion, patients with angina treated with pindolol had the same peak exercise performance as with an 8:1 equivalent dose of propranolol (clinically equivalent), although at lower levels of exercise, VO2, cardiac output and heart rate were higher from the ISA of pindolol.

Angina Pectoris↗
PubMed1987

Effects of norepinephrine and fluid administration on diaphragmatic O2 consumption in septic shock.

The effects of norepinephrine infusion and fluid administration on diaphragmatic O2 consumption during endotoxic shock were assessed in spontaneously breathing anesthetized dogs. Blood flow was measured with the microsphere technique, and diaphragmatic venous blood was obtained via a catheter inserted into the left inferior phrenic vein. One group of dogs (n = 6) received 10 mg/kg Escherichia coli endotoxin intravenously (E group). In the second and third groups, blood pressure after endotoxin injection was restored by continuous infusion of norepinephrine tartrate (N group) or by infusion of normal saline and dextran infusion (F group). The animals were observed for 2 h after endotoxin injection. Cardiac output fell significantly in the E and N group, whereas it was restored in the F group. Minute ventilation and diaphragmatic pressure-time index rose twofold in the three groups of dogs. Diaphragmatic O2 consumption (VO2 di) increased substantially in the E group to a mean value of 3.46 ml X 100 g-1 X min-1, which was achieved by higher blood flow and by an increase in O2 extraction. In the N group, VO2 di was higher than control but was lower than that of the E group (mean value of 1.43 ml X 100 g-1 X min-1), which was achieved solely by increasing O2 extraction. In the F group, VO2 di was also lower than that of the E group (mean value of 1.51 ml X 100 g-1 X min-1), which was achieved by high diaphragmatic blood flow. Thus, at any given diaphragmatic task, the diaphragm consumed less O2 in the N and F group than in the E group.

Animals↗
PubMed1987

Interobserver agreement by auscultation in the presence of a third heart sound in patients with congestive heart failure.

Although the third heart sound (S3) is well recognized as an important sign in the evaluation of patients with congestive heart failure, the interobserver variability with its observation needs to be known before general applicability can be determined. Therefore, we determined the agreement among four trained observers on the presence of S3 in 81 hospitalized patients. Agreement between pairs of observers varied between 48 and 73 percent. The kappa statistic, which adjusts for agreement by chance alone, showed that agreement between various observer pairs was moderate (kappa = 0.40-0.50) at best and slight (kappa = 0.10-0.30) at worst. The rate of agreement did not appear to be affected by the time interval between measurements, by the sex of the patient or by a training effect over the time of the study. In conclusion, although S3 may be important as a clinical sign, clinicians cannot agree reliably about whether or not it is present.

Heart Auscultation↗
PubMed1986

Respiratory muscle blood flow in oleic acid-induced pulmonary edema.

If respiratory muscle blood flow (RMBF) demands in pulmonary edema are large enough, an imbalance between supply and demand could lead to respiratory muscle failure. Therefore, to determine the magnitude of RMBF in this condition we produced pulmonary edema by injecting oleic acid into the pulmonary circulation and measured RMBF with radiolabeled microspheres injected into the left atrium. We then related changes in muscle blood flow to changes in respiratory variables including frequency of breathing (fb, breaths/min), tidal volume (VT, ml), ventilation (VE, ml . kg-1 . min-1), pleural pressure-time index (PTI, cmH2O), and dynamic compliance (Cdyn, 1/cmH2O) at 0 (control), 30, 60, and 120 min. Cardiac output and blood pressure did not change throughout the experiment, but hypoxia became progressively more severe with a final PO2 of 37 +/- 10 Torr. With pulmonary edema, fb rose from a control value of 32 +/- 13 to 111 +/- 33 at peak, VE rose from 237 +/- 90 to 806 +/- 188, but VT did not change. PTI rose from 54 +/- 16 to 180 +/- 48, and Cdyn decreased from 0.06 +/- 0.02 to 2.02 +/- 0.01. Diaphragmatic blood flow (Qdi) rose from 16.0 +/- 6.26 to 120.1 +/- 54.5 ml . min-1 X 100 g-1 and accounted for 55% of the total RMBF of 217 +/- 100 ml/min. The RMBF accounted for 11.4 +/- 4.7% of the cardiac output at peak affect. The rise in Qdi was best predicted by PTI and to a smaller extent by PO2.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Pressure-flow relations of diaphragm and vital organs with nitroprusside-induced vasodilatation.

We determined maximal conductance in the diaphragm and other vital organs in 14 anesthetized dogs, weighing 22.8 +/- 4.2 kg, which were given maximal vasodilating doses of nitroprusside (mean dose 13.9 +/- 4.3 micrograms X kg-1 X min-1) and the blood pressure was lowered in stages by hemorrhage. Blood flow in the diaphragm, brain, heart, kidney, gut, and quadriceps was measured with radiolabeled microspheres. To ensure maximal vasodilatation of diaphragmatic vessels, we stimulated the phrenic nerves to produce diaphragmatic contractions at 0.3 Hz. The mean cardiac output was 2.13 +/- 0.42 l/min (thermodilution) before nitroprusside and 4.68 +/- 1.45 after (P less than 0.001). Nitroprusside failed to break the autoregulation of the brain. Pressure-flow relations (P-F) in other regions were linear (r = 0.70 +/- 0.03, P less than 0.001) and blood pressure at zero flow (X-intercept) was always greater than venous pressure (diaphragm = 11, kidney = 19, heart = 8, gut = 8, quadriceps = 32 mmHg). The flow to the diaphragm (Qdi) could be predicted by Qdi (ml X min-1 X g-1) = [(3.13 +/- 0.56) X Pa X 10(-2)] -0.52 (r = 0.71), where Pa is mean arterial pressure. The maximal vascular conductance (i.e., slope of the P-F relation) of the diaphragm was 27% of the conductance in the kidney, 87% of the value in the gut, and 42% of that in the heart. In conclusion the maximal diaphragmatic blood flow at a given blood pressure is much larger when the muscle is stimulated than is observed in spontaneously breathing animals.

Animals↗
PubMed1985

Effects of contraction frequency and duty cycle on diaphragmatic blood flow.

The effects of diaphragmatic contraction frequency (no. of intermittent tetanic contractions/min) at a given tension-time index and of duty cycle (contraction time/total cycle time) on diaphragmatic blood flow were measured in anesthetized mongrel dogs during bilateral supramaximal phrenic nerve stimulation. Diaphragmatic blood flow was measured by the radionuclide-labeled microsphere method. Contraction frequency was varied between 10 and 160/min at duty cycles of 0.25 and 0.75. Diaphragmatic blood flow increased with contraction frequency from 1.47 +/- 0.13 ml X min-1 X g-1 (mean +/- SE) at an average of 18/min to 2.65 +/- 0.16 ml X min-1 X g-1 at 74/min (P less than 0.01) with a duty cycle of 0.25 and from 1.32 +/- 0.19 ml X min-1 X g-1 at an average of 15/min to 1.96 +/- 0.15 ml X min-1 X g-1 at 80/min (P less than 0.02) with a duty cycle of 0.75. At higher contraction frequencies diaphragmatic blood flow did not increase further at both duty cycles. In addition, diaphragmatic blood flow was higher with a duty cycle of 0.25 than 0.75 at all contraction frequencies. We conclude that frequency of contraction is a major determinant of diaphragmatic blood flow and that high duty cycle impedes diaphragmatic blood flow.

Abdomen↗