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Biomedical subjects

S Magder

Publications and source records attributed to S Magder.

At least 37 records · Page 2Linked to original sources
PubMed1999

Low systemic vascular resistance state in patients undergoing cardiopulmonary bypass.

OBJECTIVE: To determine the prevalence, hemodynamic characteristics, and risk factors for the low systemic vascular resistance (SVR) state in patients who have undergone cardiopulmonary bypass. DESIGN: Prospective cohort study. SETTING: The intensive care unit of a tertiary care hospital. PATIENTS: Seventy-nine consecutive patients who underwent coronary artery bypass graft, mitral valve, or aortic valve procedures. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Low SVR was defined as an indexed systemic vascular resistance (SVRi) of <1800 dyne x sec/cm5 x m2 at two consecutive times postoperatively. SVRi, cardiac index, mean arterial pressure, temperature, and central venous pressure were recorded before bypass and at 0, 1, 2, 4, 8, and 16 hrs after bypass. We recorded age, gender, urgency of operation, use of angiotensin-converting enzyme inhibitors and calcium channel blockers, ejection fraction, pump time, cross-clamp time, use of antifibrinolytics, type of oxygenator, amrinone use, postoperative biochemical and hematologic values, medication use, fluid balance, intensive care unit admission duration, and hospital admission duration. We assessed the role of diabetes mellitus, current smoking, and systemic hypertension. The incidence of the low-SVR state was 35 of 79 patients during a 3-month period (44%). At 8 hrs postoperatively, the SVRi in low-SVR and non-low-SVR patients was 1594+/-50 (SEM) and 2103+/-56 (SEM) dyne x sec/cm5 x m2, respectively (p < .001). In low-SVR patients, there was an initial and sustained increase in cardiac index and central venous pressure that preceded the decrease in mean arterial pressure. The decrease in mean arterial pressure was maximal at 8 hrs postoperatively. Patients with low SVR were more likely to have longer cross-clamp times, to be male, and to have lower postoperative platelet counts (p < .05 for all). Low-SVR patients were less likely to require dobutamine in the first 4 hrs postoperatively. CONCLUSIONS: Low SVR, a probable manifestation of systemic inflammatory response syndrome, is common in patients after cardiopulmonary bypass. These patients may respond better to a vasopressor to restore vascular tone than to volume loading to further increase cardiac index.

Analysis of Variance↗
PubMed1999

Hemodynamic response to norepinephrine with and without inhibition of nitric oxide synthase in porcine endotoxemia.

The objective of this study was to determine the circuit and cardiac effects of norepinephrine (NE) with and without endotoxin, and how these responses are modified by the inhibition of nitric oxide synthase (NOS). We anesthetized eight pigs and instrumented them for measurements of cardiac output (Q), arterial pressure (Part), and mean pulmonary arterial pressure (Ppa). We also placed a 40-ml balloon in the right atrium for transient obstruction of flow and measurement of the mean circulatory filling pressure (MCFP) and resistance to venous return (RVR). After baseline measurements, animals were treated with 10 microg/kg/h of Escherichia coli endotoxin. At 105 min the measurements were repeated. We then infused 12.5 mg/kg of N(G)-nitro-L-arginine methyl ester (L-NAME) for 10 min and repeated the measurements. At baseline, at the end of endotoxin infusion, and after L-NAME infusion we infused 3, 9, and 27 microg/min of NE for 10 min each, and recorded hemodynamic measurements at each dose. NE shifted the venous return curve (i.e., increased MCFP) to the right without changing RVR, and increased cardiac output (CO) both at baseline and after endotoxin. Endotoxemia markedly flattened the dose-response curves for the change in Part, Ppa, CO, and heart rate with NE. The peak response of Part to NE after endotoxemia was restored with L-NAME, but the other dose-response curves were not affected. NE also did not shift the venous return curve after L-NAME. Furthermore, the increase in Part with NE was of shorter duration after L-NAME than in the baseline condition. In conclusion, NE shifts the venous return curve to the right and improves CO in endotoxic and nonendotoxic conditions. Endotoxemia decreases the arterial responsiveness to NE. L-NAME partly restored this loss of responsiveness in arteries but not in the venous circulation.

Adrenergic alpha-Agonists↗
PubMed1998

Cardiac versus noncardiac limits to exercise after heart transplantation.

BACKGROUND: To determine whether the reduced exercise capacity of patients after heart transplantation is primarily a result of decreased cardiac or peripheral vascular factors, we examined the cardiac output (CO) and right atrial pressure (Pra) relation during graded cycle ergometry. METHODS AND RESULTS: We studied 12 male patients (51.2+/-15.3 years [mean+/-SD]) 35.3+/-12.5 weeks after heart transplantation and 6 young healthy men. Patients had a normal increase in CO with increasing oxygen uptake (VO2) (CO = 0.00597 VO2 + 4.4, r = 0.83). Mean (+/-SEM) heart rate increased from 97.0+/-5.0 beats/min at rest to 146.9+/-6.9 beats/min at peak effort compared with the increase of 67.2+/-1.9 beats/min to 187.2+/-2.5 beats/min in the normal group. Pra in patients increased from 1.6+/-1.0 mm Hg at rest to 8.9+/-1.6 mm Hg during mild exercise but did not increase further at the highest work rates, even though CO continued to increase. In the normal group there was an initial increase in Pra from rest to exercise transition but little further change in Pra with increasing CO. Aerobic capacity (peak VO2) did not increase when cardiac function was increased with dobutamine during exercise in two patients. CONCLUSIONS: The steep increase in CO relative to Pra during severe exercise in patients who undergo heart transplantation argues against the heart as the sole limiting factor during maximal effort.

Atrial Function, Right↗
PubMed1998

Role of neurosympathetic pathways in the vascular response to sepsis.

PURPOSE: The aim of this study was to determine the role of sympathetic neural activity in the hemodynamic adaptations to sepsis in pigs with an emphasis on circuit adaptations. A fall in resistance to venous return (RVR) was predicted in contrast to what was previously observed in sympathetically intact animals that had no change in RVR. MATERIALS AND METHODS: We anesthetized and ventilated 13 pigs and gave 5 mg/kg of indomethacin. We measured cardiac output (CO) by thermodilution and measured pulmonary arterial (PAP), pulmonary capillary wedge (Pcw), right atrial pressure (Pra), and arterial pressure (MAP). Intermittent inflation of a 50-mL balloon in the right atrium was used to transiently arrest the circulation for the measurement of mean circulatory filling pressure (MCFP). RVR was calculated from (MCFP - Pra)/CO. Animals were divided into two groups; 6 received 10 mg/kg of the ganglionic blocker, hexamethonium and norepinephrine to maintain MAP; 7 had their spinal cords cut at C-2. After baseline measurements, all animals received 10 microg/kg/h of endotoxin for 2 hours, and hemodynamic measurements were repeated. Plasma samples were obtained for measurements of immunoreactive endothelin-1 (ET-1), which was assayed by a radioimmunoassay. RESULTS: Hexamethonium had no significant effect on hemodynamics except for an increase in heart rate. After endotoxin, MAP and SVR fell, PAP rose, and CO and RVR did not change. Spinal section resulted in an increase in heart rate and small increase in PAP and MCFR After endotoxin, there was a further increase in heart rate, PAP, and MCFP with a marked fall in MAP and CO. RVR increased from 2.1 +/- 0.46 after spinal section to 3.6 +/- 54 mm x min/L (P < .05). ET-1 in the hexamethonium group (n = 2) rose from 2.21 +/- .14 to 11.5 +/- 2.1 pg/ml at 2 hours, and in the spinal group (n = 7) from 2.04 +/- 0.77 to 6.85 +/- 3.9 pg/mL at 45 minutes. CONCLUSION: Spinal section resulted in a more profound fall in blood pressure and less increase in MCFP than in previously studied animals with sympathetic nervous system intact, but there was still an increase in RVR and PAP ET-1 is a possible mediator of the increase in RVR and PAP.

Adaptation, Physiological↗
PubMed1998

Clinical death and the measurement of stressed vascular volume.

OBJECTIVES: To measure stressed vascular volume in humans and to review the concepts of stressed and unstressed vascular volume. DESIGN: Observational study during surgical procedure. SETTING: Operating room at a university hospital. PATIENTS: Five patients undergoing hypothermic circulatory arrest for surgery on major vessels. INTERVENTION: We measured the volume that drained from the patient to the reservoir of the pump when the pump was turned off. MEASUREMENTS AND MAIN RESULTS: Stressed volume was 20.2+/-1.0 mL/kg, which is 30% of the predicted blood volume of these patients. CONCLUSION: The amount of blood volume that determines vascular filling pressure is only about a quarter of the total predicted volume, which means that there is a large reserve of unstressed volume that can be recruited to maintain vascular filling pressure.

Animals↗
PubMed1998

Evidence for constitutive release of nitric oxide in the venous circuit of pigs.

To determine whether the venous circuit constitutively produces nitric oxide (NO), we infused the NO synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME) into anesthetized and mechanically ventilated pigs and measured venous circuit parameters. We measured cardiac output (Q) by thermodilution and obtained arterial (Part), central venous pressure (in the inferior vena cava), right atrial (Pra), pulmonary artery (PAP), and pulmonary capillary wedge pressures. A balloon was transiently inflated in the right atrium to stop venous return and obtain mean circulatory filling pressure (MCFP). Venous compliance (Cv) was measured by volume boluses. Starling curves were obtained from changes in Q with changes in Pra from the boluses. Resistance to venous return (RVR) was calculated from (MCFP - Pra)/Q. After baseline measurements, we infused 25 mg/kg of L-NAME over 10 min in seven pigs and monitored them for a further 2 h. Three others served as time controls and showed no significant hemodynamic changes. L-NAME markedly decreased cardiac output from 3.8+/-0.86 to a low of 2.0+/-0.2 L/min, and increased blood pressure from 114+/-16 to 144+/-11 mm Hg and pulmonary artery pressure from 15+/-2 to 30+/-12 mm Hg (p < 0.05). MCFP increased from 9.1+/-1.2 to 11.4+/-2.4 mm Hg (p < 0.05); Cv did not change. Cardiac function curves were markedly depressed and flattened and remained depressed for 2 h. The increase in RVR of 167% from 1.8+/-0.6 mm Hg/L/min at baseline to 5.4+/-3.7 mm Hg/L/min (p < 0.05) was similar to the 188% increase in systemic vascular resistance. These data indicate that constitutive release of NO decreases baseline venous resistance and increases capacitance. There also appears to be a worsening of cardiac function when NOS is inhibited.

Animals↗
PubMed1998

Exercise capacity and energy expenditure of morbidly obese and previously obese subjects.

OBJECTIVE: To determine whether morbidly obese and previously obese women fail to lose weight after gastric bypass surgery because of reduced energy expenditure, and whether a large, surgically induced, rapid weight loss improves exercise capacity on a treadmill. DESIGN: Cross-sectional study. PARTICIPANTS: Four groups of 5 subjects: 1) patients still obese 12 months after surgery (failure); 2) patients who achieved normal weight after surgery (success); 3) obese patients who had not yet undergone surgery (preoperative); and 4) nonobese (control) subjects. Four subjects in the preoperative group were studied again at 6 months postsurgery. MAIN OUTCOME MEASURES: Total daily energy expenditure (TDEE), and exercise capacity and peak oxygen consumption (VO2) during treadmill exercise. RESULTS: TDEE or energy expenditure (EE) above basal metabolic rate (when normalized for body size) was similar for all groups, but the absolute energy consumption was higher in the preoperative and failure groups. Treadmill endurance time was greater in the success than the failure and preoperative groups, and the endurance times of these 3 groups were less than those of the nonobese subjects. Peak VO2 body weight was similar in the success, failure and preoperative groups, which meant that the peak VO2 was lower in the success group than in the preoperative and failure groups. Six months after surgery, peak VO2 had not decreased in the preoperative group. CONCLUSION: Failure to lose weight after isolated gastric bypass surgery was not because of a lower level of activity. Aerobic capacity was impaired 1 year, but not 6 months, after a large weight loss. Exercise training may be appropriate to maintain absolute peak oxygen consumption.

Adult↗
PubMed1997

Effects of adenosine on pressure-flow relationships in an in vitro model of compartment syndrome.

Blood flow through skeletal muscle is best modeled with a vascular waterfall at the arteriolar level. Under these conditions, flow is determined by the difference between perfusion pressure (Pper) and the waterfall pressure (Pcrit), divided by the arterial resistance (Ra). By pump perfusing an isolated canine gastrocnemius muscle (n = 6) after it was placed within an airtight box, with and without adenosine infusion, we observed an interaction between the pressure surrounding a muscle (as occurs in compartment syndrome) and baseline vascular tone. We titrated adenosine concentration to double baseline flow. We measured Pcrit and Ra at box pressures (Pbox), which resulted in 100 (Pbox = 0), 90, 75, and 50% flow without adenosine; and 200, 180, 150, 100, and 50% flow with adenosine. Without adenosine, each 10% decline in flow was associated with a 5.7 mmHg increase in Pcrit (P < 0.01). With adenosine, the same decrease in flow was associated with a 2.6-mmHg increase in Pcrit (P < 0.01). Values of Pcrit at 50% of flow were almost identical. Each 10% decrease in flow was also associated with 2.2% increase in Ra with or without adenosine (P < 0.001). Ra decreased with adenosine infusion (P < 0.05), and there was no interaction between adenosine and flow (P > 0.9). We conclude that increases in pressure surrounding a muscle limit flow primarily through changes in Pcrit with and without adenosine-induced vasodilation. The interaction between Pbox and adenosine with respect to Pcrit but not Ra suggests that Pbox affects the tone of the vessels responsible for Pcrit but not Ra.

Adenosine↗
PubMed1997

The effects of changes in ventilation and cardiac output on expired nitric oxide.

The measurement of nitric oxide (NO) in expired gas is being increasingly reported in disease states such as sepsis, heart failure, and asthma. However, the effects of changes in ventilatory and cardiac parameters on expired NO are not known. Therefore, we assessed the effects of changes in minute ventilation (VE), ventilatory pattern, and cardiac output on expired gas NO levels in five anesthetized, intubated pigs. The animals were mechanically ventilated at three settings for each of respiratory rate (12 to 14, 16 to 18, and 22 to 24/min) and tidal volume (10, 15, and 20 mL/kg) applied in random sequence, yielding nine ventilatory patterns and a range of VE (3.7+/-0.1 to 13.2+/-0.8 L/min). When VE was increased, expired NO concentration declined slightly (r=-0.40, p<0.01), but the rate of excretion of NO in expired gas increased significantly (r=0.60, p<0.01). In contrast, when cardiac output was increased progressively from 3.6+/-0.1 to 4.7+/-0.3 and 5.8+/-0.4 L/min (p<0.01) by volume loading during constant eucapneic ventilation, there was no change in expired NO. Changes in VE over a physiologic range significantly affect the measurement of NO in expired gas, whereas short-term changes in cardiac output do not. To facilitate comparison between studies, we suggest that the measurement of expired NO should be reported in conjunction with data on VE.

Animals↗
PubMed1996

Circuit factors in the high cardiac output of sepsis.

PURPOSE: The increase of cardiac output (CO) in sepsis must be matched by an increase in venous return. Our goal was to determine which of the determinants of venous return are responsible in volume-loaded and nonvolume-loaded pigs with endotoxemia. The determinants include stressed volume, venous compliance (Cv), venous resistance (RVR) and right atrial pressure (Pra). We also tested the effect of the nitric oxide (NO) synthase inhibitor, N omega-nitro-L-arginine-methyl ester (L-NAME) after the hemodynamics with endotoxin stabilized. METHODS: Pigs were anesthetized and mechanically ventilated. We measured CO by thermodilution, mean circulatory filling pressure (MCFP) by inflating a balloon in the right atrium, blood volume by dye dilution, and Cv by rapid blood infusions. RVR was calculated from MCFP-Pra/CO). After baseline measurements, we infused 10 micrograms/(kg x h-1) of Escherichia coli endotoxin. Eight animals also received 30 mL x kg-1 of dextran over the 2 hours (volume treated), and seven did not (no volume). After 2 hours we injected 25 mg x kg-1 of the NO synthase inhibitor, L-NAME, and repeated the measurements. RESULTS: In volume-treated animals, CO increased from 3.9 +/- 0.7 to 5.4 +/- 0.8 L x min-1 (P < .05), and blood pressure (BP) fell from 118 +/- 9 to 76 +/- 12 mmHg. MCFP rose, and there was no change in RVR or Cv, whereas capacitance increased (ie, right shift of pressure-volume curve). Cardiac function (ie, Starling curve) did not change. In no-volume animals, CO fell from 4.47 +/- 0.64 to 2.50 +/- 0.86 L x min-1, BP from 114 +/- 10 to 9 +/- 13 mmHg and MCFP fell. Systemic vascular resistance did not change. Cardiac function was markedly depressed, and the heart rate increased from 143 +/- 13 to 203 +/- 30 beats x min-1. L-NAME restored BP in both groups but also increased RVR and depressed cardiac function. CONCLUSION: Changes in vascular tone during endotoxemia are dependent on volume status. The increased cardiac output in volume-treated septic animals occurred because of an increase in stressed volume due to the volume given in combination with a dilated vasculature. L-NAME restored arterial tone but decreased CO because of a rise in RVR and decrease in cardiac function.

Analysis of Variance↗
PubMed1996

Central venous pressure during exercise: role of muscle pump.

Central venous pressure (CVP) gives the integral result of changes in cardiac and peripheral factors. Thus, the sudden increase in CVP observed at the onset of dynamic exercise has been attributed to the action of the muscle pump but is also affected by reflex changes in cardiac response. To determine which predominates at the onset of exercise, we compared the change in CVP from rest to onset of upright exercise and after 3 min of exercise in four healthy normal subjects (N) and six patients following heart transplantation (HT), who thus had a delayed cardiac response. CVP immediately increased to a similar extent in both groups at exercise onset (by 4.6 +/- 0.6 mmHg (1 mmHg = 133.3 Pa) in HT and 4.0 +/- 0.4 mmHg in N) (mean +/- SE). After 3 min of exercise, CVP remained constant in N (2.0 +/- 1.1 vs. 2.6 +/- 1.8 at onset) but increased further in HT (7.0 +/- 0.8 vs. 3.5 +/- 1.1 at onset, p < 0.05). The immediate increase in CVP with leg movement in both groups supports an initial central shift in blood volume because of muscle contractions. During the first minute of exercise, muscle blood flow most likely continues to increase and CVP increased further in HT but not in N, which had adequate reflex cardiac adjustment. We conclude that the muscle pump increases CVP at exercise onset, but the interaction between cardiac response and circuit function determines CVP as exercise continues.

Adult↗
PubMed1995

The mechanical effects of contractions on blood flow to the muscle.

To determine whether muscle contractions can increase muscle blood flow independently from metabolic factors, we isolated the vasculature of the left diaphragm or gastrocnemius muscle of anesthetized and mechanically ventilated dogs. Arterial blood flow was controlled with a constant pressure source and the arterial pressure (Pa) was decreased in steps to obtain pressure-flow relationships (P-Q). The local vasculatures were maximally dilated with nitroprusside [mean (SD) 114.0 (32.0) micrograms.min-1], adenosine [1.43 (0.41) mmol.l-1.min-1], and acetylcholine [1.43 (0.41) mmol.l-1.min-1] and the P-Q with and without spontaneous contractions (n = 6), stimulated twitches (n = 12, 2-4 Hz), or tetanic trains (n = 7, 25 Hz) in the diaphragm and stimulated twitches (n = 6, 2-4 Hz), or tetanic contractions (n = 6, 12-16 trains) in the gastrocnemius were compared. The pressure axis intercept decreased (P < 0.5) with spontaneous contractions in the diaphragm and the slope did not change. At Pa of 13.3 kPa, flow increased from 36.2 (34.9) to 43.9 (38.2) ml.min-1.100 g-1 (P < 0.05). During twitch contractions, the slope and intercept of the P-Q were not significantly different from vasodilatation alone, but the flow at a pressure of 13.3 kPa increased slightly. In the gastrocnemius (n = 6), continuous and intermittent tetanic contractions did not affect P-Q or flow at Pa of 100 mmHg (n = 6). Furthermore, increasing venous pressure to 6.7 kPa did not affect flow in this muscle. We conclude that the muscle pump has only a small direct effect on muscle blood flow and its main effect is to reduce venous pressures.

Animals↗
PubMed1995

Monitoring complication due to a pulsatile femoral vein from tricuspid regurgitation.

This clinical report illustrates a monitoring complication due to a pulsatile femoral vein from tricuspid regurgitation. In this case, the femoral vein of a patient was inadvertently cannulated and exhibited a pulsatile tracing which was mistaken for an arterial pressure tracing. This led to the initial inappropriate use of vasopressors which actually augmented the pulsatility and delayed detection of the error. Although this may be a rare occurrence, the clinician should be aware of its possibility when using invasive monitoring in a patient with tricuspid regurgitation.

Aged↗
PubMed1995

Local and systemic effects of endotoxin in contracting skeletal muscle.

PURPOSE: This study was performed to determine the direct effect of endotoxin on force generation, O2 consumption and vascular resistance in contracting skeletal muscle. MATERIALS AND METHODS: We vascularly isolated the gastrocnemius muscle of dogs anesthetized with sodium pentobarbital and mechanically ventilated. The muscle was perfused from a proximal vessel or by a pump that withdrew blood from the contralateral leg. The nerve to the muscle was stimulated with supramaximal voltage 12 tr/min, 15-Hz impulses and a duty cycle of 0.4. Blood flow was measured with an electromagnetic flow probe, and oxygen consumption (VO2) was calculated from the flow and arterial-venous O2 content. In Protocol 1 (local infusion), contractions were stimulated for 30 minutes and endotoxin (n = 6) or saline (n = 6) was infused into the vasculature of the isolated gastrocnemius muscle after 10 minutes of contraction and continued for another 20 minutes of contraction. In Protocol 2 (systemic infusion), The normal tension and flow to the gastrocnemius were established and endotoxin (n = 5) or saline (n = 5) infused systemically. One hour later, the flow was set at the control level of contracting muscle, and contractions were stimulated for 30 minutes. RESULTS: In both groups, endotoxin did not alter the tension VO2, arterial venous oxygen difference, or vascular resistance at the end of the stimulation period. CONCLUSION: Endotoxin must affect muscle force production by acting through intermediates such as cytokines, and the effect is not apparent in the first 60 minutes.

Animals↗
PubMed1995

Effect of baroreceptor activation and systemic hypotension on plasma endothelin 1 and neuropeptide Y.

To determine whether endothelin (ET-1) and neuropeptide Y (NPY) release are controlled by the carotid sinus (CS) baroreceptor or local endothelial mechanisms, we isolated and pump perfused the CS in eight chloralose-anesthetized dogs and controlled systemic arterial pressure (SAP) with an elevated reservoir connected to both femoral arteries. This allowed the SAP to be kept constant while CS pressure was varied from 55.8 +/- 2.0 (low CS) to 192 +/- 1.9 (high CS) mmHg (1 mmHg = 133.3 Pa) or CS pressure to be kept constant while SAP was lowered to 53.9 +/- 1.8 mmHg (low SAP). There was no significant change in ET-1 when CS pressure was varied (control, 2.08 +/- 0.50; low CS, 2.18 +/- 0.51; high CS, 2.11 +/- 0.38 pg/mL), but ET-1 was significantly higher during low SAP (2.93 +/- 0.49 pg/mL, p < 0.05). This increase was not observed with vagi and CS intact in six dogs or with vagi intact and CS constant in four dogs. In contrast, plasma NPY was significantly higher in the low CS condition (619.13 +/- 66.87 pg/mL) versus high CS condition (528.88 +/- 45.19 pg/mL, p < 0.05) and did not change during hypotension. In conclusion, NPY, but not ET-1, is affected by CS baroreceptor manipulation, and plasma ET-1 increases in response to hemorrhagic hypotension when modulating reflexes are abolished.

Animals↗
PubMed1995

Effects of nifedipine on vascular waterfall and arterial resistance in canine hindlimb.

Pressure-flow relations in the canine hindlimb can be well explained by a vascular waterfall at the arteriolar level. Under these conditions, P(art) = Pcrit + Q.Rart, where P(art) is the arterial pressure, Pcrit is the waterfall pressure, Q is regional flow, and Rart is the arterial resistance of the vessels upstream from the waterfall. To determine whether calcium channels in vascular smooth muscle affect Pcrit in addition to Rart, we pump perfused canine hindlimbs and measured both variables over a range of perfusion pressures (Pper) before and during the infusion of the calcium channel blocker nifedipine. Nifedipine significantly decreased Pcrit and Rart at each Pper. Increasing Pper under control conditions from 50 to 150 mmHg significantly increased Pcrit from 24.2 +/- 1.5 to 42.5 +/- 2.2 mmHg. During nifedipine infusion, increasing Pper from 25 to 100 mmHg also increased Pcrit from 14.5 +/- 1.5 to 20.2 +/- 1.9 mmHg, but the rate of increase was less. In contrast to the rise in Pcrit with increasing Pper, Rart significantly decreased from 10.7 +/- 1.1 to 8.1 +/- 1.2 mmHg.min.100 g.ml-1 before nifedipine infusion, and from 5.7 +/- 0.4 to 2.2 +/- 0.1 mmHg.min.100 g.ml-1 during nifedipine infusion. Venous resistance (Rven) significantly decreased with increases in Pper and during nifedipine infusion. The regional elastic recoil pressure (Pel, a measure of small venular pressure) increased with both an increase in Pper and nifedipine. These results suggest that nifedipine decreases Pcrit, Rart, and Rven and that at constant Pper nifedipine increases Pel.

Animals↗
PubMed1995

NG-nitro-L-arginine and phenylephrine have similar effects on the vascular waterfall in the canine hindlimb.

Hindlimb pressure-flow relationships are well characterized by modeling a vascular waterfall at the arteriolar level. Under these conditions, Q = (Pper - Pcrit)/Rart, where Q is blood flow, Pper is perfusion pressure, Pcrit is waterfall pressure, and Rart is the resistance upstream from the waterfall. To determine the effects of endothelium-derived relaxing factor (EDRF) on Pcrit, Rart, and venous resistance (Rv), we varied Pper in the canine hindlimb between 100 and 200 mmHg before and after NG-nitro-L-arginine infusion (L-NNA, an inhibitor of EDRF synthesis). Before L-NNA, Pcrit increased with increasing Pper. After L-NNA, Pcrit was higher at each Pper, and the increase in Pcrit with increases in Pper was greater than under control conditions. In contrast to Pcrit, Rart decreased with increasing Pper before L-NNA. After L-NNA, Rart was higher at each Pper and no longer decreased with increasing Pper. Rv was not affected by Pper under control conditions but decreased with increasing Pper after L-NNA. The pressure in the small venules at each Pper decreased after L-NNA. In a second group of animals, we infused phenylephrine to control for increased tone produced by L-NNA. Results were similar to those seen with L-NNA. In conclusion, blocking EDRF synthesis increases both Pcrit and Rart, but the same response was also obtained with phenylephrine.

Animals↗