Effects of posture on the venodilatory response to nitroglycerin

To determine the effects of posture on the venodilatory response to nitroglycerin (TNG), the change in forearm venous volume after inflation of an upper arm cuff to 30 mmHg above cuff zero (VV[30]) was measured during control conditions and after TNG (0.8 mg spray) in 18 healthy young volunteers in the supine position and the sitting position. VV[30] was 3.24 +/- 0.98 ml/100 ml arm in the supine position and 2.46 +/- 1.32 ml/100 ml arm in the sitting position. TNG increased VV[30] by 0.56 +/- 0.19 ml/100 ml arm in supine subjects, but by only 0.38 +/- 0.17 ml/100 ml arm in sitting subjects (P = 0.013). When limb volume was measured in the forearm and calf without using a cuff to produce venous congestion, the increase in limb volume with TNG was significantly greater in the sitting than in the supine position. Because the fall in both systolic and diastolic pressure and the rise in heart rate were significantly greater after TNG was administered in the sitting position, it is suggested that a greater reflex venoconstriction occurred in this posture, which antagonized the TNG-induced increase in venous distensibility. In the seated position, the effect of gravity more than compensated for the impaired venodilatory response to TNG. These results suggest that TNG causes a greater reduction in venous return to the heart when administered in the sitting position than in the supine position.     

Effect of high local temperature on reflex cutaneous vasodilation

We examined the effect of high local forearm skin temperature (Tloc) on reflex cutaneous vasodilator responses to elevated whole-body skin (Tsk) and internal temperatures. One forearm was locally warmed to 42 degrees C while the other was left at ambient conditions to determine if a high Tloc could attenuate or abolish reflex vasodilation. Forearm blood flow (FBF) was monitored in both arms, increases being indicative of increases in skin blood flow (SkBF). In one protocol, Tsk was raised to 39-40 degrees C 30 min after Tloc in one arm had been raised to 42 degrees C. In a second protocol, Tsk and Tloc were elevated simultaneously. In protocol 1, the locally warmed arm showed little or no change in blood flow in response to increasing Tsk and esophageal temperature (average rise = 0.76 +/- 1.18 ml X 100 ml-1 X min-1), whereas FBF in the normothermic arm rose by an average of 8.84 +/- 3.85 ml X 100 ml-1 X min-1. In protocol 2, FBF in the normothermic arm converged with that in the warmed arm in three of four cases but did not surpass it. We conclude that local warming to 42 degrees C for 35-55 min prevents reflex forearm cutaneous vasodilator responses to whole-body heat stress. The data strongly suggest that this attenuation is via reduction or abolition of basal tone in the cutaneous arteriolar smooth muscle and that at a Tloc of 42 degrees C a maximum forearm SkBF has been achieved. Implicit in this conclusion is that local warming has been applied for a duration sufficient to achieve a plateau in FBF.     

Methylene blue inhibits hypoxic cerebral vasodilation in awake sheep.

Cerebral vasodilation in hypoxia may involve endothelium-derived relaxing factor-nitric oxide. Methylene blue (MB), an in vitro inhibitor of soluble guanylate cyclase, was injected intravenously into six adult ewes instrumented chronically with left ventricular, aortic, and sagittal sinus catheters. In normoxia, MB (0.5 mg/kg) did not alter cerebral blood flow (CBF, measured with 15-microns radiolabeled microspheres), cerebral O2 uptake, mean arterial pressure (MAP), heart rate, cerebral lactate release, or cerebral O2 extraction fraction (OEF). After 1 h of normobaric poikilocapnic hypoxia (arterial PO2 40 Torr, arterial O2 saturation 50%), CBF increased from 51 +/- 5.8 to 142 +/- 18.8 ml.min-1 x 100 g-1, cerebral O2 uptake from 3.5 +/- 0.25 to 4.7 +/- 0.41 ml.min-1 x 100 g-1, cerebral lactate release from 2 +/- 10 to 100 +/- 50 mumol.min- x 100 g-1, and heart rate from 107 +/- 5 to 155 +/- 9 beats/min (P < 0.01). MAP and OEF were unchanged from 91 +/- 3 mmHg and 48 +/- 4%, respectively. In hypoxia, 30 min after MB (0.5 mg/kg), CBF declined to 79.3 +/- 11.7 ml.min-1 x 100 g-1 (P < 0.01), brain O2 uptake (4.3 +/- 0.9 ml.min-1 x 100 g-1) and heart rate (133 +/- 9 beats/min) remained elevated, cerebral lactate release became negative (-155 +/- 60 mumol.min-1 x 100 g-1, P < 0.01), OEF increased to 57 +/- 3% (P < 0.01), and MAP (93 +/- 5 mmHg) was unchanged. The sheep became behaviorally depressed, probably because of global cerebral ischemia. These results may be related to interference with a guanylate cyclase-dependent mechanism.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of nerve block on response of forearm blood flow to local temperature

To determine the role of neurotransmitter in the response of forearm blood flow (ABF) to local (forearm) skin temperature (Tsk) we measured ABF of six subjects at Tsk from 25 to 40 degrees C before (control) and after brachial plexus block (BPB). Control experiments were conducted in an ambient temperature of 27-29 degrees C, adjusted to minimize the subject's overall thermal sensation. Tsk was regulated by blowing a controlled-temperature airstream through a plastic bag enclosing the arm. We first lowered Tsk to 25 degrees C and after 20 min began to measure ABF with Whitney strain gauges. We then raised Tsk by 2.5 degrees C steps to 40 degrees C and measured ABF every 30 s for at least 10 min at each level of Tsk. Mean ABF rose from 1.1 ml X 100 ml-1 X min-1 at Tsk of 25 degrees C to 2.1 ml X 100 ml-1 X min-1 at 32.5 degrees C to 13.7 ml X 100 ml-1 X min-1 at 40 degrees C in control experiments and from 2.8 to 4.4 to 14.8 ml X 100 ml-1 X min-1 after BPB. The effect of Tsk on ABF was highly significant (P less than 0.0001) but the effect of BPB was not (P approximately equal to 0.2). At thermoneutrality, the effect of Tsk on ABF is largely independent of neural activity, since this effect is unaffected by nerve block.     

Cardiovascular responses to lower body negative pressure in trained and untrained older men.

To determine whether aerobic conditioning alters the orthostatic responses of older subjects, cardiovascular performance was monitored during graded lower body negative pressure in nine highly trained male senior athletes (A) aged 59-73 yr [maximum O2 uptake (VO2 max) = 52.4 +/- 1.7 ml.kg-1 x min-1] and nine age-matched control subjects (C) (VO2 max = 31.0 +/- 2.9 ml.kg-1 x min-1). Cardiac volumes were determined from gated blood pool scintigrams by use of 99mTc-labeled erythrocytes. During lower body negative pressure (0 to -50 mmHg), left ventricular end-diastolic and end-systolic volume indexes and stroke volume index decreased in both groups while heart rate increased. The decreases in cardiac volumes and mean arterial pressure and the increase in heart rate between 0 and -50 mmHg were significantly less in A than in C. For example, end-diastolic volume index decreased by 32 +/- 4 ml in C vs. 14 +/- 2 ml in A (P < 0.01), mean arterial pressure declined 7 +/- 5 mmHg in C and increased by 5 +/- 3 mmHg in A (P < 0.05), and heart rate increased 13 +/- 3 beats/min in C and 7 +/- 1 beats/min in A (P < 0.05). These data suggest that increased VO2 max among older men is associated with improved orthostatic responses.     

Postural cardiovascular reflexes: comparison of responses of forearm and calf resistance vessels

Simultaneous measurements were made of changes in vascular resistance in the forearm and calf in response to moving from supine to sitting or to head-down tilt. The subjects were healthy male volunteers, 21-63 yr. Blood flows were measured by venous occlusion plethysmography using mercury-in-Silastic strain-gauges. The gauges were maintained at the same level relative to the heart during the postural changes. Arterial blood pressure was measured by auscultation; heart rate was counted from the plethysmograms. Changing from supine to sitting caused a decrease in forearm blood flow from 4.13 +/- 0.14 to 2.16 +/- 0.19 ml.100 ml-1.min-1. Corresponding calf flows were 4.21 +/- 0.32 and 4.40 +/- 0.59 ml.100 ml-1.min-1. There was no change in mean arterial blood pressure, and heart rate increased by 8.0 +/- 1.5 beats/min. Arrest of the circulation of both legs with occlusion cuffs on the thighs before sitting, to prevent pooling of blood in them, reduced the degree of forearm vasoconstriction. Neck suction (40 Torr) during sitting, to oppose the decrease in transmural pressure at the carotid sinuses, inhibited the vasoconstriction. During a 30 degrees head-down tilt, there was a dilatation of forearm but not of calf resistance vessels. A Valsalva maneuver caused a similar constriction of both vascular beds. Thus, when changes in vascular resistance in forearm and calf are compared, the major reflex adjustments to changes in posture take place in the forearm.     

N omega-nitro-L-arginine influences cerebral metabolism in awake sheep.

Cerebral vasodilation in hypoxia may involve endothelium-derived relaxing factor-nitric oxide (NO). An inhibitor of NO formation, N omega-nitro-L-arginine (LNA, 100 micrograms/kg i.v.), was given to conscious sheep (n = 6) during normoxia and again in hypocapnic hypoxia (arterial PO2 approximately 38 Torr). Blood samples were obtained from the aorta and sagittal sinus, and cerebral blood flow (CBF) was measured with 15-microns radiolabeled microspheres. During normoxia, LNA elevated (P < 0.05) mean arterial pressure from 82 +/- 3 to 88 +/- 2 (SE) mmHg and cerebral perfusion pressure (CPP) from 72 +/- 3 to 79 +/- 3 mmHg, CBF was unchanged, and cerebral lactate release (CLR) rose temporarily from 0.0 +/- 1.9 to 13.3 +/- 8.7 mumol.min-1 x 100 g-1 (P < 0.05). The glucose-O2 index declined (P < 0.05) from 1.67 +/- 0.16 to 1.03 +/- 0.4 mumol.min-1 x 100 g-1. Hypoxia increased CBF from 59.9 +/- 5.4 to 122.5 +/- 17.5 ml.min-1 x 100 g-1 and the glucose-O2 index from 1.75 +/- 0.43 to 2.49 +/- 0.52 mumol.min-1 x 100 g-1 and decreased brain CO2 output, brain respiratory quotient, and CPP (all P < 0.05), while cerebral O2 uptake, CLR, and CPP were unchanged. LNA given during hypoxia decreased CBF to 77.7 +/- 11.8 ml.min-1 x 100 g-1 and cerebral O2 uptake from 154 +/- 22 to 105.2 +/- 12.4 mumol.min-1 x 100 g-1 and further elevated mean arterial pressure to 98 +/- 2 mmHg (all P < 0.05), CLR was unchanged, and, surprisingly, brain CO2 output and respiratory quotient were reduced dramatically to negative values (P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Reflex vascular defects in the orthostatic tachycardia syndrome of adolescents.

Dependent pooling occurs in postural orthostatic tachycardia syndrome (POTS) related to defective vasoconstriction. Increased venous pressure (Pv) >20 mmHg occurs in some patients (high Pv) but not others (normal Pv). We compared 22 patients, aged 12-18 yr, with 13 normal controls. Continuous blood pressure and strain-gauge plethysmography were used to measure supine forearm and calf blood flow, resistance, venous compliance, and microvascular filtration, and blood flow and swelling during 70 degrees head-up tilt. Supine, high Pv had normal resistance in arms (26 +/- 2 mmHg x ml(-1) x 100 ml x min) and legs (34 +/- 3 mmHg x ml(-1) x 100 ml x min) but low leg blood flow (1.5 +/- 0.4 ml x 100 ml(-1) x min(-1)). Supine leg Pv (30 +/- 2 vs. 13 +/- 1 mmHg in control) exceeded the threshold for edema (isovolumetric pressure = 19 +/- 3 mmHg). Supine, normal Pv had high blood flow in arms (4.1 +/- 0.2 vs. 3.5 +/- 0.2 ml x 100 ml(-1) x min(-1) in control) and legs (3.8 +/- 0.4 vs. 2.7 +/- 0.3 ml x 100 ml(-1) x min(-1) in control) with low resistance. With tilt, calf blood flow increased steadily in POTS with high Pv and transiently increased in normal Pv. Calf volume increased in all POTS patients. Arm blood flow increased in normal Pv only with forearm maintained at heart level. These data suggest that there are (at least) two subgroups of POTS characterized by high Pv and low flow or normal Pv and high flow. These may correspond to abnormalities in local or baroreceptor-mediated vasoconstriction, respectively.     

Low-dose estrogen therapy does not change postexercise hypotension, sympathetic nerve activity reduction, and vasodilation in healthy postmenopausal women

The aim of this study was to determine whether estrogen therapy enhances postexercise muscle sympathetic nerve activity (MSNA) decrease and vasodilation, resulting in a greater postexercise hypotension. Eighteen postmenopausal women received oral estrogen therapy (ET; n=9, 1 mg/day) or placebo (n=9) for 6 mo. They then participated in one 45-min exercise session (cycle ergometer at 50% of oxygen uptake peak) and one 45-min control session (seated rest) in random order. Blood pressure (BP, oscillometry), heart rate (HR), MSNA (microneurography), forearm blood flow (FBF, plethysmography), and forearm vascular resistance (FVR) were measured 60 min later. FVR was calculated. Data were analyzed using a two-way ANOVA. Although postexercise physiological responses were unaltered, HR was significantly lower in the ET group than in the placebo group (59+/-2 vs. 71+/-2 beats/min, P<0.01). In both groups, exercise produced significant decreases in systolic BP (145+/-3 vs. 154+/-3 mmHg, P=0.01), diastolic BP (71+/-3 vs. 75+/-2 mmHg, P=0.04), mean BP (89+/-2 vs. 93+/-2 mmHg, P=0.02), MSNA (29+/-2 vs. 35+/-1 bursts/min, P<0.01), and FVR (33+/-4 vs. 55+/-10 units, P=0.01), whereas it increased FBF (2.7+/-0.4 vs. 1.6+/-0.2 ml x min(-1) x 100 ml(-1), P=0.02) and did not change HR (64+/-2 vs. 65+/-2 beats/min, P=0.3). Although ET did not change postexercise BP, HR, MSNA, FBF, or FVR responses, it reduced absolute HR values at baseline and after exercise.     

Captopril attenuates reflex adrenergic response in essential hypertension

An attenuation of adrenergic activity during the inhibition of endogenous angiotensin II formation was evaluated by determining plasma norepinephrine concentration after a single oral administration of captopril compared to that after nifedipine in essential hypertension. Captopril produced a fall in mean arterial pressure (-24 +/- 2 mmHg, p less than 0.01) which magnitude was the same as that gained by nifedipine (-22 +/- 3 mmHg, p less than 0.01). Reflex tachycardia due to hypotension was produced (+13 +/- 1 beats/min, p less than 0.01) after nifedipine but not after captopril (-1 +/- 2 beats/min, p greater than 0.05). Although the enhancement of plasma renin activity induced by captopril (+1.54 +/- 0.56 ng/ml/hr, p less than 0.05) was similar (p greater than 0.05) to that by nifedipine (+1.44 +/- 0.47 ng/ml/hr, p less than 0.05), plasma norepinephrine concentration increased less (p less than 0.01) after captopril (+100 +/- 23 ng/ml, p less than 0.05) than after nifedipine (+283 +/- 51 ng/ml, p less than 0.05). Thus, the diminished adrenergic activity is a likely candidate for the abolished reflex tachycardia after the inhibition of angiotensin I converting enzyme activity by captopril in essential hypertension.     

Heterogeneous responses of human limbs to infused adrenergic agonists: a gravitational effect?

Unlike quadrupeds, the legs of humans are regularly exposed to elevated pressures relative to the arms. We hypothesized that this "dependent hypertension" would be associated with altered adrenergic responsiveness. Isoproterenol (0.75-24 ng x 100 ml limb volume-1 x min-1) and phenylephrine (0.025-0.8 microg x 100 ml limb volume-1 x min-1) were infused incrementally in the brachial and femoral arteries of 12 normal volunteers; changes in limb blood flow were quantified by using strain-gauge plethysmography. Compared with the forearm, baseline calf vascular resistance was greater (38.8 +/- 2.5 vs. 26.9 +/- 2.0 mmHg x 100 ml x min x ml-1; P < 0.001) and maximal conductance was lower (46.1 +/- 11.9 vs. 59.4 +/- 13.4 ml x ml-1 x min-1 x mmHg-1; P < 0.03). Vascular conductance did not differ between the two limbs during isoproterenol infusions, whereas decreases in vascular conductance were greater in the calf than the forearm during phenylephrine infusions (P < 0.001). With responses normalized to maximal conductance, the half-maximal response for phenylephrine was significantly less for the calf than the forearm (P < 0.001), whereas the half-maximal response for isoproterenol did not differ between limbs. We conclude that alpha1- but not beta-adrenergic-receptor responsiveness in human limbs is nonuniform. The relatively greater response to alpha1-adrenergic-receptor stimulation in the calf may represent an adaptive mechanism that limits blood pooling and capillary filtration in the legs during standing.     

Influence of menstrual cycle on shivering, skin blood flow, and sweating responses measured at night

In 10 women, external cold and heat exposures were performed both in the middle of luteal phase (L) and in the early follicular phase (F) of the menstrual cycle. Serum progesterone concentrations in L and F averaged 46.0 and 0.9 nmol X l-1, respectively. The experiments took place between 3:00 and 4:30 A.M., when the L-F core temperature difference is maximal. At neutral ambient temperature, esophageal (Tes), tympanic (Tty), rectal (Tre), and mean skin (Tsk) temperatures averaged 0.59 degrees C higher in L than in F. The thresholds for shivering, chest sweating, and cutaneous vasodilation (heat clearance technique) at the thumb and forearm were increased in L by an average of 0.47 degrees C, related to mean body temperature [Tb(es) = 0.87Tes + 0.13 Tsk] and to Tes, Tty, Tre, or Tsk. The above-threshold chest sweat rate and cutaneous heat clearances at the thumb and forearm were also enhanced in L, when related to Tb(es) or time. The metabolic rate, arm blood flow, and heart rate at thermoneutral conditions were increased in L by 5.0%, 1.1 ml X 100 ml-1 X min-1, and 4.6 beats X min-1, respectively. The concomitant increase in threshold temperatures for all autonomic thermoregulatory responses in L supports the concept of a resetting of the set point underlying the basal body temperature elevation in L. The effects of the increased threshold temperatures are counteracted by enhanced heat loss responses.     

Homeostatic responses to caloric restriction: influence of background metabolic rate.

The biological responses to caloric restriction (CR) are generally examined in rats with elevated metabolic rates due to being housed at ambient temperatures (T(a)) below the zone of thermoneutrality. We determined the physiological and behavioral responses to 2 wk of 30-40% CR in male FBNF1 rats housed in cool (T(a) = 12 degrees C) or thermoneutral (TMN; T(a) = 30 degrees C) conditions. Rats were instrumented with telemetry devices and housed continuously in home-cage calorimeters for the entire experiment. At baseline, rats housed in cool T(a) had reduced rate of weight gain; thus a mild CR (5%) group at thermoneutrality for weight maintenance was also studied. Rats housed in cool T(a) exhibited elevated caloric intake (cool = 77 +/- 1; TMN = 54 +/- 2 kcal), oxygen consumption (Vo(2); cool = 9.9 +/- 0.1; TMN = 5.5 +/- 0.1 ml/min), mean arterial pressure (cool = 103 +/- 1; TMN = 80 +/- 2 mmHg), and heart rate (cool = 374 +/- 3; TMN = 275 +/- 4 beats/min). Cool-CR rats exhibited greater CR-induced weight loss (cool = -62 +/- 3; TMN = -42 +/- 3 g) and reductions in Vo(2) (cool = -2.6 +/- 0.1; TMN = -1.5 +/- 0.1 ml/min) but similar CR-induced reductions in heart rate (cool = -59 +/- 1; TMN= -51 +/- 7 beats/min). CR had no effect on arterial blood pressure or locomotor activity in either group. Unexpectedly, weight maintenance produced significant reductions in Vo(2) and heart rate. At thermoneutrality, a single day of refeeding effectively abolished CR-induced reductions in Vo(2) and heart rate. The results reveal that rats with low or high baseline metabolic rate exhibit comparable compensatory reductions in Vo(2) and heart rate and suggest that T(a) can be used to modulate the metabolic background on which the more prolonged effects of CR can be studied.     

Tracheobronchial perfusion during exercise in ponies

Tracheobronchial circulation during exercise has previously not been examined. Therefore blood flow to the trachea and bronchi (up to 7th generation of branching) was studied in seven healthy adult ponies at rest and during the 3rd and 10th min of exercise performed at a treadmill speed setting of 25 km/h. The ambient air temperature varied from 19 to 20 degrees C and humidity from 35 to 45%. To determine blood flow radionuclide-labeled 15-microns-diameter microspheres were injected into the left ventricle via a catheter advanced from the left carotid artery (exposed using local anesthesia), and a reference sample was obtained from the aorta. Adequate mixing of microspheres with blood was demonstrated by similar perfusion values for left and right kidneys. Exercise increased heart rate (194 +/- 9 and 200 +/- 7 beats/min) and mean aortic pressure (169 +/- 8 and 156 +/- 4 mmHg) of ponies at 3rd and 10th min. Tracheal blood flow (6.7 +/- 0.5 ml.min-1 x 100 g-1) of resting ponies was only one-third of the bronchial blood flow (21.6 +/- 4.9 ml.min-1 x 100 g-1) Significant changes in tracheal perfusion did not occur at 3rd or 10th min of exercise. Although bronchial perfusion also did not change at the 3rd min of exercise, it rose dramatically to 202.8 +/- 30.3 ml.min-1 x 100 g-1 during the 10th min. Concomitantly, renal blood flow decreased at 10th min of exertion. The large increase in bronchial blood flow at 10th min of exertion may have been necessitated by the need to help dissipate body heat.     

Modification of the cutaneous vascular response to exercise by local skin temperature

This study examined how local forearm temperature (Tloc) affects the responsiveness of the cutaneous vasculature to a reflex drive for vasoconstriction. We observed responses in forearm blood flow (FBF) and arterial blood pressure to a 5-min bout of supine leg exercise of moderate intensity (125-175 W) after the forearm had been locally warmed to 36, 38, 40, or 42 degrees C for 48 min. With exercise, FBF fell by 1.82 +/- 0.23, 4.06 +/- 0.58, and 3.64 +/- 1.48 ml X 100 ml-1 X min-1 at 36, 38, and 40 degrees C, respectively, and rose by 2.16 +/- 0.57 ml X 100 ml X min-1 at a Tloc of 42 degrees C (mean +/- SE). Forearm vascular conductance (FVC) fell with the onset of exercise by averages of 2.77 +/- 0.57, 7.02 +/- 0.51, 5.36 +/- 0.85, and 4.17 +/- 0.79 ml X 100 ml-1 X min-1 X 100 mmHg-1 at 36, 38, 40, and 42 degrees C, respectively. Second-order polynomial regression analysis indicated that the reductions in FVC were greatest near a Tloc of 39 degrees C and that at a Tloc of 40 or 42 degrees C the cutaneous vasoconstrictor response to the onset of exercise is attenuated. Although elevated Tloc can be used to increase base-line FBF levels to make cutaneous vasoconstrictor responses more obvious, the direct effects of Tloc on this response must also be considered. We conclude that the optimum Tloc for observing reflex cutaneous vasoconstriction is near 39 degrees C.     

External compression increases forearm perfusion.

Application of compression stockings to the lower extremities is a widely used therapeutic intervention to improve venous return, but there is little information about the effects of compression on local arterial perfusion. Therefore, we tested the hypothesis that a positive external pressure increases forearm perfusion. The relation of increasing external pressure induced by standardized compression to the arterial inflow and arterial flow reserve of the forearm was critically evaluated in a group of healthy young men (n = 9). Flow was measured with venous occlusion plethysmography after a 10-min application of six different stockings with compression pressure increasing from 13 to 23 mmHg. During compression, the arterial inflow increased significantly from 3.7 +/- 0.85 to 8.8 +/- 2.01 ml.min(-1).100 ml tissue(-1) (P < 0.001) and the arterial flow reserve increased from 17.7 +/- 4.7 to 28.3 +/- 7.0 ml.min(-1).100 ml tissue(-1). The flow increase was persistent after 3 h of constant application of external pressure and also during simultaneous low-intensity hand grip. Similar results obtained with occlusion plethysmography were seen with MRI. During the interventions, forearm temperature was unchanged, and the volunteers reported no discomfort. In conclusion, 1) arterial perfusion of the human forearm increases more than twofold during application of external compression over a pressure range of 13-23 mmHg, and 2) the result is interpreted as an autoregulatory response following the decrease of the vascular transmural pressure gradient.     

Atrial natriuretic peptide inhibits compensatory responses when cardiac performance is depressed.

We tested the hypothesis that the atrial natriuretic peptide (ANP) mediated decrease in baroreceptor sensitivity that is seen in normal rats is more pronounced in a state of depressed cardiac performance. Holtzman rats (n = 15) were injected with Adriamycin (1 mg/kg i.p. 3 times/week for 8-10 weeks). Control rats (n = 17) were injected with 0.9% saline. Experiments were done in conscious animals that had been catheterized for i.v. infusions and for measurement of arterial blood pressure (ABP) and heart rate (HR). ANP (250 ng.kg-1.min-1) or saline vehicle was infused i.v. Graded periodic bolus injections of phenylephrine or sodium nitroprusside were given to assess baroreceptor sensitivity (beats.min-1.mmHg-1) up to 60 mmHg (1 mmHg = 133.3 Pa) above and below resting ABP. The following day the experiment was repeated with the ANP-vehicle regimen reversed. Finally, the rats were anesthetized and the rate of left ventricular pressure increase (dP/dt) was measured. Data evaluation included calculation of least squares linear regression slopes of peak delta HR vs. peak delta ABP, applying corrections for experimental errors in both the dependent and independent variables. Adriamycin rats (A) did not differ significantly from control rats (C) with respect to either initial ABP (A = 105 +/- 5; C = 100 +/- 3; mean mmHg +/- SEM) or initial HR (335 +/- 9 vs. 312 +/- 13 beats.min-1). However, their indices of cardiac performance were significantly depressed.(ABSTRACT TRUNCATED AT 250 WORDS)     

Rapid blunting of sympathetic vasoconstriction in the human forearm at the onset of exercise.

The purpose of this study was to test the hypothesis that sympathetic vasoconstriction is rapidly blunted at the onset of forearm exercise. Nine healthy subjects performed 5 min of moderate dynamic forearm handgrip exercise during -60 mmHg lower body negative pressure (LBNP) vs. without (control). Beat-by-beat forearm blood flow (Doppler ultrasound), arterial blood pressure (finger photoplethysmograph), and heart rate were collected. LBNP elevated resting heart rate by approximately 45%. Mean arterial blood pressure was not significantly changed (P = 0.196), but diastolic blood pressure was elevated by approximately 10% and pulse pressure was reduced by approximately 20%. At rest, there was a 30% reduction in forearm vascular conductance (FVC) during LBNP (P = 0.004). The initial rapid increase in FVC with exercise onset reached a plateau between 10 and 20 s of 126.6 +/- 4.1 ml. min(-1). 100 mmHg(-1) in control vs. only 101.6 +/- 4.1 ml. min(-1). 100 mmHg(-1) in LBNP (main effect of condition, P = 0.003). This difference was quickly abolished during the second, slower phase of adaptation in forearm vascular tone to steady state. These data are consistent with a rapid onset of functional sympatholysis, in which local substances released with the onset of muscle contractions impair sympathetic neural vasoconstrictor effectiveness.     

Effects of airflow and work load on cardiovascular drift and skin blood flow

Cardiovascular drift (CVD) can be defined as a progressive increase in heart rate (HR), decreases in stroke volume (SV) and mean arterial pressure (MAP), and a maintained cardiac output (Q) during prolonged exercise. To test the hypothesis that the magnitude of CVD would be related to changes in skin blood flow ( SkBF ), eight healthy, moderately trained males performed 70-min bouts of cycle ergometry in a 2 X 2 assortment of airflows (less than 0.2 and 4.3 m X s-1) and relative work loads (43.4% and 62.2% maximal O2 uptake). Ambient temperature and relative humidity were controlled to mean values of 24.2 +/- 0.8 degrees C and 39.5 +/- 2.4%, respectively. Q, HR, MAP, SkBF , skin and rectal temperatures, and pulmonary gas exchange were measured at 10-min intervals during exercise. Between the 10th and 70th min during exercise at the higher work load with negligible airflow, HR and SkBF increased by 21.6 beats X min-1 and 14.0 ml X 100 ml-1 X min-1, respectively, while SV and MAP decreased by 16.4 ml and 11.3 mmHg. The same work load in the presence of 4.3 m X s-1 airflow resulted in nonsignificant changes of 7.6 beats X min-1, 4.0 ml X (100 ml-1 X min)-1, -2.7 ml, and -1.7 mmHg for HR, SkBF , SV, and MAP. Since nonsignificant changes in HR, SkBF , SV, and MAP were observed at the lower work load in both airflow conditions, the results emphasize that CVD occurs only in conditions which combine high metabolic and thermal circulatory demands.(ABSTRACT TRUNCATED AT 250 WORDS)     

Reversible impairment of forearm vasodilation after forearm casting

To examine whether the resumption of normal physical activity after forearm immobilization would reverse impaired vasodilation, the minimal vascular resistance was examined in six subjects who had forearm casts placed for broken forearm bones. Each subject was examined twice, once within 48 h after forearm cast removal and again approximately 29 days later. The formerly casted forearm and the opposite forearm (noncasted) were examined. Minimal vascular resistance decreased in the casted forearm from 3.0 +/- 0.4 to 2.6 +/- 0.5 mmHg.ml-1.min.100 ml (P less than 0.014). There was no change in the noncasted forearm: 2.5 +/- 0.3 vs. 2.5 +/- 0.3 mmHg.ml-1.min.100 ml. This study shows that maximal vasodilation improves with the resumption of normal physical activity and therefore demonstrates that immobilization is associated with a reduced forearm vasodilator capacity.