LIMB BLOOD FLOW AND VASCULAR RESISTANCE CHANGES IN DOGS DURING HEMORRHAGIC HYPOTENSION AND SHOCK

1946 ◽  
Vol 147 (4) ◽  
pp. 685-694 ◽  
Author(s):  
R. W. Eckstein ◽  
I. M. Liebow ◽  
C. J. Wi'ggers
Keyword(s):  
Blood Flow ◽  
Vascular Resistance ◽  
Limb Blood Flow ◽  
Hemorrhagic Hypotension

Local vasoconstriction in spinal cord-injured and able-bodied individuals

2007 ◽  
Vol 103 (3) ◽  
pp. 1070-1077 ◽  
Author(s):  
M. Kooijman ◽  
M. de Hoog ◽  
G. A. Rongen ◽  
H. J. M. van Kuppevelt ◽  
P. Smits ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Blood Flow ◽  
Vascular Resistance ◽  
Venous Occlusion ◽  
Myogenic Response ◽  
Cuff Inflation ◽  
Limb Blood Flow ◽  
Percent Increase ◽  
Spinal Cord Injured ◽  
Forearm Vascular Resistance

Local vasoconstriction plays an important role in maintaining blood pressure in spinal cord-injured individuals (SCI). We aimed to unravel the mechanisms of local vasoconstriction [venoarteriolar reflex (VAR) and myogenic response] using both limb dependency and cuff inflation in SCI and compare these with control subjects. Limb blood flow was measured in 11 male SCI (age: 24–55 yr old) and 9 male controls (age: 23–56 yr old) using venous occlusion plethysmography in forearm and calf during three levels of 1) limb dependency, and 2) cuff inflation. During limb dependency, vasoconstriction relies on both the VAR and the myogenic response. During cuff inflation, the decrease in blood flow is caused by the VAR and by a decrease in arteriovenous pressure difference, whereas the myogenic response does not play a role. At the highest level of leg dependency, the percent increase in calf vascular resistance (mean arterial pressure/calf blood flow) was more pronounced in SCI than in controls (SCI 186 ± 53%; controls 51 ± 17%; P = 0.032). In contrast, during cuff inflation, no differences were found between SCI and controls (SCI 17 ± 17%; controls 14 ± 10%). Percent changes in forearm vascular resistance in response to either forearm dependency or forearm cuff inflation were equal in both groups. Thus local vasoconstriction during dependency of the paralyzed leg in SCI is enhanced. The contribution of the VAR to local vasoconstriction does not differ between the groups, since no differences between groups existed for cuff inflation. Therefore, the augmented local vasoconstriction in SCI during leg dependency relies, most likely, on the myogenic response.

Pial vessel caliber and cerebral blood flow during hemorrhage and hypercapnia in the rabbit

1984 ◽  
Vol 247 (1) ◽  
pp. H40-H51 ◽  
Author(s):  
U. I. Tuor ◽  
J. K. Farrar
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Vascular Resistance ◽  
Hemorrhagic Hypotension ◽  
Pial Vessels ◽  
Vascular Dilatation ◽  
Pial Vessel ◽  
The Relationship ◽  
Arteriolar Diameter ◽  
Hydrogen Clearance

We examined the relationship between cerebral blood flow (CBF) and pial vessel caliber responses to graded hemorrhagic hypotension at both normocapnia and hypercapnia in 31 anesthetized rabbits. Changes in CBF (hydrogen clearance) and pial arteriolar diameter (image splitting) were predictably related at all perfusion pressures (PP). Three autoregulatory regions were identified. 1) At PP greater than 65 mmHg, autoregulation was complete as CBF and the CBF response to hypercapnia remained at control levels. The pial vessels dilated progressively, and their response to hypercapnia increased. 2) At PP between 65 and 35 mmHg autoregulation continued but was incomplete. CBF decreased proportionately less than the corresponding reductions in PP due to continued pial vascular dilatation. Both the CBF and pial vessel responses to hypercapnia diminished. 3) At PP less than 35 mmHg, autoregulation was abolished. Pial arteriolar caliber and CBF decreased pressure passively, and there were no responses to hypercapnia. A comparison of changes in pial vascular resistance and total precapillary resistance indicated that the responses of pial vessels (particularly those less than 50 micron) paralleled the responses of the intraparenchymal arterioles.

Hypercapnia potentiates renal vasoconstriction during hemorrhagic hypotension in awake rabbits

1984 ◽  
Vol 246 (5) ◽  
pp. H671-H674
Author(s):  
D. W. Busija
Keyword(s):  
Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Renal Blood Flow ◽  
Vascular Resistance ◽  
Renal Vasoconstriction ◽  
Hemorrhagic Hypotension ◽  
Severe Hypotension ◽  
Unanesthetized Animals ◽  
Renal Vascular

Although both hemorrhagic hypotension and hypercapnia increase renal vascular resistance (RVR) modestly, effects of interaction between these stimuli on RVR have not been examined systematically in unanesthetized animals. The purpose of this study was to test the hypothesis that renal vasoconstriction during hemorrhagic hypotension is affected by arterial CO2 tension (PCO2). Unanesthetized rabbits were placed into an environmental chamber, and six were exposed to normocapnia (PCO2 approximately 29 mmHg) and six to hypercapnia (PCO2 approximately 62 mmHg). Renal blood flow (RBF) was measured with 15-micrograms microspheres during 1) normotension [mean arterial pressure (MAP) 84-88 mmHg]; 2) moderate hemorrhagic hypotension (MAP 61-64 mmHg); and 3) severe hemorrhagic hypotension (MAP 44-50 mmHg). When MAP was normal, RBF was 437 +/- 59 and 345 +/- 59 ml X min-1 X 100 g-1 in the normocapnic and hypercapnic groups, respectively (NS; P greater than 0.05). In addition, RVR (MAP/RBF) was 0.22 +/- 0.04 in the normocapnic group and 0.32 +/- 0.08 mmHg X ml-1 X min X 100 g in the hypercapnic group (NS; P greater than 0.05). During moderate hypotension, RVR was 0.48 +/- 0.18 in the normocapnic group and 1.74 +/- 0.36 mmHg X ml-1 X min X 100 g in the hypercapnic group (P less than 0.05, comparison between groups). During severe hypotension, RVR was 0.46 +/- 0.14 and 3.13 +/- 1.13 mmHg X ml-1 X min X 100 g during normocapnia and hypercapnia, respectively (P less than 0.05, comparison between groups). Thus, in unanesthetized rabbits, although hypercapnia does not increase RVR compared with normocapnia when arterial pressure is normal, hypercapnia greatly potentiates renal vasoconstriction during hemorrhagic hypotension.

PERIPHERAL VASCULAR EFFECTS OF THE INSECTICIDE ENDRIN

1965 ◽  
Vol 43 (4) ◽  
pp. 531-539 ◽  
Author(s):  
Thomas E. Emerson Jr. ◽  
Lerner B. Hinshaw
Keyword(s):  
Blood Flow ◽  
Vascular Resistance ◽  
Small Vessel ◽  
Peripheral Vascular ◽  
Limb Blood Flow ◽  
Small Artery ◽  
Vascular Effects ◽  
Systemic Hypotension ◽  
Small Vein ◽  
Anesthetized Dogs

The peripheral vascular actions of insecticides are relatively unexplored. The effects of the chlorinated hydrocarbon insecticide endrin on vascular resistances were investigated in forelimbs of anesthetized dogs. Total arterial, small-vessel, and venous segmental resistances were determined in innervated and denervated limbs following lethal infusions of endrin. Limb weight was recorded continuously in some experiments. Endrin administration resulted in large increases in total limb vascular resistance, most of which were due to an increase in small-vessel (small artery to small vein) resistance. Arterial and venous segmental resistances also increased. Early responses of innervated and denervated limbs were similar. Limb blood flow decreased markedly, and when measured, limb weight fell progressively. These effects appear to result primarily from an increased level of circulating catecholamines. Hyperexcitability to noise, bradycardia, and hypertension preceded the development of systemic hypotension.

Diaphragmatic perfusion heterogeneity during exercise with inspiratory resistive breathing

1990 ◽  
Vol 68 (5) ◽  
pp. 2177-2181 ◽  
Author(s):  
M. Manohar
Keyword(s):  
Blood Flow ◽  
Exercise Capacity ◽  
Vascular Resistance ◽  
Maximal Exercise ◽  
Perfusion Pressure ◽  
Work Of Breathing ◽  
Regional Distribution ◽  
Resistive Breathing ◽  
Exercise Induced

Regional distribution of diaphragmatic blood flow (Q; 15-microns-diam radionuclide-labeled microspheres) was studied in normal (n = 7) and laryngeal hemiplegic (LH; n = 7) ponies to determine whether the added stress of inspiratory resistive breathing during maximal exercise may cause 1) redistribution of diaphragmatic Q and 2) crural diaphragmatic Q to exceed that in maximally exercising normal ponies. LH-induced augmentation of already high exertional work of breathing resulted in diminished locomotor exercise capacity so that maximal exercise in LH ponies occurred at 25 km/h compared with 32 km/h for normal ponies. The costal and crural regions received similar Q in both groups at rest. However, exercise-induced increments in perfusion were significantly greater in the costal region of the diaphragm. At 25 km/h, costal diaphragmatic perfusion was 154 and 143% of the crural diaphragmatic Q in normal and LH ponies. At 32 km/h, Q in costal diaphragm of normal ponies was 136% of that in the crural region. Costal and crural diaphragmatic Q in LH ponies exercised at 25 km/h exceeded that for normal ponies but was similar to the latter during exercise at 32 km/h. Perfusion pressure for the three conditions was also similar. It is concluded that diaphragmatic perfusion heterogeneity in exercising ponies was preserved during the added stress of inspiratory resistive breathing. It was also demonstrated that vascular resistance in the crural and costal regions of the diaphragm in maximally exercised LH ponies remained similar to that in maximally exercising normal ponies.

Sexual dimorphism in regional blood flow responses to vasopressin in conscious rats

1997 ◽  
Vol 273 (3) ◽  
pp. R1126-R1131 ◽  
Author(s):  
Y. X. Wang ◽  
J. T. Crofton ◽  
S. L. Bealer ◽  
L. Share
Keyword(s):  
Blood Flow ◽  
Vascular Resistance ◽  
Regional Blood Flow ◽  
Pressor Response ◽  
Peripheral Resistance ◽  
Female Rats ◽  
Sexually Dimorphic ◽  
Arterial Blood ◽  
Vasoconstrictor Response ◽  
Renal Vascular

The greater pressor response to vasopressin in male than in nonestrous female rats results from a greater increase in total peripheral resistance in males. The present study was performed to identify the vascular beds that contribute to this difference. Mean arterial blood pressure (MABP) and changes in blood flow in the mesenteric and renal arteries and terminal aorta were measured in conscious male and nonestrous female rats 3 h after surgery. Graded intravenous infusions of vasopressin induced greater increases in MABP and mesenteric vascular resistance and a greater decrease in mesenteric blood flow in males. Vasopressin also increased renal vascular resistance to a greater extent in males. Because renal blood flow remained unchanged, this difference may be due to autoregulation. The vasopressin-induced reduction in blood flow and increased resistance in the hindquarters were moderate and did not differ between sexes. Thus the greater vasoconstrictor response to vasopressin in the mesenteric vascular bed of male than nonestrous females contributed importantly to the sexually dimorphic pressor response to vasopressin in these experiments.

scholarly journals Adrenergic control of vascular resistance varies in muscles composed of different fiber types: influence of the vascular endothelium

2011 ◽  
Vol 301 (3) ◽  
pp. R783-R790 ◽  
Author(s):  
Bradley J. Behnke ◽  
Robert B. Armstrong ◽  
Michael D. Delp
Keyword(s):  
Blood Flow ◽  
Vascular Resistance ◽  
Vascular Endothelium ◽  
Fold Increase ◽  
Male Rats ◽  
Type I ◽  
Fiber Types ◽  
Fast Twitch Muscle ◽  
Dose Responses ◽  
Fast Twitch

The influence of the sympathetic nervous system (SNS) upon vascular resistance is more profound in muscles comprised predominately of low-oxidative type IIB vs. high-oxidative type I fiber types. However, within muscles containing high-oxidative type IIA and IIX fibers, the role of the SNS on vasomotor tone is not well established. The purpose of this study was to examine the influence of sympathetic neural vasoconstrictor tone in muscles composed of different fiber types. In adult male rats, blood flow to the red and white portions of the gastrocnemius (GastRed and GastWhite, respectively) and the soleus muscle was measured pre- and postdenervation. Resistance arterioles from these muscles were removed, and dose responses to α1-phenylephrine or α2-clonidine adrenoreceptor agonists were determined with and without the vascular endothelium. Denervation resulted in a 2.7-fold increase in blood flow to the soleus and GastRed and an 8.7-fold increase in flow to the GastWhite. In isolated arterioles, α2-mediated vasoconstriction was greatest in GastWhite (∼50%) and less in GastRed (∼31%) and soleus (∼17%); differences among arterioles were abolished with the removal of the endothelium. There was greater sensitivity to α1-mediated vasoconstriction in the GastWhite and GastRed vs. the soleus, which was independent of whether the endothelium was present. These data indicate that 1) control of vascular resistance by the SNS in high-oxidative, fast-twitch muscle is intermediate to that of low-oxidative, fast-twitch and high-oxidative, slow-twitch muscles; and 2) the ability of the SNS to control blood flow to low-oxidative type IIB muscle appears to be mediated through postsynaptic α1- and α2-adrenoreceptors on the vascular smooth muscle.

scholarly journals Human muscle length-dependent changes in blood flow

2012 ◽  
Vol 112 (4) ◽  
pp. 560-565 ◽  
Author(s):  
John McDaniel ◽  
Stephen J. Ives ◽  
Russell S. Richardson
Keyword(s):  
Blood Flow ◽  
Knee Joint ◽  
Joint Angle ◽  
Muscle Blood Flow ◽  
Muscle Length ◽  
Limb Blood Flow ◽  
Knee Joint Angle ◽  
Femoral Blood Flow ◽  
Femoral Blood ◽  
Cyclic Changes

Although a multitude of factors that influence skeletal muscle blood flow have been extensively investigated, the influence of muscle length on limb blood flow has received little attention. Thus the purpose of this investigation was to determine if cyclic changes in muscle length influence resting blood flow. Nine healthy men (28 ± 4 yr of age) underwent a passive knee extension protocol during which the subjects' knee joint was passively extended and flexed through 100–180° knee joint angle at a rate of 1 cycle per 30 s. Femoral blood flow, cardiac output (CO), heart rate (HR), stroke volume (SV), and mean arterial pressure (MAP) were continuously recorded during the entire protocol. These measurements revealed that slow passive changes in knee joint angle did not have a significant influence on HR, SV, MAP, or CO; however, net femoral blood flow demonstrated a curvilinear increase with knee joint angle ( r2 = 0.98) such that blood flow increased by ∼90% (125 ml/min) across the 80° range of motion. This net change in blood flow was due to a constant antegrade blood flow across knee joint angle and negative relationship between retrograde blood flow and knee joint angle ( r2 = 0.98). Thus, despite the absence of central hemodynamic changes and local metabolic factors, blood flow to the leg was altered by changes in muscle length. Therefore, when designing research protocols, researchers need to be cognizant of the fact that joint angle, and ultimately muscle length, influence limb blood flow.

Does calcium chloride increase blood pressure and uterine blood flow during hemorrhagic hypotension in hypermagnesemic gravid ewes?

1991 ◽  
Vol 75 (3) ◽  
pp. A822-A822
Author(s):  
R D Vincent ◽  
D H Chestnut ◽  
S L Sipes ◽  
C S Thompson ◽  
S A Bleuer ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Calcium Chloride ◽  
Increase Blood Pressure ◽  
Uterine Blood Flow ◽  
Hemorrhagic Hypotension

Lower vascular tone and larger plasma volume in Parkinson's disease with orthostatic hypotension

2011 ◽  
Vol 111 (2) ◽  
pp. 443-448 ◽  
Author(s):  
J. T. Groothuis ◽  
R. A. J. Esselink ◽  
J. P. H. Seeger ◽  
M. J. H. van Aalst ◽  
M. T. E. Hopman ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Blood Flow ◽  
Orthostatic Hypotension ◽  
Vascular Resistance ◽  
Plasma Volume ◽  
Venous Pressure ◽  
Dilution Method ◽  
Significant Difference ◽  
Head Up Tilt

The pathophysiology of orthostatic hypotension in Parkinson's disease (PD) is incompletely understood. The primary focus has thus far been on failure of the baroreflex, a central mediated vasoconstrictor mechanism. Here, we test the role of two other possible factors: 1) a reduced peripheral vasoconstriction (which may contribute because PD includes a generalized sympathetic denervation); and 2) an inadequate plasma volume (which may explain why plasma volume expansion can manage orthostatic hypotension in PD). We included 11 PD patients with orthostatic hypotension (PD + OH), 14 PD patients without orthostatic hypotension (PD − OH), and 15 age-matched healthy controls. Leg blood flow was examined using duplex ultrasound during 60° head-up tilt. Leg vascular resistance was calculated as the arterial-venous pressure gradient divided by blood flow. In a subset of 9 PD + OH, 9 PD − OH, and 8 controls, plasma volume was determined by indicator dilution method with radiolabeled albumin (125I-HSA). The basal leg vascular resistance was significantly lower in PD + OH (0.7 ± 0.3 mmHg·ml−1·min) compared with PD − OH (1.3 ± 0.6 mmHg·ml−1·min, P < 0.01) and controls (1.3 ± 0.5 mmHg·ml−1·min, P < 0.01). Leg vascular resistance increased significantly during 60° head-up tilt with no significant difference between the groups. Plasma volume was significantly larger in PD + OH (3,869 ± 265 ml) compared with PD − OH (3,123 ± 377 ml, P < 0.01) and controls (3,204 ± 537 ml, P < 0.01). These results indicate that PD + OH have a lower basal leg vascular resistance in combination with a larger plasma volume compared with PD − OH and controls. Despite the increase in leg vascular resistance during 60° head-up tilt, PD + OH are unable to maintain their blood pressure.

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