bluuebunny/crossref_metadata_2025 huggingface dataset:
Reduced myocardial reflow and increased coronary vascular resistance following prolonged myocardial ischemia in the dog.
Authors: Willerson J T , Watson J T , Hutton I , Templeton G H , Fixler D E
Published: June 2012

Studies were performed to determine whether an alteration in coronary vascular resistance and a reduction in the reflow phenomenon occurred in the blood-perfused, heparinized canine heart after various periods of myocaridal ischemia. Regional myocardial blood flow was measured with radioactive microspheres. Proximal left anterior descending coronary artery blood flow was measured with a periarterial flow transducer. Reduced reflow to the ischemic portion of the left ventricle and increased resistance in the left anterior descending coronary artery were present after 120 minutes of myocardial ischemia. The reduction in reflow was specific to the subendocardium of the ischemic area. Saline and isosorbide dinitrate (Isordi) did not prevent the increase in coronary vascular resistance or the significant reduction in reflow to the subendocardial portion of the ischemic area. Hypertonic mannitol given so as to increase serum osmolality 40 mosmoles/kg prevented the increase in coronary vascular resistance and modified the reduction in the reflow phenomenon to the subendocardial portion of the ischemic area. Thus, both an increase in coronary vascular resistance and a significant reduction in reflow to the subendocardial portion of the ischemic area occur in the canine heart after 120 minutes of myocardial ischemia. Moreover, the increase in coronary vascular resistance can be prevented and the reduction in reflow to the subendocardial portion of the ischemic area can be modified by the administration of hypertonic mannitol.
Transmural gradients in ventricular tissue metabolites produced by stopping coronary blood flow in the dog.
Authors: Dunn R B , Griggs D M
Published: June 2012

To determine whether transmural metabolite gradients develop in the contracting, ischemic left ventricle due to factors other than a nonuniform distribution of myocardial blood flow, right and left coronary artery inflow was completely stopped with vessel occluders in open-chest dogs for 15 or 30 seconds before a transmural myocardial tissue sample was obtained for regional analysis of creatine phosphate, adenosine triphosphate (ATP), and lactate. Heart rate was controlled, and the decline in left ventricular systolic pressure during the period in which coronary blood flow was stopped was attenuated by aortic constriction. Studies were also performed in dogs that were (1) pretreated with propranolol, (2) subjected to ventricular fibrillation, and (3) volume loaded. Control studies revealed no transmural metabolite gradients in the normally perfused ventricle, but creatine phosphate was slightly lower in the inner region than it was in the outer and middle ventricular wall regions. With coronary blood flow stopped for 30 seconds, a significant lactate gradient, increasing from the outer to the inner region, was present. Propranolol-treated dogs with their coronary blood flow stopped for 30 seconds also exhibited a lactate gradient, but dogs with ventricular fibrillation and their coronary blood flow stopped for 30 seconds did not. Volume-loaded dogs with their coronary blood flow stopped for only 15 seconds had a significant lactate gradient. Reciprocal gradients occurred in creatine phosphate but not in ATP. The findings suggest that the contracting ventricle uses energy unevenly and that in myocardial ischemia one of the factors causing greater subendocardial vulnerability is a greater energy need in this region.
Static linear and nonlinear elastic properties of normal and arterialized venous tissue in dog and man.
Authors: Wesly R L , Vaishnav R N , Fuchs J C , Patel D J , Greenfield J C
Published: June 2012

Ten normal and four transplanted canine jugular vein segments and four human saphenous vein segments were studied to determine the in vitro static elastic properties of venous tissue and their modification by transplantation into the arterial system. Both the intraluminal pressure and the longitudinal force were varied, and the resulting dimensions were recorded photographically. Venous segments manifested a hysteresis response but showed minimum tendency to creep. The pressure-strain relationships were curvilinear with an initial, highly compliant phase over the physiological venous pressure range followed by a relatively noncompliant phase. This transition occurred at lower pressures for jugular segments than it did for saphenous segments. In contrast, comparable-sized canine carotide artery segments did not show this essentially noncompliant phase over the pressure range studied (0 to 200 cm H2O). At comparable pressures and strains, the jugular vein segments were stiffer than the saphenous vein segments in both the circumferential and the longitudinal directions. At comparable strains, the saphenous vein moduli were similar to those in the carotid artery segments. Jugular segments transplanted into arterial circuits became virtually noncompliant and markedly inhomogeneous, with wall thickening and a histologic picture of intimal proliferation. They showed no tendency to "arterialize," that is, they failed to assume either the elastic or the histologic characteristics of arterial tissue.
Pathogenesis of acute renal failure following temporary renal ischemia in the rat.
Authors: Arendshorst W J , Finn W F , Gottschalk C W
Published: June 2012

In this study, we characterized the sequence of several intrarenal events and evaluated their relative importance in the pathogenesis of unilateral oliguric acute renal failure induced experimentally in rats by complete occlusion of a renal artery for 1 hour. Kidneys were studied prior to occlusion and 1-3 hours and 22-26 hours after release of the temporary occlusion. Renal blood flow measured by an electromagnetic flow transducer was reduced to 40-50% of control during both postocclusion periods. Flow of tubular fluid was markedly reduced, and the damaged kidneys were oliguric. Proximal and distal convolutions were filled with fluid and dilated 1-3 hours after occlusion; their pressures were greatly heterogeneous and were elevated, on the average, to 31 and 16 mm Hg, respectively. Glomerular capillary pressure at this time was normal or slightly increased. Histological sections showed extensive tubular obstruction. We conclude that initially the oliguria is primarily due to intraluminal obstruction in the absence of predominant increases in preglomerular vascular resistance. Observations at 22-26 hours after occlusion indicated acute tubular necrosis. Moreover, the combined involvement of preglomerular vasoconstriction, presisting tubular obstruction, and passive backflow of tubular fluid appeared to be important in the maintenance of the oliguria. Glomerular capillary, proximal intratubular, and peritubular capillary hydrostatic pressures were reduced below control values. After acute volume expansion, the reduced pressures and renal blood flow were reversed, yet the experimental kidneys remained oliguric. Thus, it is clear that tubular obstruction is a significant factor responsible for both the genesis and the maintenance of oliguria in this experimental model of ischemia-induced acute renal failure.
Interaction of the chemoreflex and the pulmonary inflation reflex in the regulation of coronary circulation in conscious dogs.
Authors: Vatner S F , McRitchie R J
Published: June 2012

The interaction of chemoreflex and pulmonary inflation reflex control of the coronary circulation was examined in conscious dogs by comparing the responses to chemoreflex stimulation (intracarotid injection of nicotine) when ventilation was allowed to increase with those when ventilation was controlled. The responses were also compared with those elicited by both forced mechanical and spontaneous hyperinflation. When the heart rate was constant, intracarotidly administered nicotine induced an increase in the depth of respiration followed closely by an increase in late diastolic coronary flow from 48 +/- 2 to 106 +/- 8 ml/min and a reduction in late diastolic coronary resistance from 1.62 +/- 0.08 to 0.78 +/- 0.06 mm Hg/ml min-1. After beta-receptor and cholinergic blockade, a similar coronary dilation in response to nicotine occurred only when ventilation was allowed to increase. However, when ventilation was controlled, intracarotidly administered nicotine increased coronary resistance after combined beta-receptor and cholinergic blockade. The reflex coronary dilation was not observed after carotid sinus nerve section or after alpha-receptor blockade. Thus, nicotine stimulation of the carotid chemoreflex results in a striking coronary dilation that has two components. The minor component involves a chemoreflex with its efferent pathway in tthe vagi. The major component of coronary dilation follows an increase in the depth of respiration, and its efferent component appears to involve withdrawal of alpha-adrenergic constrictor tone. An almost identical period of reflex coronary dilation followed either forced mechanical or spontaneous hyperinflation in the conscious dog.
Effect of stimulation of carotid chemoreceptors on total and regional cerebral blood flow.
Authors: Heistad D D , Marcus M L , Ehrhardt J C , Abboud F M
Published: June 2012

This study was performed to determine whether stimulation of the carotid chemoreceptors increases total or regional cerebral blood flow and whether activation of arterial chemoreceptors contributes to cerebral vasodilation during systemic hypoxemia. In anesthetized and ventilated dogs, carotid chemoreceptors were stimulated with nicotine or hypoxic and hypercapnic blood. To measure total and regional cerebral blood flow, we used labeled 15-mu microspheres. Stimulation of chemoreceptors did not increase cerebral blood flow or produce significant redistribution of cerebral blood flow, even though the chemoreflex was intact in these animals (as manifested by vasoconstriction in muscle, kidney, and small bowel) and the cerebral vessels dilated in response to systemic hypercapnia. In other studies in anesthetized, ventilated dogs and rhesus monkeys, cerebral vasodilator responses to systemic hypoxemia were observed before and after denervation of carotid and aortic chemoreceptors. Systemic hypoxemia produced large and equivalent increases in cerebral blood flow before and after chemodenervation. We conclude that stimulation of carotid chemoreceptors does not produce cerebral vasodilation and that chemoreceptors do not contribute significantly to cerebral vasodilation during systemic hypoxemia.
Renal blood flow and its response to angiotensin II. An interaction between oral contraceptive agents, sodium intake, and the renin-angiotensin system in healthy young women.
Authors: Hollenberg N K , Williams G H , Burger B , Chenitz W , Hoosmand I , Adams D F
Published: June 2012

A variety of estrogen- and progestin-containing oral contraceptive agents reduced renal blood flow (RBF) significantly in 23 healthy, nonhypertensive young women, to a mean of 75 +/- 3.3% of the value expected for their age and dietary sodium intake (P less than 0.001). There was also significant activation of the renin-angiotensin system: renin substrate was increased approximately 3-fold in association with a striking increase in the circulating renin activity and angiotensin II levels in relation to sodium intake and excretion. Two observations suggest that the RBF reduction was directly mediated by angiotensin II. A correlation was demonstrable between circulating angiotensin II and RBF (P less than 0.01), and renal vascular responsiveness to angiotensin II infused into the renal artery was reduced significantly (P less than 0.001). Moreover, the oral contraceptive agents modified the basic relationship between sodium balance and vascular responsiveness to angiotensin II, suggesting that the agents acted through some mechanism other than alteration in the state of sodium balance. These observations provide further evidence for an important role of angiotensin II as a determinant of RBF. Renal vasoconstriction may contribute to the genesis of a number of complications, such as sodium retention and hypertension, associated with oral contraceptive use.
Inhibition of hypoxic pulmonary vasoconstriction by calcium antagonists in isolated rat lungs.
Authors: McMurtry I F , Davidson A B , Reeves J T , Grover R F
Published: June 2012

The role of a transmembrane calcium influx in hypoxic pulmonary vasoconstriction was studied in isolated, blood-perfused, rat lungs. We reasoned that, if the influx of extracellular calcium mediated the hypoxic mechanism, pressor responses to alveolar hypoxia (2.5% O2) would be susceptible to inhibition by the calcium antagonists verapamil (2 X 10(-5) to 2 X 10(-1) mM) and SKF 525A (2.6 to 260 mM). Susceptibility of hypoxic pressor responses to inhibition by these calcium antagonists was contrasted to that of pressor responses elicited by the humoral vasoconstrictors angiotensin II(1 or 0.5 mug) and prostaglandin F2alpha (10 myg). Since neither saralasin (0.5 muM), a competitive antagonist of angiotensin II, nor meclofenamate (6.8 muM), an inhibitor of prostaglandin synthesis, depressed hypoxic pressor responses, it was concluded that these humoral transmitters were not directly involved in the hypoxic mechanism, and therefore served as independent reference agonists. The order of susceptibility of pulmonary pressor responses to inhibition by verapamil was hypoxia greater than angiotensin II greater than prostaglandin F2alpha. SKF 525A also reduced pressor responses to hypoxia more readily than those to angiotensin II. The greater inhibition of hypoxic pulmonary vasoconstriction by both calcium antagonists suggested that the hypoxic mechanism was critically dependent on the transmembrane influx of extracellular calcium. Mediation of the hypoxic response by this type of excitation-contraction coupling is consistent with the idea that hypoxia has a direct depolarizing effect on the vascular smooth muscle. It also provides a unifying explanation for inhibition of the hypoxic mechanism by various agents that have depressant or stabilizing actions on membranes in addition to other pharmacological effects.
Evidence for a dual innervation affecting local blood flow in the hypothalamus of the conscious rabbit.
Authors: Rosendorff C , Mitchell G , Scriven D R , Shapiro C
Published: June 2012

We have attempted to evaluate the role of adrenergic nerves which arise from the superior cervical ganglia or which are intracerebral throughout their course, in the control of local cerebral blood flow (CBF). Hypothalamic blood flow (HBF) was measured in the conscious rabbit by the 133Xe-clearance technique. Stimulation of the upper brainstem, using 5-Hz, 3-V, 1-msec, square wave pulses, increased by HBF by a mean of 7.6 ml/100 g per min (P less than 0.005). This effect was abolished by the intrahypothalamic injection of the beta-adrenoreceptor blocker, propranolol, and by chemical sympathectomy of the hypothalamus or of the upper brainstem with 6-hydroxydopamine, but was not altered by bilateral cervical ganglionectomy. Intrahypothalamic injection of 0.1 mug of tyramine caused a mean decrease in HBF of 15.6 ml/100 g per min (P less than 0.001). This effect of intrahypothalamic injection of tyramine was abolished by bilateral cervical sympathectomy but not by chemical sympathectomy of the upper brainstem. These results support the idea that local CBF, at least in the hypothalamus, is mediated by two distinct pathways. The first consists of the sympathetic nerves which arise in the cervical ganglia, and which activate intrahypothalamic alpha-receptors to cause constriction. The second is an entirely intracerebral noradrenergic pathway which stimulates beta-receptors to cause vasodilation.
The effects of tension on acetylstrophanthidin-induced transient depolarizations and aftercontractions in canine myocardial and Purkinje tissues.
Authors: Ferrier G R
Published: June 2012

Transmembrane potentials and contractile activity were recorded from isolated canine Purkinje and ventricular muscle preparations exposed to acetylstrophantidin (AS) and subjected to a resting tension equal to 80% of that required to elicit peak developed tension. AS induced transient depolarizations (TD's) accompanied by aftercontractions in Purkinje tissue. AS also induced aftercontractions in 11 muscle preparations, and in seven of these the mechanical events were associated with TD's. Aftercontractions and TD's in both and the coupling intervals were directly related to the preceding basic cycle length (BCL). The amplitudes of aftercontractions and TD's reached a maximum at a coupling interval of 600-700 msec. Tension increased the amplitude of TD's in Purkinje tissue and promoted the appearance of TD's in muscle. TD's in muscle occasionally reached threshold in the presence of tension. The results of this study suggest that stretch or increased resting tension may promote the types of cardiac arrhythmias that are causally related to digitalis-induced TD's. The results are compatible with the hypothesis that TD's are caused either by a transmembrane influx of calcium or by an internal release of calcium ions.
Relationships between pressure and flow in the umbilical and uterine circulations of the sheep.
Authors: Berman W , Goodlin R C , Heymann M A , Rudolph A M
Published: June 2012

We studied the relationship of fetal and maternal vascular pressures to umbilical and uterine blood flow in the unanesthetized ewe and in the sheep fetus in utero by placing electromagnetic flow transducers around both the common umbilical and uterine arteries. Reductions in umbilical arterial pressure or elevations in umbilical venous pressure decreased umbilical blood flow without affecting either the uterine arterial blood flow or other maternal cardiovascular variables which were studied. Elevations in uterine venous pressure or reductions in uterine arterial pressure decreased uterine arterial flow but these interventions had no effect on umbilical blood flow until fetal hypoxemia and bradycardia occurred. When the bradycardia of the fetal hypoxic response was inhibited by atropine, alterations in maternal vascular pressure had no effect on umbilical arterial flow. These data do not support the presence of a "sluice" or "waterfall" effect in the umbilical-placental circulation of the sheep fetus in utero.
The vascular basis for acute renal failure in the rat. Preglomerular and postglomerular vasoconstriction.
Authors: Venkatachalam M A , Rennke H G , Sandstrom D J
Published: June 2012

Myohemoglobinuric acute renal failure (ARF) was induced in dehydrated, salt-deficient, salt-loaded, and untreated rats by intramuscular injection of glycerol, and the renal vasculature was studied after 24 hours. Kidneys were prepared for examination by rapid freezing in vivo to -160 degrees C and freeze substitution in -80 degrees C alcohol, and by perfusion fixation with 1% glutaraldehyde in Ringer's solution at 120 mm Hg. Frozen kidneys were examined by light microscopy after paraffin and epoxy resin embedding. Techniques used in examining the perfusion-fixed kidneys were: (1) vascular injection with silicone rubber and clearing in glycerol, (2) electron microscopy, and (3) morphometric evaluation of lumen to wall area ratios of glomerular arterioles. Kidneys of all rats with ARF showed renal cortical arterial and glomerular arteriolar (afferent and efferent) vasoconstriction. The degree of constriction, estimated by lumen to wall ratios, correlated with the degree of azotemia (r = -0.71; P less than 0.001). Differences between all ARF groups and respective controls were highly significant (P less than 0.001). Vasoconstriction was maximal in the dehydrated group, intermediate in the untreated and Na-deficient rats, and lowest in the salt-loaded animals. Glomerular and peritubular capillaries were patent and free of endothelial swelling or thrombi. Glomerular basement membranes and epithelial foot processes showed no morphological alterations. The observations suggest that marked pre- and postglomerular vasoconstriction occurs in established myohemoglobinuric ARF, that it is related to azotemia, and that mechanical vascular obstruction does not play a major role in this experimental model.
Substructure of intercellular junctions in freeze-fractured alveolar-capillary membranes of mouse lung.
Authors: Schneeberger E E , Karnovsky M J
Published: June 2012

The purpose of this study was to examine by freeze-fracture the ultrastructure of intercellular junctions between mouse pulmonary endothelial and epithelial cells, and to relate this fine structure to that deduced from previous physiological and ultrastructural studies using tracer techniques. Junctions between capillary endothelial cells consist of one to three interconnected rows of particles which show occasional discontinuities. Small gap junctions are associated with these rows of particles in the arteriolar end of the capillary bed. At the venular end, the junctions consist of low profile ridges on the protoplasmic fracture (PF) face or complimentary grooves on the exoplasmic fracture (EF) face some of which have a sparse number of associated particles. The vascular junctions are similar to those of vessels in rat omentum and mesentery, and resemble "leaky" junctions described in renal proximal convoluted tubular cells. Tight junctions (zonulae occludentes) between type I pneumocytes or between types I and II pneumocytes consist of a band of interconnecting ridges on the PF face and complimentary interconnecting grooves on the EF face. These continuous epithelial junctions have a structure that is typical of tight occluding junctions. Occasionally zonulae occludentes between type I and type II pneumocytes are discontinuous; this may be the result of cell translocation as pneumocytes are shed into the alveolus. Intravascular perfusion fixation at high pressure (140 cm H2O) had no discernible effect on the structure of endothelial or epithelial junctions. The appearance in our study of freeze-fractured pulmonary endothelial and epithelial junctions reveals clearly the physical basis for the results of ultrastructural tracer and physiological studies which have suggested that it is the alveolar epithelium rather than the endothelium that is the chief permeability barrier to small, water-soluble molecules.
Effects of chronic anemia on the coronary and coronary collateral vasculature in dogs.
Authors: Scheel K W , Brody D A , Ingram L A , Keller F
Published: June 2012

We compared coronary resistances and collateral (retrograde) flows for a group of normal dogs (hematocrit 40) to values for a group of dogs with severe chronic anemia (hematocrit 17). We used an isolated heart preparation in which the vessels were maximally dilated by dipyridamole. All data were compared for a hematocrit of 40. The results showed a significant decrease in coronary resistances with anemia; average resistances (+/-SE) of the anterior descending, circumflex, and right coronary arteries of the control dogs were 1.04 +/- 0.09,0.74 +/- 0.01, and 2.63 +/- 0.17 mm Hg/[(ml/min)/100 g], respectively, and 0.6 +/- 0.04,0.41 +/- 0.05,and 1.17 +/- 0.15 for the anemic dogs. Average coronary collateral flows increased in anemia but statistical significance could not be shown. We conclude that increased vascularity is a long-term regulatory mechanism in response to a hypoxic stimulus.
Pharmacological mechanisms for left ventricular unloading in clinical congestive heart failure. Differential effects of nitroprusside, phentolamine, and nitroglycerin on cardiac function and peripheral circulation.
Authors: Miller R R , Vismara L A , Williams D O , Amsterdam E A , Mason D T
Published: June 2012

We compared cardiocirculatory actions of the commonly employed systemic vasodilators, intravenous (iv) nitroprusside (NP), iv phentolamine (PH), and sublingual nitroglycerin (NTG), causing left ventricular (LV) unloading in 29 chronic coronary subjects with congestive failure to determine whether they produce disparate responses in LV function by different relaxing actions on systemic resistance and capacitance beds. Each drug equally lowered systemic arterial pressures to a small extent, whereas heart rate rose slightly with NTG. Cardiac catheterization showed a decline in end-diastolic pressure with NTG (19 to 8 mm Hg) which was greater (P less than 0.05) than with NP and PH (21 to 11). Cardiac index increased (P less than 0.05) during NP (2.68 to 2.93 liters/min per m2) and PH (2.60 to 3.02) but was unchanged (2.83) by NTG. Stroke work increased with PH, ejection fraction rose with NP and PH, and mean ejection rate increased with each, whereas pressure-time per minute fell and end-diastolic volume decreased with each agent. Total systemic vascular resistance declined (P less than 0.001) during NP and PH (1,475 to 1,200 dynes sec cm-5) but was unchanged (1,487) by NTG. Plethysmographically, forearm vascular resistance (FVR) decreased (P less than 0.01) with NP and PH (61.6 to 39.1 mm Hg/ml per 100 g/min) but not (52.4) by NTG. The decreases in venous tone (VT) with NTG (18.2 to 9.3 mm Hg/ml) and NP (18.5 to 9.8) were greater (P less than 0.05) than with PH (18.8 to 13.1) FVR/VT percent changes of 0.96, 1.62, and 0.53 with NP, PH, and NTG indicated balanced systemic arteriolovenous relaxation by iv NP, greater arteriolar dilation with iv PH, and predominant venous dilation by sublingual NTG. Thus, vasodilators produce disparate modifications of LV function by their differing alterations of preload and impedance, which are dependent upon relative extents of relaxation of systemic resistance and capacitance vessels characteristic of each agent as used clinically.
Progressive perfusion impairment during prolonged low flow myocardial ischemia in dogs.
Authors: Frame L H , Powell W J
Published: June 2012

Recent studies have shown that after total coronary artery occlusion, there is impaired "reflow" of blood accompanied by myocardial and capillary endothelial cell swelling. To investigate the effect of prolonged low flow myocardial ischemia on coronary vascular resistance, regional hypoperfusion of the distal left anterior descending coronary artery was studied in 31 autonomically blocked dogs on right heart bypass. Heart rate, aortic pressure, and, during ischemia, left ventricular end-diastolic pressure were held constant. The distal left anterior descending coronary artery was perfused at a substantially reduced perfusion pressure which resulted in an antegrade coronary blood flow that usually was between 3% and 7% (0.5-1 ml/min) of control. When relative hypothermia (33-34 degrees C) was induced in nine dogs, left anterior descending coronary artery vascular resistance did not change during 2.5-3 hours of low flow ischemia. Under euthermic conditions (37-40 degrees C) in 17 dogs there was a consistent progressive increase in distal left anterior descending coronary artery vascular resistance starting at 90 minutes (median) after onset of ischemia. By 110-140 minutes ischemic antegrade flow decreased by 35 +/- 4% (SEM) (P less than 0.01). Directionally similar flow changes were observed in six euthermic experiments using the krypton-85 washout technique. Light microscopy did not reveal hemorrhage as a cause of the increased vascular resistance. The perfusion impairment did not occur in two euthermic, nonischemic hearts. In five dogs elevation of serum osmolality by 23 +/- 11 mOsmol/liter with mannitol attenuated the progressive decrease in flow. Thus, a progressive perfusion defect exists in the ischemic low flow state in the heart which presumably contributes to the extent of eventual necrosis.
Low renal papillary plasma flow in both Dahl and Kyoto rats with spontaneous hypertension.
Authors: Ganguli M , Tobian L , Dahl L
Published: June 2012

Abnormally low plasma flow to renal papilla characterizes Dahl hypertension. When eating a normal Na diet (0.3% NaCl) both hypertension-sensitive (S) rats and hypertension-resistant (R) rats, 16 weeks old, have fairly normal blood pressure (BP), averaging 144 and 129 mm Hg, respectively. However, even in this barely hypertensive state, 18 S rats had a 31% lower papillary plasma flow (Lilienfield method) than 22 R rats, 19.2 ml/100 g of papilla per min compared to 25.6 (P less than 0.001). When a high (8%) NaCl diet was fed for 7 days, R rats increased papillary plasma flow from 25.6 on 0.3% NaCl to 33.8 on 8% NaCl, a 32% rise (P less than 0.001). S rats increased papillary flow from 20.4 to 24.8, a 22% rise (P less than 0.05). When a high (8%) NaCl diet was fed for 4 weeks, R rats increased papillary plasma flow from 25.7 ml/100 g per min on 0.3% NaCl to 29.5 ml/100 g per min on 8% NaCl, a 15% rise (P less than 0.025). S rats increased papillary flow from 17.7 to 20.0 ml/100 g per min (not significant). S rats on 8% NaCl had a papillary flow 32% lower than R rats on 8% NaCl (P less than 0.001). BP of S rats rose to 162 mm Hg after 4 weeks on 8% NaCl; in R rats, BP did not rise at all. S rats on 0.3% NaCl have a low papillary flow even in a borderline hypertensive state. When challenged with 8% NaCl, R rats increased papillary flow, an adaptation possibly important for the natriuresis. S rats failed to achieve this same high papillary flow. Lacking this adaptation, hypertension may then conceivably occur in S rats to accomplish natriuresis through a "pressure natriuresis" mechanism. Papillary flow also decreased by 11% in 26 Kyoto 17-week-old spontaneously hypertensives (BP, 182 mm Hg) compared to 24 Kyoto normotensives (BP, 118 mm Hg), 29.5 vs 33.2 ml/100 g per min (P less than 0.001). Thus, low papillary flow exists in both hypertensions.
Interaction of capillary and tissue forces in the cat small intestine.
Authors: Mortillaro N A , Taylor A E
Published: June 2012

We measured steady state capillary hydrostatic pressure (P c,i), plasma and lymph protein concentrations, lymph and blood flow, and capillary filtration coefficients in an in situ loop of cat small intestine at venous outflow pressures (PV) of 0, 5, 10, 15, 20, 25, and 30 mm Hg. The data were used to calculate colloid osmotic pressure of lymph and plasma, interstitial fluid pressure (Pt), pre- and postcapillary resistances, and a tissue pressure-volume curve of the intestinal interstitium. When PV was elevated from 0 to 30 mm Hg, lymph protein concentration decreased from 3.8 to 1.9 g/100 ml (representing a change in colloid osmotic pressure of 6.2 mm Hg), lymph flow increased 7-fold (or an equivalent imbalance in Starling forces of 4.3 mm Hg), and the calculated PT increased from 1.8 to +5.3. Because lymph flow draining the loop decreased during the determination of Pc, i at venous pressures between 15 and 30 mm Hg, the corresponding calculated PT may be in error by 1-2 mm Hg. The tissue pressure-volume relationship calculated from the data indicates that the intestinal interstitial volume expands nonlinearly and this expansion is characterized by two distinctly different compliant components: (1) tissue compliance is low at PV between 0 and 15 mm Hg (0.4 ml/mm Hg), and (2) at PV greater than 15 mm Hg the tissue compliance is relatively high (4 ml/mm Hg). We found that when PV was elevated from 0 to 15 mm Hg, increases in PT are the major tissue adjustments that oppose the increased filtration pressures. Furthermore, at Pv of 20-30 mm Hg, tissue protein concentration decreases, lymph flow relative to the filtration coefficient (deltaP DROP) increases and, to a much lesser extent, PT increases. Finally, the combination of these changes in tissue force at high filtration pressures represent a maximum tissue edema "safety factor" of 10 mm Hg; further increases in filtration pressures result in large volume movements into the intestinal lumen.
Transcapillary escape rate of albumin and right atrial pressure in chronic congestive heart failure before and after treatment.
Authors: Hesse B , Parving H H , Lund-Jacobsen H , Noer I
Published: June 2012

The transcapillary escape rate of albumin (TERalb), i.e., the fraction of intravascular mass of albumin that passes to the extravascular space per unit of time, was determined from the disappearance of intravenously injected 125I-labeled human serum albumin during the first 60 minutes after injection in 10 subjects with chronic right heart failure. The investigation was repeated after sodium and water depletion. Before treatment TERalb was significantly elevated (mean 8.3 +/- 1.6% (SD)/hour, in comparison to values for normal subjects (mean 5.4 +/- 1.1%/hour, P less than 0.001). With treatment TERalb decreased significantly (mean 5.9 +/- 1.2%/hour, P less than 0.01). Right atrial pressure decreased from an average of 10 mm Hg to 6 mm Hg during treatment. A statistically significant, positive correlation was found between TERalb and right atrial pressure (r = 0.77, P less than 0.001). Our results best can be explained by increased filtration, mainly through the venous end of the microvasculature, due to the increased venous pressure in heart failure.
Effect of exercise conditioning on the intrinsic contractile state of cat myocardium.
Authors: Williams J F , Potter R D
Published: June 2012

Fourteen adult cats were exercised on a motor-driven treadmill 5 days each week for 6 weeks to determine the effect of exercise conditioning on the intrinsic contractile state of the myocardium. The exercise program was sufficient to produce a cardiovascular training effect manifested by slower exercising heart rates and resting heart rates after atropine by the end of the 6th week. The mechanical function of the isolated right ventricular papillary muscle from exercised cats was compared with that of 17 sedentary adult cats. There were no significant differences between exercised and control cats in in heart weight-body weight ratios, resting and active lenght - tension relations, maximal rate of isometric force development at the peak of the length-tension curve (Lmax), time to peak force at Lmax, maximal force development with paired stimulation and norepinephrine, or force-velocity relations. These results indicate that the intrinsic state of feline myocardium is unaffected by exercise conditioning.
Effects of sodium pentobarbital anesthesia on left ventricular function and distribution of cardiac output in dogs, with particular reference to the mechanism for tachycardia.
Authors: Manders W T , Vatner S F
Published: June 2012

Sodium pentobarbital (PB), 30 mg/kg, iv, was administered to 30 conscious dogs instrumented for measurement of cardiac output and regional blood flow distribution, left ventricular (LV) diameter, LV pressure, dP/dt, and dD/dt, i.e., velocity of myocardial fiber shortening. Ventilation was controlled during anesthesia to maintain arterial blood gases at control values for conscious dogs. The anesthetic produced an initial transient, peripheral vasodilation but the steady state effects 15-30 minutes later were characterized by slight reductions in mesenteric flow and cardiac output and increases in mesenteric and systemic resistances, whereas iliac and renal resistances were not significantly different from control. When heart rate rose, PB increased end-systolic diameter and decreased coronary resistance, LV end-diastolic diameter, dP/dt/P (42%), and shortening velocity (36%). When heart rate was controlled, PB still increased end-systolic diameter and decreased shortening velocity and dP/dt/P, as occurred during spontaneous rhythm, but end-diastolic diameter rose instead of falling and coronary resistance did not change. After recovery from bilateral cervical section of both carotid sinus and aortic nerves, PB failed to elicit tachycardia. Thus, PB affects systemic and regional hemodynamics only slightly, but depresses the myocardium markedly. The tachycardia associated with PB anesthesia in intact, trained dogs appears not to be only vagolytic, as previously thought, but is predominantly mediated through the arterial baroreceptor reflex.
Single-passage extraction and permeability estimation of sodium in normal dogs lungs.
Authors: Yipintsoi T
Published: June 2012

Bolus injections of 24NaCl, 131I-albumin, and indocyanine green dye were made into the right atria of anesthetized, ventilated dogs. Blood was sampled from the femoral artery, and from the dilution curves, instantaneous extractions, E2(t), and area averaged extractions, E3(t), were calculated for sodium at various plasma flows (Fp). Flow reduction was produced by transient inferior vena cava obstruction. E2(t) and E3(t) within any dilution curve generally started off with a high value, then decreased with time. The E3 that occurred at the peak of the albumin-dilution curve were about 0.11 for plasma flow of 0.75 liter/min and tended to decrease as flow increased. Parallel study of the sodium extravascular space at equilibrium gave values of 0.3-0.4 g of plasma sodium per g of tissue, suggesting that this volume is not infinitely small. Since the E was low it is unlikely that the high initial E(t) and the decreasing E(t) were due to early back flux. Calculation of capillary permeability surface area product [PS = Fp loge (1 - E)] showed an increasing PS with plasma flows. The injection of 9-mum microspheres at low and high total blood flow gave evidence supporting a decrease of capillary surface area (S) with decreasing total blood flow. Regional pulmonary blood flow also showed marked heterogeneity. Because of the low average extraction of sodium in the lung, insensitivity of the method in normal lungs cannot be excluded.
The Relation of a Venous-Arteriolar Reflex to Transmural Pressure and Resistance in Small and Large Systemic Vessels
Authors: HADDY FRANCIS J. , GILBERT ROBERT P.
Published: June 2012

Data are presented which indicate that, even in pressure ranges well above critical closing pressures, transmural pressure is an important factor in determining systemic vascular resistance but that a mechanism is present which actively limits these pressure changes in resistance when transmural pressure is varied on the venous side.
The Continuous Recording of Central Venous Pressure Changes from an Arm Vein
Authors: GAUER OTTO H. , SIEKER HERBERT O.
Published: June 2012

With the subject in the right lateral decubitus position, changes of central venous pressure can be recorded accurately and conveniently from a vein in the antecubital fossa of the dependent arm. Theoretically the hydrostatic, pressure transforms the venous bed between the heart and the site of puncture into uninterrupted wide channels with relatively low distensibility. Simultaneous recordings of pressure by the method described and by catheterization of the central veins showed that induced changes of central venous pressure were identically recorded from both sites. The mean pressure gradient between the peripheral and central veins was 35 mm. of water.
Effect of X-irradiation and Beta Emanation on Circulation in the Hamster Cheek Pouch
Authors: FULTON GEORGE P. , LUTZ BRENTON R. , KAGAN ROMA
Published: June 2012

The small venules of the hamster cheek pouch were rendered susceptible to hemorrhage by total body x-irradiation, cheek pouch x-irradiation and beta emanations from strontium-90 glass beads imbedded in the cheek pouch, as determined by negative pressure and moccasin venom tests. Petechiae were formed without vessel rupture and ceased without formation of platelet plug or fibrin clot. Increased susceptibility to petechiae preceded thrombocytopenia. Endothelial damage was indicated by increased leukocytic adhesiveness to walls of venules. Vasodilation, tortuosity, newlyformed capillaries, and occasional "sausage-shaped" segments of constriction in arterioles were characteristic vascular responses. Near death, erythrocytes circulated in aggregates varying from typical rouleau formation to discrete masses, resembling "sludged blood" but without formation of occluding thrombi.
The Reduction of Autoprothrombin II Activity with Dicumarol
Authors: JOHNSON SHIRLEY A. , SEEGERS WALTER H.
Published: June 2012

It is generally considered that the administration of dicumarol is followed by a decrease in prothrombin concentration, and it has been suggested that another plasma factor may also decrease. We have found that there are two derivatives of prothrombin called autoprothrombin and autoprothrombin II. In this paper we present data which show that the concentration of autoprothrombin II can be reduced practically to zero with the use of Dicumarol without observing a bleeding tendency. The decrease in concentration coincides with a decrease in prothrombin concentration but is relatively more rapid.
Theoretic Limitations of the Nitrous Oxide Method for the Determination of Regional Blood Flow
Authors: SAPIRSTEIN LEO A. , OGDEN ERIC
Published: June 2012

The nitrous oxide method for regional blood flow determination is based on the assumption that concentration equilibrium for nitrous oxide between the organ and its venous blood is reached. This assumption is examined, and it is shown mathematically that faulty equilibrium is not revealed by presently available criteria. It is shown that quantitatively and qualitatively erroneous results may be obtained by the use of this method for the estimation of regional blood flow.
The Action of Acetylcholine and Epinephrine on the Cellular Membrane Potentials and Contractility of Rat Atrium
Authors: WEBB J. LEYDEN , HOLLANDER PHILIP B.
Published: June 2012

Acetylcholine diminished the developed tension of contraction in rat atria; simultaneously there was a slight increase in resting potential, no appreciable change in action potential, a decrease in the rate of conduction, only a minor alteration of the form of contraction, and, most strikingly, a decrease in the duration of the action potential or the area enclosed by it. The rate of repolarization subsequent to the action potential was markedly accelerated. Epinephrine, in general, produced the opposite effects and slowed the repolarization rate as it augmented atrial contraction. Cholinesterase does not seem to play a direct role in cardiac membrane potentials or ion transfer since physostigmine had no effect of its own on the electric manifestations. Certain aspects of the mechanisms involved are discussed.
Influence of Pulmonary Arterial and Left Atrial Pressures on Pulmonary Vascular Resistance
Authors: BORST HANS G. , MCGREGOR MAURICE , WHITTENBERGER JAMES L. , BERGLUND ERIK
Published: June 2012

A method has been developed by which flow to each lung, as well as pulmonary artery and left atrial pressures can be measured and varied at will. Vascular resistances were determined over a wide range of these variables. Both pressures have a marked effect on vascular resistances; the higher either pressure, the lower the resistances. This effect is most marked at low levels of pressure and flow. The absolute levels of the pressures, by affecting vascular distension, are major determinants of pulmonary vascular resistance.
Effects of Fat on Blood Viscosity in Dogs
Authors: SWANK ROY L.
Published: June 2012

Intravenous fat injections cause significant increases in blood viscosity. Nonemulsified or poorly emulsified oil produces pulmonary and other embolization. Plasma is lost rapidly and in alarming degree. The hematocrit increases rapidly and is accompanied by a nearly parallel increase in blood viscosity. Oil in stable emulsion in blood plasma or lymph can be injected in greater doses. Slow, but significant increases in the blood viscosity develop to maximum in 10 to 24 hours. Varying degrees of paralysis follow. The loss of plasma is not so marked, and increase in hematocrit is not sufficient to account for increase in viscosity.
Adrenergic Drugs and Blockade on Coronary Arterioles and Myocardial Contraction
Authors: DENISON ADAM B. , BARDHANABAEDYA SUTHIP , GREEN HAROLD D.
Published: June 2012

The 3 adrenergic substances, epinephrine, levarterenol and isopropylarterenol, were injected into a coronary artery of anesthetized dogs while recording the coronary artery flow (electromagnetic meter) and pressure. The effects of these substances on the peripheral coronary pressure (PCP) were recorded by occluding the flow proximal to the pressure gage. All 3 substances caused a qualitatively similar increase in myocardial contraction and dilation of the coronary arterioles.
Fractionation of the Cardiac Output of Rats with Isotopic Potassium
Authors: SAPIRSTEIN LEO A.
Published: June 2012

A single injection of K
42
given intravenously is initially distributed among the organs in proportion to the blood flow through them. By determining the organ content of K
42
after such an injection the cardiac output may be fractionated. The conditions and limitations of the method are discussed and values are given for the fractional distribution of the cardiac output in the rat.
Cardiac lysosomal derangements in mouse heart after long-term exposure to nonmetabolizable sugars.
Authors: Wildenthal K , Dees J H , Buja L M
Published: June 2012

Hearts of late fetal mice were maintained in organ culture in the presence of 30-100 mM sucrose or mannitol. Activities of several lysosomal enzymes (cathepsin D, beta-acetylglucosaminidase, acid phosphatase) were increased by up to 30% after 18-24 hours and by up to 50% after 48-72 hours, as compared to enzyme activities in litter-matched hearts maintained in control medium or medium supplemented with equimolar urea. Simultaneously, the ratio of nonsedimentable to sedimentable enzyme activity was significantly increased, suggesting increased lysosomal fragility. Light and electron microsopic examination of the hearts revealed marked vacuolization in myocytic, interstitial, and endothelial cells. The vacuoles were limited by single membranes, often contained particulate or amorphous cellular debris resulting from autophagocytosis, and in cytochemical preparations frequently exhibited an electron-dense reaction product indicative of acid phosphatase activity. Hydrocortisone failed to prevent the marked lysosomal activation induced by the sugars. In conclusion, prolonged exposure to nonmetabolizable sugars induces severe lysosomal derangements with prominent autophagy, in fetal mouse heart maintained in organ culture.
Cardiac output and renal blood flow in glycerol-induced acute renal failure in the rat.
Authors: Hsu C H , Kurtz T W , Waldinger T P
Published: June 2012

Cardiac output (CO) and renal blood flow (RBF) were simultaneously evaluated by the microsphere method in water-drinking and chronic saline-drinking rats at 3, 12 and 24 hours after induction of acute renal failure by glycerol injection. Threee hours after glycerol injection CO and RBF decreased to 36% and 20% of the respective controls in water-drinking rats and to 41% and 24% of the controls in saline-drinking rats. Renal vascular resistance (RVR) increased significantly in both groups at this time. Isoncotic plasma expansion (3% of body weight) restored the RBF and RVR to normal in water-drinking rats 3 hours post-glycerol injection, althought CO increased to only 70% of the control. Twelve hours after glycerol injection, CO and RBF returned to normal in saline-drinking rats, whereas they remained lower than controls in water-drinking rats. Twenty-four hours post-glycerol injection, when acute renal failure was evident as indicated by blood urea nitrogen (BUN) values of 116.9 and 63.8 mg/100 ml in water- and saline-drinking rats, respectively, CO and RBF returned to normal, except that the CO of of water-drinking rats was slightly higher than control. Thus, we conclude that decreased CO is an important determinant of the early decrease in renal perfusion in glycerol-induced acute renal failure. Furthermore, the observed earlier return of CO and RBF to normal in saline-drinking rats may be partly responsible for reproducing the severity of acute renal failure.