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PubMed1980

Immunohistochemical localization and vascular effects of vasoactive intestinal polypeptide in skeletal muscle of the cat.

Scattered vasoactive intestinal polypeptide (VIP)-immunoreactive nerves were found in the striated muscle of the hind limb of the cat, where they usually were associated with small blood vessels. VIP-immunoreactive nerves were also demonstrated in the sciatic nerve; after ligation an abundance of intensely immunoreactive VIP fibres were seen proximal to the ligation. Intraarterial infusion of VIP into isolated hind limb of the cat had dramatic effects on different sections of the vascular bed. Thus, VIP dilated the resistance vessels leading to a marked increment in muscle blood flow. VIP also relaxed the capacitance vessels causing regional pooling of blood; it increased the capillary surface area available for fluid exchange. Infusions of VIP at a dose of 8 microgram/min significantly inhibited the vasoconstriction, induced by electrical stimulation of the regional sympathetic nerves. It is suggested that local nervous release of VIP may act as a modulator of vascular tone in skeletal muscle.

Animals↗

PubMed1982

[Effect of adrenoreceptor blockade and stimulation on the resistance and capacitance of intestinal vessels].

Resistography and extracorporeal venous flow in cats revealed that i. a. administration of noradrenaline (NA) increased the intestine vascular resistance, adrenaline (A) decreased it and novodrine (N) sharply decreased it in all the experiments. After the alpha-adrenoreceptors blockade with dihydroergotoxin, NA as well as A decreased the vascular resistance whereas N exerted just the same dilator response as before blockade. Blockade of B-adrenoreceptors with obsidan augmented the NA constriction of the arterial vessels, sharply decreased their N dilatation and induced obvious constrictor responses to A. The vascular resistance after the alpha-blockade decreased by 7% whereas after the beta-blockade it increased by 26%. The venous outflow from the intestine increased after A and N disregarding the alpha-blockade but being prevented with the beta-blockade. Irregular changes of the venous outflow in response to NA preserved after the blockade of both types of adrenoreceptors.

Animals↗

PubMed1982

Vasomotor dynamics associated with cardiac operations. I. Venous tone and the effects of vasodilators.

Vasomotor dynamics were studied in 52 patients undergoing direct coronary revascularization or mitral valve replacement utilizing cardiopulmonary bypass. Emphasis was placed on the study of venous tone. Operation resulted in a general vasoconstrictive response with increased arterial resistance and reduced venous capacitance. These changes were magnified in patients who underwent mitral valve replacement for mitral valve stenosis related or partially related to reduced cardiac performance before and after operation. Nine patients became hypertensive following coronary artery bypass and were treated with nitroprusside; eight patients were given nitroglycerin to reduce venous tone and prevent hypertension. A comparison of these two vasodilators, with their somewhat different actions on the vascular bed, reveals that afterload reduction and increase of cardiac output were equivalent with both. However, nitroglycerin had the effect of increasing venous capacitance, while nitroprusside had little effect on the venous circulation. In addition, nitroglycerin was especially effective in reducing venous tone and left ventricular preload following mitral valve replacement. Relative merits of pharmacologic reduction of venous tone as a part of overall relief of increased vascular resistance following cardiac operation should be considered when attempting to obtain an optimal hemodynamic state.

Adult↗

PubMed2002

Dynamic changes in three-dimensional architecture and vascular volume of transmural coronary microvasculature between diastolic- and systolic-arrested rat hearts.

BACKGROUND: The phase difference of coronary arterial and venous flows indicates the importance of intramyocardial capacitance vessels in storing diastolic flow and in discharging volume in systole. However, the anatomic and functional characteristics of the capacitance vessels are unclear. We aimed to clarify those characteristics with their transmural difference by 3D visualization of transmural microvessels under diastole and systole. METHODS AND RESULTS: We performed complete intracoronary filling of a contrast medium into Langendorff's Wistar rat hearts under (1) St Thomas-perfused diastolic arrest (D-mode) and (2) BaCl(2)-induced systolic arrest (S-mode). Precise transmural 3D architectures of capillaries and of pre- and post-capillary microvessels (ie, microvessels larger than capillaries) were visualized clearly with a confocal laser scanning microscope and x-ray microcomputed tomography (microCT), respectively. Vascular volume fraction (VF) and systolic-induced VF reduction rate from D- to S-mode were analyzed. The net capillary VF in D-mode (20.4 +/- 0.9%) was 10 times that of larger microvessels and was reduced in S-mode by 32% without capillary collapse. Systolic-induced VF reduction rate was smaller in capillaries than in larger microvessels (48%; P<0.05). The larger microvessel VF in D-mode (2.2 +/-0.2%) was reduced in S-mode, accompanied by complicated 3D deformation. CONCLUSIONS: Capillaries were relatively resistant to the systolic extravascular compression compared with pre- and post-capillary microvessels, conveniently beneficial for the myocardial oxygen delivery throughout a cardiac cycle. Nevertheless, a larger change in the absolute volume of capillaries may function as effective capacitance. On one hand, the pre- and post-capillary microvessels showed a larger phasic change in resistance, which may function to maintain the capillary patency during systole.

Animals↗

PubMed1989

Adrenergic and non-adrenergic mechanisms in sympathetic vascular control of the nasal mucosa.

1. Co-existence of NA and NPY-LI was observed in the dense network of sympathetic nerves around both resistance and capacitance vessels in the nasal mucosa from most species including man. NPY-LI seems also to be present together with VIP-LI and PHI-LI in periglandular and some perivascular parasympathetic fibres in some species. 2. A new in vivo model was developed in the pig which allowed parallel recordings of arterial blood flow (BF), capacitance function (V) and superficial movement of blood cells (LDF signal) of the nasal mucosa upon SNS and/or local intra-arterial injection of various pharmacological agents. SNS reduced both BF and V. The V response was maximal already at low frequency. The LDF signal was increased when the SNS-evoked BF reduction was under 40% but was reduced upon larger BF response. After pretreatment with the alpha-adrenoceptor antagonist PBZ, the vascular responses to SNS were significantly attenuated but clear-cut reductions of BF, V and LDF responses remained even to a single impulse. Exogenous NA induced dose-dependent reductions of the BF, V and LDF signal, which were abolished by PBZ treatment. ATP caused biphasic vascular effects with short-lasting vasoconstriction followed by vasodilatation. NPY and mATP caused reduction of the vascular parameters via non-adrenergic mechanisms. 3. A frequency-dependent increase of NA overflow was observed in the nasal venous effluent upon SNS in control pigs, whereas detectable release of NPY-LI occurred only at high frequency. Pretreatment with PBZ significantly increased the SNS-evoked NA and NPY-LI overflow, while DMI enhanced both the functional response and NA release but reduced the NPY-LI overflow. These data suggest that NA and NPY release in the pig nasal mucosa is regulated by prejunctional alpha-adrenoceptor mechanisms. During tachyphylaxis to mATP, the NA and NPY-LI overflow and the vasoconstrictor responses to SNS were unmodified in controls. 4. Reserpine pretreatment induced a marked depletion of both NA and NPY-LI in the pig nasal mucosa. The reduction of NA was not influenced by preganglionic denervation while the depletion of NPY then was prevented. Slowly developing, frequency-dependent and long-lasting vascular responses remained (up to 80% of control) upon SNS in reserpinized and decentralized animals. In these animals, the NA overflow was abolished while release of NPY-LI was enhanced. Stimulation with irregular bursts, caused both larger vascular responses and more NPY-LI overflow in comparison with continuous stimulation.(ABSTRACT TRUNCATED AT 400 WORDS)

Adenosine Triphosphate↗

PubMed1999

Peptidergic innervation of human cerebral blood vessels and saccular aneurysms.

Peptidergic innervation of the human cerebral vasculature has not yet been described in detail and its role in the maintenance of cerebral autoregulation still needs to be established. Similarly, few data exist on the innervation of vascular malformations. The aim of this study was to clarify the peptidergic innervation patterns of human cerebral arteries of various sizes, and, for the first time, that of saccular aneurysms. Light microscopic study of whole-mount preparations of human cerebral arteries and aneurysm sacs resected either during tumor removal or after neck-clipping were carried out by means of silver-intensified light microscopic immunocytochemistry visualizing neuropeptide-Y, calcitonin gene-related peptide and substance P immunoreactivity. Systematic morphological investigations confirmed the presence of longitudinal fiber bundles on the adventitia and a network-like deeper peptidergic system at the adventitia-media border, while in smaller pial and intraparenchymal vessels, only sparse longitudinal immunopositive axons could be detected. The innervation pattern was totally absent in the wall of saccular aneurysms with the complete disappearance of peptidergic nerve fibers in some areas. To the best of our knowledge neither the disappearance of this network on small pial and intraparenchymal vessels, nor the absence of an innervation pattern in saccular aneurysms have been described before. Nonhomogeneous peptidergic innervation of the human cerebral vascular tree might be one of the factors responsible for the distinct autoregulatory properties of the capacitance and resistance vessels. Malfunction of this vasoregulatory system might lead to the impairment of autoregulation during pathological conditions such as subarachnoid hemorrhage.

Cerebral Arteries↗

PubMed1981

Body fluid homeostasis in man. A contemporary overview.

In the steady state, urinary excretion of sodium is closely matched to dietary salt intake. Given rigorous defense of extracellular fluid osmolality, it is the quantity of sodium in the extracellular fluid that determines the volume of this compartment. Changes in extracellular fluid volume are detected by volume sensors located in the intrathoracic vascular bed, kidney and other organs. These mechanoreceptors gauge the adequacy of intravascular volume, relative to capacitance, at various sites within the circulation. The perception of a change in the normal relationship between intravascular volume and circulatory capacity evokes a host of renal effector mechanisms that lead ultimately to physiologically appropriate changes in urinary sodium excretion. These effector mechanisms involve physical adjustments in the glomerular filtration rate, renal microvascular hemodynamics and peritubular capillary Starling forces, tubule fluid composition, flow rate and transtubular ion gradients. Neural and humoral pathways are also involved and, among the latter, angiotensin II, aldosterone, prostaglandins and kinins have been studied extensively. The continuous interaction between these sensor and effector mechanisms serves to ensure near-constancy of the extracellular fluid volume, a condition essential for optimal circulatory performance.

Aldosterone↗

PubMed1999

Liver microvascular architecture: an insight into the pathophysiology of portal hypertension.

Structural adaptations in the liver to constantly receive and release a large volume of circulating blood at low pressure are present at many levels; alteration of these structures can modify flow and perturb pressure gradients. Liver growth multiplies the lobule number by a factor of 4-5 after birth. Lobule configuration conforms with observations in space division, each unit being bordered by planes; curvature will impede expansibility and retractability among units. Lobular organization with hepatocytic plates and sinusoids, being radial centrally and reticular peripherally, maximizes its reversible distensibility. Resistance sites in the portal, sinusoidal, and hepatic system are subject to species variations; real portal sphincters are photographed in the frog. Small venules are demonstrably resistive. In endothelin-1-induced rat portal hypertension, the distal segment of preterminal portal venules constricts most intensely, whereas the terminal portal venules and sinusoids are flaccid. Their pericytes and arachnocytes (stellate cells, Ito cells, retinol-storing cells), respectively, possess no effective contractile machinery. In the dog, the initial sublobular veins react with venoconstriction to many stimulations. Well-developed musculature in hepatic veins, as in man and pig, can regulate flow by junctional constriction. These histoarchitectonics provide hepatic hemodynamics with high capacitance and high compliance properties. The hepatic artery supplies oxygenated blood to five stromal compartments: peribiliary vascular plexus, portal tract interstitium, portal vein vasa vasorum, hepatic capsule, and central-sublobular-hepatic vein vasa vasorum. Its role as the nutrient vessel to the veins is established, but what influence it may have in the pathophysiology of portal hypertension awaits clarification.

Animals↗

PubMed1998

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

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

Animals↗

PubMed1988

Sympathetic vascular control of the pig nasal mucosa (2): Reserpine-resistant, non-adrenergic nervous responses in relation to neuropeptide Y and ATP.

The possible occurrence of non-adrenergic mechanisms in the sympathetic vascular control of the nasal mucosa was studied in vivo using reserpine-treated pigs (1 mg kg-1, i.v., 24 h earlier) in combination with pharmacological blockade of alpha-adrenoceptors by local phenoxybenzamine (1 mg kg-1, i.a.) infusion. The nasal mucosal depletion (99%) of the content of noradrenaline (NA) in reserpinized animals was not influenced by preganglionic denervation while the depletion (44%) of neuropeptide Y (NPY) was prevented. Upon stimulation with single shocks, 25% of the arterial blood flow reduction and 47% of the nasal mucosal volume reduction (reflecting contraction of venous sinusoids) were still present after reserpine as compared with controls. In reserpinized animals, the vascular responses were slow developing and long-lasting, and about 60% remained at 0.59 Hz and more than 80% at 6.9 Hz. The vascular effects after reserpine were, however, subjected to fatigue, which may explain why phenoxybenzamine treatment still reduced the functional effects in the absence of NA. Local intra-arterial injections of NA, NPY and the metabolically stable adenosine-5'-triphosphate analogue alpha, beta-methylene ATP (mATP) caused reduction in both arterial blood flow and nasal mucosal volume. The C-terminal fragment of NPY (NPY 13-36) also induced nasal vasoconstriction although with a fivefold lower potency than NPY 1-36. Adenosine-5'-triphosphate caused a biphasic vascular effect with vasodilatatory actions at low doses and a short-lasting vasoconstriction followed by vasodilatation at very high doses (100-fold higher than the threshold response to mATP). In contrast to the response to NA, the long-lasting vascular effects of NPY and mATP were resistant to phenoxybenzamine treatment. In conclusion, although NA is likely to mediate most of the sympathetic vascular responses to low-frequency stimulation in the pig nasal mucosa, a large resistance and capacitance vessel component upon high-frequency stimulation seems to be non-adrenergic and mimicked by NPY rather than ATP.

Adenosine Triphosphate↗

PubMed1992

Elevated mean systemic filling pressure due to intermittent positive-pressure ventilation.

To clarify the effect of intermittent positive-pressure ventilation (IPPV) on systemic circulation, mean systemic filling pressure (Psf) and circulating blood volume were measured together with other hemodynamic parameters of capacitance vessel. Change in circulating blood volume was determined by dilution with 51Cr-labeled erythrocytes. Vascular compliance (Cvas) was measured from the change in Psf caused by a bolus injection of blood. These parameters were measured during both spontaneous respiration and IPPV in male Wistar rats anesthetized with pentobarbital sodium. The shift from spontaneous respiration to IPPV reduced cardiac output (CO) by 20.9%. Psf increased significantly, from 7.1 +/- 1.2 to 8.6 +/- 1.1 mmHg. Central venous pressure (Pcv) also increased significantly. The pressure gradient for venous return decreased by 15.6% (from 6.4 to 5.4 mmHg). The resistance to venous return did not change significantly, but there was a significant increase in total peripheral resistance. Neither Cvas nor circulating blood volume was changed significantly by IPPV. These results indicate that during IPPV the increased Pcv attenuates the pressure gradient for venous return and decreases CO and that the compensatory increase in Psf is caused by a blood shift from unstressed to stressed blood volume.

Animals↗

PubMed1995

Specificity of different organic nitrates to elicit NO formation in rabbit vascular tissues and organs in vivo.

1. In the present study we assessed the formation of nitric oxide (NO) from classical and thiol-containing organic nitrates in vascular tissues and organs of anaesthetized rabbits, and established a relationship between the relaxant response elicited by nitroglycerin (NTG) and NO formation in the rabbit isolated aorta. Furthermore, the effect of isolated cytochrome P450 on NO formation from organic nitrates was investigated. 2. Rabbits received diethyldithiocarbamate (DETC; 200 mg kg-1 initial bolus i.p. and 200 mg kg-1 during 20 min, i.v.) and either saline, or one of the following organic nitrates: nitroglycerin (NTG, 0.5 mg kg-1), isosorbide dinitrate (ISDN), N-(3-nitratopivaloyl)-L-cysteine ethylester (SPM 3672), S-carboxyethyl-N-(3-nitratopivaloyl)-L-cysteine ethylester (SPM 5185), at 10 mg kg-1 each. After 20 min the animals were killed, blood vessels and organs were removed, and subsequently analyzed for spin-trapped NO by cryogenic electron spin resonance (e.s.r.) spectroscopy. 3. In the saline-treated control group, NO remained below the detection limit in all vessels and organs. In contrast, all of the nitrates tested elicited measurable NO formation, which was higher in organs (liver, kidney, heart, lung, spleen) (up to 4.8 nmol g-1 20 min-1) than in blood vessels (vena cava, mesenteric bed, femoral artery, aorta) (up to 0.7 nmol g-1 20 min-1). Classical organic nitrates (NTG, ISDN) formed NO preferentially in the mesenteric bed and the vena cava, while the SPM compounds elicited comparable NO formation in veins and arteries. 4. Using a similar spin trapping technique, NO formation was assessed in vitro in phenylephrine-precontracted rabbit aortic rings. The maximal relaxation elicited by a first exposure (10 min) to NTG (0.3 to 10 microM) was positively correlated (r = 0.8) with the net increase (NTG minus basal) of NO spin-trapped during a second exposure to the same concentration of NTG in the presence of DETC. 5. Cytochrome P450 purified from rabbit liver enhanced NO formation in a NADPH-dependent fashion from NTG, but not from the other nitrates, as assessed by activation of purified soluble guanylyl cyclase. 6. We conclude that the vessel selective action of different organic nitrates in vivo reflects differences in vascular NO formation. Thus, efficient preload reduction by classical organic nitrates can be accounted for by higher NO formation in venous capacitance as compared to arterial conductance and resistance vessels. In contrast, NO is released from cysteine-containing nitrates (SPMs) to a similar extent in arteries and veins, presumably independently of an organic nitrate-specific biotransformation. Limited tissue bioavailability of NTG and ISDN might account for low NO formation in the aorta, while true differences in biotransformation seem to account for differences in NO formation in the other vascular tissues.

Animals↗

PubMed1978

[Cardiac and vascular components of the systemic circulatory reaction to orthostasis].

The orthostatic test (OT) induced regular constrictor responses of the resistance vessels and less regular those of the capacitance vessels under conditions of extracorporeal circulation (by passing the left ventricle) in anesthetized cats. Responses of the resistance vessels were eliminated by ganglionic blockade, while blood pooling rised only in half of experiments under these conditions. In case of natural circulation, the ganglionic blockade entailed an obvious initial hypotension followed by lowering of compensatory elevation of arterial pressure (AP) while responses of the cardiac output to OT remained unchanged. By the method of extracorporeal circulation combined with the "working" heart significant lowering of the cardiac output to OT was achieved; this response was accompanied by constrictor responses of the resistance vessels. Compensatory responses of AP reveal themselves mainly by the vascular component of the systemic reaction.

Animals↗

PubMed1982

Unloading effects of vasodilators on peripheral circulation and cardiac hemodynamics in patients with acute myocardial infarction.

Effects of three representative vasodilators on peripheral and cardiac hemodynamics were studied in 20 patients with heart failure due to acute myocardial infarction (PCWP greater than 18 mmHg, C1 greater than 2.20 L/min/m2) using venous occlusion plethysmography and a Swan-Ganz catheter. Sublingual isosorbide dinitrate (ISDN) significantly increased calf venous capacitance (CVC) from 5 to 60 min (p less than 0.01) and calf blood flow (CBF) in the initial 15 min (p less than 0.05), while simultaneously lowering PCWP (p less than 0.05) and central venous pressure (p less than 0.05). Calf vascular resistance (CVR), cardiac index, blood pressure, and total systemic peripheral resistance (TSPR) were not affected significantly. Nitroglycerin ointment (NGO) significantly decreased CVR (p less than 0.05) and increased CVC (p less than 0.05) from 60 to 240 min, simultaneously with lowering of PCWP (p less than 0.01), central venous pressure (p less than 0.05), and TSPR (p less than 0.05). Oral prazosin (Pz) increased CBF (p less than 0.01) and CVC (p less than 0.05) from 60 to 240 min, simultaneously with significant lowering of PCWP (p less than 0.01) and TSPR (p less than 0.05), resulting in increased stroke work index (p less than 0.05). These data confirm that ISDN predominantly causes capacitance vessel dilatation and reduce excessive venous return, while Pz and NGO dilate not only capacitance vessels but also resistance vessels, consequently reducing systemic vascular resistance and resulting in increased peripheral blood flow and cardiac performance. It was observed that the higher the base-line calf vascular resistance rose, the better the response to the vasodilator treatment appeared in terms of a decrease in calf vascular resistance.

Adult↗

PubMed1982

[Effect of nitrates, nitrate-like substances, calcium antagonists and beta-adrenergic receptor blockers on peripheral circulation].

The effectiveness of organic nitrates in the therapy of angina pectoris can be explained from their direct relaxing action on vascular smooth muscle. At conventional dosage the most important action of nitrates is a pooling of blood in the large systemic venous capacitance vessels which leads to a decrease of central venous pressure and ventricular filling pressure. The resulting reduction in left ventricular volume lowers, at virtually constant arterial pressure, systolic wall tension and hence myocardial oxygen consumption. Only at higher dosage, is a distinct dilatation of systemic resistance vessels affected. The fundamental action of the "Ca antagonists", i.e. the inhibition of transmembrane calcium influx in the myocardium and the vascular smooth muscle, includes various beneficial effects for the treatment of angina pectoris. The lowering of myocardial oxygen consumption after application of calcium antagonist is mainly due 1. to the decrease in afterload of the left ventricle, caused by the relaxation of peripheral resistance vessels, 2. to the reduction in ventricular preload by a peripheral venodilation. By a direct inhibitory effect on the coronary vascular tone, coronary blood flow at rest in patients with angina pectoris increases. In addition, Ca antagonists are very efficacious in relieving angiospastic angina. The primary mode of action of beta-blocking drugs in angina pectoris affects, in contrast to the peripheral mechanisms of nitrates and Ca antagonists, is on the heart directly. By the reduction in the extent of exercise heart rate, the increase in cardiac output and, hence, the mean arterial pressure is also significantly lower during exercise under beta-blockade. Beta-blockers also depress the contractile state of myocardium. Therefore, the main factors of the myocardial oxygen consumption (mean arterial pressure, size of the left ventricle, contractility and heart rate) may be essentially influenced. By the decrease in heart rate and the longer diastolic period a better myocardial oxygen delivery results. Besides the immediate cardiac effects of beta-adrenergic blockade, a decline in peripheral resistance combined with a fall in blood pressure occur in hypertensive patients during long-term drug administration. Different hypotheses have been proposed in the last years to explain the antihypertensive mode of action of beta-blockers. Some possible mechanisms are discussed.

Adrenergic beta-Antagonists↗

PubMed1976

Correlative changes in total vascular capacity and resistance in carotid sinus reflex.

To attain a quantitative understanding of carotid sinus reflex control of circulation, we studied the correlation between changes in total vascular capacity (V) and total peripheral resistance (R). We used a newly devised, accurate and simple method to measure changes in V while both mean central venous and arterial pressures being kept constant. In 7 open chest dogs (7-11 Kg, mean 8.9 Kg), bilateral carotid occlusion after vagotomy reduced V by as much as 58 +/- 9 (SE) ml or approximately 8% of total blood volume while R increased by 36 +/- 5% from 0.08 +/- 0.01 mmHg-min/ml. Similar responses were obtained either in the reflex before vagotomy or with infusion of norepinephrine. Mathematical analysis with Poiseuille's law suggested that internal radius of an average resistance vessel decreased approximately 1.5 to 3 times as much as that of an average capacitance vessel. The wall to lumen ratio of the average resistance vessel estimated from the correlation was 0.3 to 0.6, being within physiological range. Therefore, the difference in vascular sensitivity may be partly owing to the wall to lumen ratio of resistance vessels. Moreover, the correlative changes in the capacitance and resistance vessels were elucidated to be significantly responsible for the characteristic hemodynamic changes in carotid sinus reflex.

Animals↗

PubMed1994

Three-dimensional transmural mechanical interaction between the coronary vasculature and passive myocardium in the dog.

The "garden hose" effect of coronary perfusion on diastolic left ventricular (LV) mechanics has been proposed to cause changes in systolic function by altering diastolic sarcomere length. We measured transmural distributions of three-dimensional shape change using radiopaque markers implanted in the LV free wall of eight isolated arrested canine hearts as functions of coronary arterial perfusion pressure (Pp) and LV pressure (PLV) and related these deformations to the local muscle fiber architecture. Increased Pp from 0 to 110 mm Hg produced a 10% reduction in LV chamber volume (P < .01) and 25% to 40% decreases in local three-dimensional wall strain at matched PLV, indicating myocardial stiffening. Significant decreases in the magnitudes of local deformation occurred preferentially in the cross-fiber and radial directions (P < .02), with no change in fiber strain. This suggests that changing coronary Pp does not alter diastolic fiber length; hence, the Frank-Starling law may not mediate the Gregg effect. Since the myocardial microvessels are primarily oriented parallel to the muscle fibers, the observed myocardial stiffening occurs in the directions transverse to the microvessels rather than along their length. Local myocardial wall volume in the unloaded LV demonstrated a uniform 5% increase from the unperfused state to Pp of 50 mm Hg. With further increases in Pp up to 110 mm Hg, the change in regional wall volume from the unperfused state developed a substantial transmural gradient increasing by 7% at the epicardium and 15% at the subendocardium. This reflects a significant increase (P < .02) in intramyocardial coronary capacitance from epicardium to endocardium, which may be related to a transmural gradient in coronary distensibility or vascularity.

Animals↗

PubMed1989

Nasal cryosurgery and cautery: should the septum be treated and is a diagnosis relevant?

Posterior rhinometric measurements of nasal resistance were conducted on two groups of patients with perennial rhinitis: those whose symptom of nasal stuffiness responded to a topical steroid spray and those in whom it did not. The anterior ends of the inferior turbinates in 48 patients were treated with either cryosurgery or cautery, and in half of the subjects the erectile tissue of the septum was also thermally ablated. Measurements were made before and 10-16 weeks after therapy. It is concluded from statistical comparison that there is no benefit to treating the septum, and that cryosurgery is more effective in those whose symptoms respond to topical steroids, while cautery works better in those who do not. Histology showed no change in the capacitance vessels (sinusoids) after either modality, and xylometazoline caused a marked decrease in nasal resistance, suggesting that vascular smooth muscle function was intact. Irrespective of the change in airway resistance, most subjects felt that there had been an improvement. The mechanism is discussed.

Adult↗