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PubMed1989

[Hemodynamic effects of the Bezold-Jarisch reflex in rabbit].

The Bezold-Jarisch reflex induced by intracoronary injection of nicotine (ICIN) of 5 micrograms/kg was studied in 40 anesthetized rabbits. Heart rate (HR), arterial blood pressure (ABP), left ventricular pressure (IVP), left ventricular dp/dt (LV dp/dt) and cardiac output (CO) were monitored and total peripheral resistance (TPR) was calculated. HR, ABP, LVP and LV dp/dt were decreased following ICIN. These inhibitory responses induced by ICIN were enhanced by sino-aortic denervation but abolished by bilateral vagotomy. Decreases in CO and TPR were also observed in response to ICIN. With the heart paced artificially to prevent bradycardia, the decreases in CO, TPR and ABP were still significant. Bilateral stellate ganglion section plus atropinization which abolished the decreases in HR and CO, did not significantly change the hypotensive response to ICIN. These data suggest that the hypotension evoked by Bezold-Jarisch reflex in rabbit is largely due to the decreases in TPR and partially caused by the decrease in CO.

Animals↗

PubMed1989

Turbinate perimeter ratio as an indicator of conchal atrophy for diagnosis of atrophic rhinitis in pigs.

Transverse sections of snouts from 171 cross-bred (principally Yorkshire X American Landrace) pigs were evaluated for evidence of turbinate atrophy by use of conventional (atrophic rhinitis [AR] score) and morphometric methods. Of the 171 pigs, 35 were clinically normal (AR score, 0), 65 had mild AR (AR score, 1), 41 had moderate AR (AR score, 2), and 30 had severe AR (AR score, 3). Turbinate cross-sectional area (TA) and the ratio of TA to nostril cross-sectional area, called turbinate area ratio (TAR), had the lowest correlations (r = 0.24 to 0.55) with conventional AR score. Among clinically normal pigs, TA was greater in older pigs as expected, but the TAR values also were significantly (P less than 0.0001) different between 15-week-old pigs (55 kg) and 22-week-old pigs (100 kg). Turbinate perimeter and turbinate perimeter ratio (TPR) were not influenced by pig age or source. The TPR values were closely correlated with subjective visual AR scores (r = 0.73), with AR scores derived by measuring the space between the ventral portion of the scroll and the floor of the nasal cavity (r = 0.72), and the actual size of this space in millimeters (r = 0.71). Mean TPR values for pigs assigned visual AR scores of 0, 1, 2, or 3 were 1.54, 1.25, 0.97, and 0.73, respectively. The 95% confidence intervals around these mean TPR values were discreet and did not overlap. Turbinate perimeter ratio, therefore, may be a more reliable morphometric measure of atrophic rhinitis and also provides parametric data suitable for quantitative analysis.

Animals↗

PubMed1985

Endogenous angiotensin II facilitates sympathetically mediated hemodynamic responses in pithed rats.

The influence of endogenous angiotensin II on the hemodynamic responses to electrical stimulation of the sympathetic outflow was assessed in pithed male normotensive Wistar rats fitted with aortic flow probes for continuous measurement of cardiac output (CO). The frequency-related increments (0.25-4.0 Hz) in blood pressure (BP) and total peripheral resistance (TPR) were significantly attenuated by treating animals with the angiotensin converting enzyme inhibitor captopril (5 mg/kg i.v.) or the angiotensin II receptor antagonist saralasin (10 micrograms/kg/min i.v.). However, the increments in CO and heart rate during neural stimulation were unaffected by blockade of the renin-angiotensin system. After captopril treatment, infusion of angiotensin II (40 ng/kg/min i.v.) to replace the loss of endogenous angiotensin II restored stimulation-induced TPR and BP responses toward precaptopril levels; CO and heart rate responses to stimulation were not altered. The hemodynamic responses to exogenous norepinephrine were affected by inhibition of the renin-angiotensin system with captopril and saralasin in a manner analogous to the neurally mediated responses. The results obtained with nerve stimulation and norepinephrine indicate that endogenous angiotensin II selectively interacted with sympathetic neural control of vascular resistance, whereas cardiac responsiveness to noradrenergic neurons was not altered. Moreover, in the absence of nerve stimulation, the antagonism of the renin-angiotensin system lowered base-line BP by reducing CO without measurably affecting TPR. Infusion of angiotensin II reversed these effects and restored BP toward precaptopril levels by increasing CO without measurably affecting TPR.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗

PubMed1985

Hemodynamic responses to upright tilt at sea level and high altitude.

Hemodynamic responses to upright tilt were studied in eight young men at sea level (SL); after 1 h at 4,300 m simulated altitude (SA); and at 18 h, 66 h and 114 h during residence at 4,300 m (HA). Heart rate (HR), stroke volume (SV), cardiac output (CO), calf blood flow (CBF), blood pressure (BP) and total peripheral resistance (TPR) were obtained during supine rest and after 13 min of 60 degrees head-up tilt using an impedance monitor and electrosphygmomanometer. SL to HA changes in blood volume (BV) were calculated from hematocrit and hemoglobin values. Plasma norepinephrine (Nor) was measured at SL and after 18 h and 66 h of HA. Supine HR, TPR and BP were increased while SV, CO and CBF were reduced SL to HA (p less than 0.05). HR and BP in the upright position were increased SL to HA (p less than 0.05). The responses to tilt (delta supine to upright) were unaltered SL vs SA. With prolonged exposure, SV, CO, TPR and CBF responses to tilt were reduced (p less than 0.05). The reduced responses to tilt at HA were associated with a 10% decline in BV (p less than 0.01) and a 40% increase in Nor (p less than 0.05). It was concluded that the reduction in SV during tilt at SL and SA was compensated for by increases in HR and TPR in order to maintain BP. After 18 h HA, BP in the upright position was maintained only by an increase in HR.

Adult↗

PubMedDate not supplied

Hemodynamic effects of chronic alteration in hematocrit in spontaneously hypertensive rats.

This study describes the effect of a chronic decrease in hematocrit on blood pressure, cardiac output (CO), total peripheral resistance (TPR), and plasma volume in spontaneously hypertensive rats (SHR), and all but plasma volume in normotensive Wistar rats (NWR). Hematocrit was decreased by treatment with either heparin, vitamin K inhibitor ( pelentan ), or by repeated blood letting (BL). The results show that in SHR, a decrease in hematocrit, regardless of how produced, was associated with a significant decrease (p less than 0.01) in blood pressure. Prevention of heparin-induced decrease in hematocrit by repeated transfusions of red blood cells abolished the blood-pressure-lowering effect of heparin. By using combined data on hematocrit and systolic blood pressure in all five SHR groups, a significantly positive correlation and linear regression between hematocrit and blood pressure were obtained. When compared to control untreated SHR, heparin- or pelentan -treated SHR showed a significant (p less than 0.001) decrease in TPR and a significant increase in CO, while in SHR BL, no difference in TPR or CO was found. Plasma or blood volume did not differ among the groups. In NWR, heparin treatment resulted in significantly decreased hematocrit, decreased TPR, and increased CO compared to control normotensive rats. However, blood pressure did not change. Results confirming the authors' previous study and those of other investigators indicate a direct association between hematocrit and systemic hypertension. Lowering the hematocrit can effectively lower an elevated blood pressure. Moreover, the data suggest that heparin or pelentan induces a vasodilator effect that cannot be attributed to a decrease in hematocrit alone.

Animals↗

PubMed1978

[Hemodynamic effects of obzidan in vasorenal hypertension in dogs in ontogeny].

Vasorenal hypertension was reproduced in experiments on 18--22 day-old and 2--3-month-old puppies and on sexually-mature dogs by bilateral stenosis of the renal arteries. Two weeks later all the animals were given intravenous infusion of obzidan in a dose of 2 mg/kg. The arterial pressure, the minute and systolic volumes (MV, SV), total peripheral resistance (TPR), and the work, strength, and phase structure of the left ventricle were recorded. In animals aged 18--22 days with elevated pressure, obzidan infusion promoted its normalization, led to a decrease in the increased MO to subnormal values, a decrease in TPR and the heart beat rate, and normalization of the increased SV. In puppies aged 2--3 months, obzidan normalized the pressure by causing a fall in the minute output which was already reduced in hypertension, and a certain decrease in TPR with hardly any changes occurring in SV. In adult dogs, despite a sharp decrease in MV, arterial pressure did not significantly change due to the increase in TPR. Energy expenditure per each liter of MV was normalized by obzidan only in puppies.

Age Factors↗

PubMed1983

[Hemodynamic changes after application of vasoactive substances in cats with unilateral renal artery constriction in addition to sinoaortal baroreceptor deafferentation].

The relationship between total peripheral resistance (TPR), cardiac output (CO) and venous return (VR) and their role in the response of mean arterial pressure (MAP) on intravenous adrenalin (10 micrograms/kg) and angiotensin II (0.5 micrograms/kg), resp., were investigated in normal cats (A), cats with unilateral renal artery stenosis (B) and cats with sinoaortal baroreceptor deafferentation (C). In the maximum MAP increase in group A there participated both TPR and VR through altered CO. In group B the MAP increased after angiotensin II only in consequence of an enhanced TPR, whereas the VR response was dampened; only after adrenalin the VR contributed a little to MAP increase through CO. In group C, the MAP increase after both substances was due exclusively to increased TPR; at a restricted ejection capacity of the heart the VR cannot act on the level of blood pressure.

Angiotensin II↗

PubMed1981

Augmented venous return: a model of left ventricular afterload reduction during the course of endotoxin shock.

Utilizing a canine model of endotoxin shock (E coli, 4 mg/kg, B6:026) the major determinants of cardiac output (preload, afterload, contractility, and heart rate) were simultaneously followed for 5 hr in four study groups: Group I: time-matched controls, Group II: endotoxin shock, Group III: endotoxin shock and femoral-femoral A-V shunt, and Group IV: A-V shunt control. Groups II and III demonstrated an initial, abrupt increase in total peripheral resistance (TPR), coronary vascular resistance (CVR), and pulmonary vascular resistance (PVR), and a decrease in cardiac output (CO), coronary flow (CF) and heart rate (HR) and stroke work (P less than 0.05). Group II then demonstrated a decrease in TPR, CVR, PVR with an increase in CO and CF but systemic arterial pressure did not return to control values. At approximately 3 hr, Group II developed a progressive increase in TPR, CVR, and PVR, and a decrease in CO, CF, and SW. Heart rate did not change. In contrast, at 3 hr Group III demonstrated no significant increase in TPR, CVR, or PVR, a progressive increase of CO and CF, and preservation of SW. It is hypothesized that endotoxin shock is characterized by an initial phase characterized by an increase in resistance and decrease in flow that is not affected by an augmented venous return. However, in the intermediate and latter stages of shock, there is a progressive increase in resistance and decrease in flow, increasing impedance to left ventricular ejection that results in an imbalance between myocardial oxygen supply and demand, contributing to the observed myocardial failure. An augmented venous return, by decreasing resistance (afterload) and increasing venous return (preload) preserves cardiac output and myocardial function and thus serves as a model of left ventricular afterload reduction during the course of endotoxin shock.

Animals↗

PubMed1995

Role of endothelin-converting enzyme in the systemic hemodynamics and regional circulatory effects of proendothelin-1 (1-38) and diaspirin cross-linked hemoglobin in rats.

Diaspirin cross-linked hemoglobin (DCLHb) is a promising hemoglobin-based, oxygen-carrying resuscitative solution. DCLHb (400 mg/kg, iv) produces significant cardiovascular effects, along with an increase in plasma endothelin-1 (ET-1) level, when administered to conscious or anesthetized rats. Present studies were performed to determine whether the cardiovascular effects of DCLHb are due to an increase in the conversion of proendothelin-1 (1-38) (proET-1) to ET-1 by endothelin-converting enzyme (ECE). The regional circulatory and systemic hemodynamic effects of proET-1 (20 micrograms/kg, iv) and DCLHb (400 mg/kg, iv) were determined by using a radioactive microsphere technique in control rats and rats pretreated with phosphoramidon (ECE inhibitor). Administration of proET-1 produced an immediate increase in mean arterial pressure (MAP)(52%) and total peripheral resistance (TPR) (55%); stroke volume (SV) and cardiac output were not affected in the initial phase but were decreased subsequently. Heart rate (HR) was not affected after administration of proET-1. A significant increase in blood flow to the heart (39%), brain (46%), kidneys (74%), portal system (40%), and gastrointestinal tract (GIT) (42%) was also observed after administration of proET-1. Vascular resistance was found to be significantly increased in the mesentery and pancreas (168%) and in the musculoskeletal system (147%) and decreased in the kidneys (-11%) after administration of proET-1. Phosphoramidon (4 mg/kg, iv) pretreatment attenuated the increase in MAP and TPR induced by proET-1. Phosphoramidon pretreatment significantly attenuated the proET-1-induced increase in blood flow to the heart, brain, kidneys, portal system, and GIT. The increase in vascular resistance induced by proET-1 in the mesentery and pancreas and in the musculoskeletal system was also attenuated by phosphoramidon. DCLHb increased MAP (63%) and TPR (54%) without affecting HR. DCLHb increased blood flow to the heart (95%), GIT (45%), portal system (43%), and skin (79%) and increased vascular resistance in the musculoskeletal system (58%). In phosphoramidon-treated rats, DCLHb increased MAP (99%), HR (25%), cardiac output (37%), and TPR (60%). DCLHb increased blood flow to the heart (104%), brain (66%), kidneys (49%), GIT (59%), portal system (63%), and skin (100%) when administered to phosphoramidon-treated rats. Phosphoramidon did not attenuate any of the DCLHb-induced cardiovascular effects. It is concluded that proET-1 increases blood flow to various organs and that phosphoramidon, an ECE inhibitor, could block the proET-1-induced increases in regional blood flow.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1995

Comparison of 7.5% NaCl/6% dextran-70 resuscitation of hemorrhage between euhydrated and dehydrated sheep.

7.5% NaCl/6% dextran-70 (HSD) has been shown to be an effective, small volume resuscitation fluid following hemorrhage (HEM) in euhydrated (E) sheep. However, there is controversy whether hypertonic solutions would be effective in dehydrated (D) animals. Therefore, we used two groups (E and 4 days D) of chronically instrumented ewes to evaluate the responses to HSD following HEM. All sheep were bled and maintained at 50 mmHg mean arterial pressure (MAP) for 2 h, then resuscitated with a 4 mL/kg bolus of HSD. Dehydration did not affect baseline MAP, heart rate (HR), or total peripheral resistance (TPR), whereas cardiac output (CO: E, 5.28 +/- .31; D, 4.00 +/- .31 L/min), stroke volume (SV: E, 61 +/- 4; D, 44 +/- 4 mL/beat), urine flow rate (V: E, .51 +/- .11; D, .34 +/- .07 mL/min), and sodium excretion (UNa V: E, 22 +/- 8; D, 6 +/- 2 microEq/min) were reduced and plasma sodium (PNa: E, 150 +/- 3; D, 157 +/- 2 mEq/L) and protein (PTP E, 7.8 +/- .1; D, 8.8 +/- .6 g/dL) were elevated. The only difference between groups during HEM were HR (E, 98 +/- 8; D, 150 +/- 17 bpm), SV (E, 31 +/- 3; D, 14 +/- 2), and TPR (E, 23 +/- 2; D, 32 +/- 3). Resuscitation with HSD restored MAP (E, 92 +/- 3; D, 92 +/- 2), CO (E, 6.2 +/- .3; D, 4.2 +/- .2), and TPR (E, 15 +/- 1; D, 23 +/- 1) to baseline values. SV was increased above hemorrhage values but was not restored to baseline values in either group (E, 50 +/- 7; D, 27 +/- 3). HR increased further following HSD (E, 143 +/- 11; D, 158 +/- 5). PNa was raised 10 and 16 mEq/L in the E and D sheep, respectively, following HSD infusion, but no adverse effects associated with elevated PNa were observed in either group. Thus, HSD was effective in restoring MAP, CO, and TPR to baseline values in D sheep but it was at the expense of a lower SV and a higher HR than in E sheep.

Animals↗

PubMed1976

Haemodynamic effects of propranolol in hypertension: a review.

Like hypertension which is a multifactorial disease, the blood pressure response to propranolol cannot be explained by one mechanism alone to the exclusion of all others. Acute (intravenous) administration of propranolol lowers cardiac output and slows heart rate but does not significantly alter blood pressure. With continued therapy however, blood pressure (in responders) is gradually reduced while cardiac output and rate remains low, indicating a readaptation of total peripheral resistance (TPR) to the new haemodynamic conditions. This relatively complex interplay of factors and the predominant role of TPR in blood pressure response help explain why haemodynamic indices (such as elevated heart rate and cardiac output) were found of little value in predicting response to therapy and the failure of propranolol to control transient pressor responses associated with stress; although the increase of output in response to stress was blocked pressure rose due to increase in TPR. Therefore, despite the obvious cardiac effects of beta-adrenergic blockade, a blood pressure response to propranolol cannot be used as an index of cardiac participation in that hypertension. The long-term changes in TPR were significantly (P less than 0-02) correlated with reduction in plasma renin activity (PRA). This association does not necessarily imply a causal relationship since PRA suppression occurs at lower doses and much more rapidly than alterations in blood pressure. Further, the hypotensive effect obtained by adding propranolol to diuretic therapy was not associated with a significant reduction in PRA. However, the absence of correlation in a group of patients between blood pressure response to propranolol and its effect on other biological variables does not mean that these variables have no role in the hypotensive response. In fact, in some specific conditions the change in one variable might assume particular importance; thus in the markedly hyperkinetic circulation induced by potent vasodilators, reducing cardiac rate and output may play a major role in controlling persistent hypertension.

Animals↗

PubMed1994

Acute effects of ethanol on cardiac output and its derivatives in spontaneously hypertensive and normotensive rats.

This study investigated the influence of small to moderate doses of ethanol on arterial pressure (MAP), heart rate, cardiac index (CI), stroke volume (SV) and total peripheral resistance (TPR) of anesthetized spontaneously hypertensive rats (SHRs) and two age-matched normotensive strains, Wistar Kyoto (WKY) and Sprague-Dawley (SD) rats. Compared with WKY values, the significantly higher MAP of SHRs (175 +/- 4 vs. 118 +/- 4 mm Hg) was the result of a significantly elevated TPR (6.1 +/- 0.3 vs. 3.1 +/- 0.2 mm Hg/ml/min/100 g; P < .05), because Cl was significantly lower (31 +/- 1.6 vs. 41 +/- 2.5 ml/min/100 g; P < .05). A lower SV (261 +/- 13 vs. 394 +/- 20 microliters/min; P < .05) accounted for the reduced Cl in SHRs, because HR was similar (318 +/- 4 vs. 328 +/- 11 beats/min). In spite of similar MAP (114 +/- 3.9 vs. 118 +/- 4 mm Hg) of SD and WKY rats, Cl was significantly higher (33 +/- 2 vs. 41 +/- 2.5 ml/min/100 g; P < .05) due to a higher SV (339 +/- 19 vs. 394 +/- 20 microliters/min; P < .05) and TPR was significantly lower (3.7 +/- 0.2 vs. 3.1 +/- 0.2 mm Hg/ml/min/100 g; P < .05) in the latter strain. Low dose ethanol (0.1-0.25 g/kg) had no effect, whereas a moderate dose of 0.5 g/kg elicited strain-dependent hemodynamic responses which comprised significant increases in Cl and SV in normotensive rats, but not in SHRs. However, because of a reduction in TPR, MAP did not change.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1993

[Peripheral and central participation in hemodynamic effects of serotonin2 receptor stimulation].

The systemic and regional haemodynamic effects of DOI were investigated in the anaesthetized rat. DOI (1-300 micrograms/kg i.v.) increased mean arterial pressure (MAP), total peripheral resistance (TPR) and all regional vascular resistances studied (hindquarters, mesenteric and renal). DOI was more effective on renal vascular bed. Cardiac output (CO) and heart rate (HR) did not change. The effects of DOI were antagonized by LY 53857 (10 micrograms/kg i.v.) and spiperone (10 or 100 micrograms/kg i.v.), selective 5-HT2 receptor antagonists. Intracerebroventricular administration of DOI (100 micrograms/kg) increased MAP, TPR, regional vascular resistances and did not change HR and CO. Pretreatment with xylamidine (10 micrograms/kg i.v.), a selective peripheral 5-HT2 receptor antagonist, blocked i.v. and i.c.v. effects of DOI. These results suggest that: 1) the increase in MAP induced by the stimulation of 5-HT2 receptors is due to an increase in TPR. All regional vascular resistances participate in the increase of TPR. 2) Peripheral and central 5-HT2 receptors seem to be implicated in the control of regional vascular resistances.

Amphetamines↗

PubMed1993

Hemodynamic responses to changes in carotid sinus pressure after endotoxin and ibuprofen.

The hemodynamic responses to changes in carotid sinus pressure (CSP) were evaluated in nine pentobarbital-anesthetized dogs during control, endotoxin-treatment, and ibuprofen (after endotoxin) treatment periods. Both carotid sinuses were isolated and perfused at varying pressures with oxygenated blood in the vagotomized animal. Alterations in carotid sinus pressure and the resultant responses were measured at 15-min intervals during a 30-min control period, for 60 min after 1 mg/kg endotoxin, and for 60 min after 10 mg/kg ibuprofen given after endotoxin. The results showed a reduction in calculated gain for mean arterial pressure (MAP) (change in arterial pressure/change in CSP), heart rate, and peripheral resistance (TPR) after endotoxin, without a corresponding reduction in cardiac output (CO) gain. These gain changes were accompanied by a decrease in absolute MAP, CO, and TPR. An indicator for cardiac performance gain also increased. Relatively, arterial pressure was partially maintained by an increase in CO despite a loss in ability to vasoconstrict. Ibuprofen failed to correct the MAP gain, and only partially restored MAP, but shifted a greater relative response to peripheral resistance. To test if TPR would also decrease if the decrease in CO was prevented, three additional animals were studied with a pump in series with the heart to maintain CO; TPR again dropped after endotoxin. The results indicate a loss of peripheral arterial tone after endotoxin, partially restored by ibuprofen. The CO response indicates a peripheral vascular failure rather than a central or carotid sinus failure mechanism.

Animals↗

PubMed1995

[Hemodynamic effects of sub-chronic NO synthase inhibition in conscious dogs: role of EDRF/NO in muscular exertion].

Acute and chronic administration of nitric oxide (NO) synthase (NOS) inhibitors increase mean arterial blood pressure (MAP) in rats but their hemodynamic effects in other species remain unknown. Moreover, the role of NO in the control of exercise-induced vasodilation is still debated. To answer these questions, six dogs were instrumented for the continuous measurement of cardiac output (CO, electromagnetic flow probe on the aorta), MAP (aortic catheter) and left ventricular pressure (Konigsberg gauge). Total peripheral resistance (TPR) was calculated as MAP/CO ratio and dP/dt was used as an index of cardiac inotropism. The dogs were treated from day 0 (D0) to 7 (D7) by the NOS inhibitor, N omega-nitro-L-arginine (L-NNA), 20 mg/kg/day (IV). Such a dose regimen resulted in NOS inhibition evidenced (a) in vivo by a reduction of the hypotensive responses to graded doses of acetylcholine and bradykinin, (b) ex vivo by a decrease in the relaxation of the femoral artery to acetylcholine (EC 50 = 2.2 +/- 0.6 10(-7) M after L-NNA vs 2.2 +/- 0.8 10(-8) M in controls). One month after instrumentation, the dogs being conscious, MAP measured at rest remained unchanged following one week L-NNA treatment (from 90 +/- 2 at D0 to 91 +/- 5 mmHg at D7). However, TPR increased (from 3,600 +/- 290 at D0 to 6,300 +/- 510 dyn.s.cm-5 at D7) and CO decreased (from 2.1 +/- 0.2 at D0 to 1.2 +/- 0.1 l/min at D7) (all p < 0.01), partly as the result of a marked bradycardia (from 100 +/- 7 at D0 to 60 +/- 7 beats/min at D7). L-NNA induced-increase in TPR was completely reversed by a bolus injection of nitroglycerin (10 micrograms/kg). During treadmill exercise (12 km/h), heart rate (251 +/- 9 at D0 vs 226 +/- 11 beats/min at D7), CO (6.3 +/- 0.9 at D0 vs 4.3 +/- 0.7 l/min at D7) and stroke volume remained significantly lower, and TPR significantly higher (1,662 +/- 278 at D0 vs 2,621 +/- 489 dyn.s.cm-5 at D7) after L-NNA than in the control state. Thus, NOS inhibition in resting conscious dogs by L-NNA markedly increases peripheral resistance but does not increase arterial pressure. In addition, L-NNA blunts both exercise-induced peripheral vasodilation and increase in cardiac output, despite metabolic vasodilation.

Acetylcholine↗

PubMed1998

Hemodynamics after aortic valve replacement with St. Jude Medical valve for patients with small aortic annulus and severe left ventricular hypertrophy.

BACKGROUND AND AIMS OF THE STUDY: Cardiac function after aortic valve replacement (AVR) for patients with small aortic annulus and increased left ventricular (LV) wall thickness has not been clearly defined. The study aim was to examine a potential relationship between postoperative catheterization data (or radionuclide LV cardiac function) and the size of the aortic valve ring of a small St. Jude Medical prosthesis. METHODS: Sixty-one patients with small prosthesis (< or = 23 mm) were allocated to three groups based on the diameter of the native aortic annulus or aortic valve ring of the prosthesis (group I, 19 mm; group II, 21 mm; group III, 23 mm). Pre- and postoperative cardiac function was evaluated from catheterization data and radioisotope (RI) ventriculography. RESULTS: There were no significant inter-group differences in preoperative pulmonary artery pressures (PAPs), total pulmonary resistance (TPR), LV ejection fraction, peak ejection rate (PER) and peak filling rate (PFR). The mean postoperative PAPs and TPR of group I were significantly elevated in ICU compared with those of groups II or III (PAP: group I, 20+/-5; group II, 17+/-4; group III, 14+/-4 mmHg; p <0.01. TPR: group I, 505+/-268; group II, 316+/-134; group III, 276+/-125 dynes.s.cm-5; p <0.05). Postoperative PAPs and TPR of group I at one month after surgery were decreased, and no significant difference was found between the three groups. Cardiac function by RI study showed that postoperative PER and PFR improved in all three groups compared with the preoperative values. CONCLUSIONS: Postoperative reversibility of PAPs and improvement of PER and PFR in patients with a prosthesis of 19 mm or 21 mm showed that a small-sized aortic SJM valve had hemodynamic advantages. However, careful postoperative management in the ICU must be applied to patients with a small aortic annulus of 19 mm and severe concentric hypertrophy.

Aged↗

PubMed1999

Ethanol counteraction of I1-imidazoline but not alpha-2 adrenergic receptor-mediated reduction in vascular resistance in conscious spontaneously hypertensive rats.

Our recent findings have shown that ethanol selectively counteracts decreases in blood pressure (BP) evoked via activation of central I1-imidazoline receptors but not alpha-2 adrenoceptors in conscious spontaneously hypertensive rats (SHRs). This study investigated the role of sympathetic activity, cardiac output and total peripheral resistance (TPR) in the differential effect of ethanol on centrally mediated hypotension. Changes in plasma norepinephrine (NE), as index of sympathetic activity, BP, heart rate, cardiac index, stroke volume, and TPR elicited by rilmenidine or alpha-methylnorepinephrine (selective I1 and alpha-2 receptor agonists, respectively) and subsequent ethanol (0.5 or 1 g/kg) or saline, were evaluated in conscious SHRs. Intracisternal rilmenidine (25 microg) or alpha-methylnorepinephrine (alpha-MNE; 4 microg) elicited similar decreases in BP, TPR, and plasma NE, but cardiac index was not changed. Ethanol (0.5 g/kg i.v.) had no effect on hemodynamic responses to rilmenidine or alpha-MNE. The higher dose (1 g/kg i.v.) of ethanol counteracted the hypotensive response to rilmenidine and significantly (P <.05) elevated TPR and plasma NE. In contrast, ethanol (1 g/kg) had no effect on the hypotensive responses to alpha-MNE but significantly (P <.05) elevated plasma NE. However, this increase in NE was approximately one third of the increase evoked by ethanol when given after rilmenidine. These findings suggest that the selective counteraction by ethanol of the hypotension evoked via activation of central I1 but not alpha-2 receptors may relate, at least in part, to its greater ability to reverse the sympathoinhibition and the associated decrease in vascular resistance mediated by I1 receptors.

Adrenergic alpha-Agonists↗

PubMed2004

Evaluation of kidney damage in patients with acute lymphoblastic leukemia in long-term follow-up: value of renal scan.

In order to evaluate potential long-term kidney damage of childhood leukemia and risk factors affecting renal damage, we studied 116 children treated for acute lymphoblastic leukemia (ALL) using the St. Jude Total XI and XIII protocols in 1991-1998. The median follow-up period after the completion of treatment was 35 months. The following parameters were examined: urinalysis, urinary creatinine (Cr), calcium (Ca), phosphorus, beta2-microglobulin, glomerular filtration rate (GFR), tubular phosphorus reabsorption (TPR), and renal function tests. Radiological evaluation included renal ultrasonography (US), and renal scans with DMSA or MAG-3 were performed. Blood chemistry and renal US patients were normal in all patients except two. GFR, TPR, urinary Ca/Cr, beta2-microglobulin, and renal scan were abnormal in 19.0%, 16.4%, 13.8%, 6.0%, and 40.5% of patients, respectively. The abnormality rate in GFR was significantly higher in patients <2 years of age. TPR abnormality was found to be significantly higher in patients who did not have G-CSF. An abnormal renal scan was associated with Hb < 10 g/dL, kidney infiltration, or hypertension at presentation and also occurred patients who underwent methotrexate treatment with frequent intervals during the follow-up period. Patients should be followed-up after cessation of therapy with the conventional tests mentioned above. In case of any abnormality, further detailed tests should be performed; renal scan seems to be more predictive for renal damage.

Adolescent↗