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PubMed2005

Calpains: a physiological regulator of the endothelial barrier?

The intracellular protease calpain, abundant in endothelial cells (EC), is assumed to be inactive under physiological conditions but may account for Ca2+ -linked pathophysiological events. However, nonstimulated EC contained autolyzed, activated calpain. Adding 12-48 microM calpain inhibitor I (CI) or 0.5-1 microM of the novel, membrane-permeable conjugate of calpastatin peptide-penetratin (CPP) caused rapid rounding and retraction of cultured EC (phase contrast, capacitance) and translocation of Syk, Rac, and Rho to the membrane, signifying activation upon inhibition of calpain. Isolated hearts (guinea pig) perfused with 12 microM CI or 0.5 muM CPP developed coronary leak. We conclude that calpain is constitutively active in EC and regulates vascular permeability by governing cell-cell attachment.

Animals↗
PubMed1976

Sex and estrogens in protection against circulatory stress reactions.

From Wistar rats, data are presented which indicate that inbred females a) have a greater ability to clear particulate matter from the blood stream than do males of the same strain; b) are significantly more resistant to two different forms of lethal circulatory stress (e.g., intestinal ischemia and whole-body trauma) than are males; and c) exhibit a greater resistance to undergo reticuloendothelial system (RES) phagocytic depression after both forms of lethal trauma than do males. Estradiol treatment of males, using either acute, massive (1 or 10 mg/kg) or multiple, low dose (10 or 100 mug/kg) regimens, confers trauma resistance on such animals. Such estradiol treated male rats exhibit hyperactive RES's. These estradiol-treated males, when subjected to either lethal ischemia or trauma, fail to demonstrate the early RES phagocytic depression seen in untreated controls. Untreated female as well as estradiol-treated male rats exhibit significantly higher arterial blood pressures post-trauma than do untreated male rats. Direct microscopic observation of rat mesenteries indicr whole-b0dy trauma, the untreated females as well as the estradiol-treated males exhibit significantly less dilatation of microscopic capacitance vessels (i.e., venules) than do untreated male rats. The data reported herein could be used to suggest that estrogenic hormones may play pivotal roles in a) the amelioration of an organism's reaction to systemic stress; and b) control of macrophage and peripheral vascular functions.

Animals↗
PubMed1993

Regional blood volume distribution during positive and negative airway pressure breathing in supine humans.

To assess the effects of continuous positive (CPAP) or negative airway pressure (CNAP) breathing (+/- 10-12 cmH2O, duration 25 min) on blood content in the body's capacitance vasculature, regional distribution of labeled red blood cells was evaluated in seven spontaneously breathing supine volunteers. Counts were acquired by whole body scans and detectors overlying the liver, intestine, left ventricle, and lower arm, and arterial pressure, heart rate, calf blood flow and vascular resistance, hematocrit, vasopressin, and atrial natriuretic peptide plasma concentrations were also obtained. With CPAP, thoracic, cardiac, and left ventricular counts diminished significantly by 7-10%, were accompanied by significant increases in counts over both the gut and liver, and remained decreased during CPAP but reversed to baseline with zero airway pressure. Calf blood flow and vascular resistance significantly decreased and increased, respectively, whereas limb counts, arterial pressure, heart rate, and hormone concentrations remained unchanged. With CNAP, in contrast, regional counts and other variables did not change. Thus, moderate levels of CPAP deplete the intrathoracic vascular bed and heart, shifting blood toward the gut and liver but not toward the limbs. No short-term compensation increasing cardiac filling during CPAP was seen. In contrast, CNAP did not alter intrathoracic or organ blood content and, therefore, does not simply mirror the effects evoked by CPAP.

Adult↗
PubMed1987

Effect of total spinal anesthesia on arterial and venous responses to dopamine and dobutamine.

To test whether acute denervation alters the vascular effects of dopamine and dobutamine, we anesthetized 16 greyhounds and placed them on total cardiopulmonary bypass (CPB). Eight dogs received total spinal anesthesia before drug testing; eight dogs were tested in the absence of total spinal anesthesia. During dopamine and dobutamine infusions, venous capacitance [determined by the volume of the CPB venous reservoir (VR)] and mean arterial pressure (MAP) were monitored. The CPB pump flows remained constant throughout our studies. Every dog received six increasing doses of both drugs. In the absence of total spinal anesthesia, both dopamine and dobutamine increased VR (decreased venous capacitance) in a dose-dependent manner. Dobutamine decreased MAP in a dose-related fashion but dopamine had no significant effect on MAP. After total spinal anesthesia, both dopamine and dobutamine produced greater dose-related increases in VR (i.e., decreases in venous capacitance) than in the absence of spinal anesthesia. Dopamine increased MAP but dobutamine had no significant effect. These data demonstrate how dopamine and dobutamine differ in their effects on the arterial circulation in the presence or absence of spinal anesthesia. The acute denervation of spinal anesthesia altered venous and arterial dose-response relationships of both drugs. Finally, our study demonstrates the effectiveness of dobutamine and, perhaps even more so, dopamine as possible alternatives to ephedrine for the pharmacologic correction of the noncardiac circulatory sequelae of spinal anesthesia.

Anesthesia, Spinal↗
PubMed1989

Prediction of the thermoregulatory response for clothed immersion in cold water.

A multi-compartmental thermoregulatory model was applied to data of ten resting clothed males immersed for 3 h in water at 10 and 15 degrees C. Clothing consisted of a dry suit and either a light or heavy undergarment, representing a total insulation of 0.15 (0.95) or 0.20 m2 degrees CW-1 (1.28 clo), respectively. Data were grouped according to low (less than 14%) and high (14 to 24%) body fat individuals. Mean decreases in rectal temperature ranged from 0.79 to 1.38 degrees C, mean decreases in the mean weighted skin temperature ranged from 6.3 to 10.2 degrees C, and mean increases in the metabolic rate ranged from 33.9 to 80.8 W. The model consists of eight segments, each representing a specific region of the body. Each segment is comprised of compartments representing the core, muscle, fat, skin, and clothing. Each compartment is assigned thermophysical values of heat conduction and heat capacitance, and with the exception of clothing, physiological values of blood flow and metabolic heat production. During cold exposure, responses are directed towards increased heat production in the form of shivering and heat conservation in the form of vasoconstriction and convective heat exchange at the vascular level. Agreement between the model predictions and the experimental observations was obtained by adjusting the parameters governing these responses.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Flow Velocity↗
PubMed1999

Changes of intracellular calcium concentrations by phenylephrine in renal arterial smooth muscle cells.

In smooth muscle cells isolated from swine renal interlobar arteries, phenylephrine (PE) at concentrations of 1-10 microM produced biphasic increases of the intracellular calcium concentration. An early transient rise was followed by a maintained plateau. The maintained component was sensitive to extracellular calcium, in contrast to the early transient, which was still observed in nominally calcium-free solution. Nifedipine (1 microM) and NiCl2 (100 microM) only weakly affected the calcium signal, suggesting that voltage-sensitive calcium channels play only a minor role in the PE-induced changes in intracellular calcium. Thapsigargin (0.5 microM) elevated the intracellular calcium concentration and depressed both the early transient and the maintained component of the PE response. In calciumfree medium PE induced a transient rise of the intracellular calcium concentration with a depressed plateau. Readmission of calcium elevated the intracellular calcium concentration above the baseline. Both components of the PE-induced calcium signal were completely abolished when the cells were pretreated with the phospholipase C (PLC) inhibitor U73122 (2 microM). LaCl3 (100 microM, 1 mM), an inhibitor of calcium-release-activated current (ICRAC), had no effect on the PE-induced calcium signal. GdCl3 (50 microM), SKF 96365 (10 microM) and flufenamic acid (100 microM), reported to inhibit nonselective cation channels, blocked or transiently reduced the maintained calcium signal. Several protein kinase inhibitors such as genistein (10 microM), H7 (50 microM), H89 (1 microM) and bisindolylmaleimide (0.2 microM) reduced the maintained calcium signal. We conclude that the initial transient spike of the PE-induced calcium signal is due to release of calcium from inositol 1,4,5-trisphosphate-sensitive calcium stores evoked by alpha 1-adrenoceptor-coupled stimulation of PLC and that the maintained component is due to capacitative calcium entry, which is modulated by protein kinases.

Adrenergic alpha-Agonists↗
PubMed1984

Unloading the heart in congestive heart failure.

Depressed contractile performance of the heart in congestive heart failure is aggravated by increases in preload and afterload related in part to arterial and venous constriction. Vasodilator drugs have a salutary effect on left ventricular performance by reducing aortic impedance and/or increasing venous capacitance resulting in an increase in stroke volume and a lowering of filling pressure. Vasodilators may act by counteracting the heightened neurohumoral vasoconstriction tone in heart failure (inhibition of the sympathetic nervous system, inhibition of the renin-angiotensin system) or by more directly affecting vascular smooth muscle tone (direct vasodilators, calcium antagonists). The immediate effects of these drugs on resting hemodynamics must be supplemented by knowledge of their effects on the circulatory response to exercise and of their efficacy during long-term administration before a rational choice can be made as to the ideal agent or combination of agents to use in the long-term management of congestive heart failure.

Calcium↗
PubMed1997

Mobilization of internal Ca2+ by vasoactive intestinal polypeptide in endothelial cells.

The aims of the present study were to establish whether vasoactive intestinal polypeptide (VIP) could mobilize internally-stored Ca2+ and whether Ca2+ release could trigger Ca2+ influx from the extracellular space. Bovine pulmonary artery endothelial cells from an established cell line were loaded with fura-2/AM and cells were studied in suspension or were imaged in monolayers at 40-80% confluency. In Ca2+ imaging studies, VIP evoked Ca2+ transients in Ca2+-free medium containing 50 microM EGTA. This was observed in 33 out of 122 cells examined on 29 separate trials. With each cell, the spread of Ca2+ appeared to occur from the periphery of the cell to the central core. Cells which did not respond to VIP responded to other stimulants such as bradykinin, endoplasmic reticulum Ca2+ pump inhibitors, (cyclopiazonic acid and thapsigargin), and endoplasmic reticulum Ca2+ release channel opener, ryanodine. The reintroduction of Ca2+ following VIP-induced Ca2+ release did not evoke a Ca2+ response in 5 cells imaged. Cells in suspension showed typical biphasic responses to bradykinin, thapsigargin or cyclopiazonic acid in the presence of external Ca2+. Stimulation with VIP caused transient Ca2+ responses in Ca2+-free physiological saline containing 50 microM EGTA. However, only 1 out of 4 cells tested showed a response to Ca2+ when it was reintroduced to the bathing medium. This study provided direct evidence for the first time in these bovine endothelial cells for VIP-mediated elevation of cytosolic concentration of Ca2+. The results also suggested that other mechanisms might prevail preventing capacitative Ca2+ entry following the release of internally-stored Ca2+.

Animals↗
PubMed1992

[Vascular effects of ketamine during anesthesia with diazepam and fentanyl].

Twenty-six adults undergoing elective cardiac surgery were anaesthetized with diazepam and fentanyl (induction with 200 micrograms.kg-1 and 30 micrograms.kg-1 respectively, maintenance with incremental doses). Normothermic constant perfusion output cardiopulmonary bypass was carried out with a membrane oxygenator, haemodilution with Ringer's lactate solution, and cardioplegia with St. Thomas's Hospital solution. The patients were randomly assigned to two groups. They were given either 2 mg.kg-1 of ketamine (group 1) or placebo (5 ml of normal saline) (group 2) via the venous line of the oxygenator. The non pulsatile flow was then kept at a steady rate of 2.41 x min-1.m-2, and no other infusion or treatment was started during the study period (ten minutes). The mean arterial pressure and blood reservoir level were measured every min during this period. The systemic vascular resistances did not change significantly in either group, but remained 27% lower in the ketamine group than in the placebo group (p less than 0.01). The blood reservoir level was 37% higher in the ketamine group (p less than 0.01), suggesting a decreased venous capacitance. It is therefore concluded that ketamine leads to venous constriction, and probably arterial dilation, during fentanyl-diazepam anaesthesia and normothermic cardiopulmonary bypass. The venous effects of ketamine could explain why it is usually well tolerated in hypovolaemic states.

Aged↗
PubMed1978

Role of the venous system in circulatory control.

The systemic venous system is a dynamic component of the cardiovascular system, and it has a key role in the maintenance of the appropriate filling of the chambers of the heart and hence of the stroke volume. Studies in man and animals have characterized the different mechanisms that control the three major components--the splanchnic, muscle, and cutaneous vascular beds--and have provided information on the changes caused by disease and by chemical agents. Concerning man, much of the information has of necessity been derived from the behavior of the limb veins, the control of which is different from that of the splanchnic capacitance vessels. Studies of the behavior of the splanchnic capacitance vessels are needed before the action of drugs that affect the cardiovascular system of man is fully understood.

Adrenal Gland Neoplasms↗
PubMed1993

Left ventricular diastolic chamber stiffness and intramyocardial coronary capacitance in isolated dog hearts.

BACKGROUND: Because the myocardium is perfused primarily during diastole, changes in diastolic properties of the left ventricle (LV) should influence the intramyocardial circulation. METHODS AND RESULTS: We examined the influence of LV diastolic properties on the magnitude and localization of intramyocardial coronary capacitance by analyzing the coronary pressure-venous flow relation in isolated, isovolumic dog heart preparations. After sudden occlusion of the left coronary artery during a long diastole, we measured precapacitance and postcapacitance resistances (RPRE and RPOST) and calculated intramyocardial coronary capacitance (CIM) from RPOST and the time constant of the coronary venous flow decay. Using this method, we characterized the effects of coronary vasodilation, LV diastolic volume, and LV diastolic chamber stiffness on the coronary circulation. The magnitude of CIM increased from 0.09 +/- 0.01 to 0.24 +/- 0.20 mL.mm Hg-1 x 100 g-1 (P < .01) after adenosine-induced vasodilation, whereas both RPOST and RPRE decreased significantly. The ratio of RPOST to RPRE+RPOST decreased from 0.35 +/- 0.02 to 0.23 +/- 0.02 (P < .01), suggesting redistribution of CIM to the distal portion of the coronary vascular tree. An increase in LV volume and wall stress was imposed to increase LV diastolic pressure from 2 +/- 0.1 to 25 +/- 1 mm Hg: this increased RPOST significantly but not RPRE and decreased the magnitude of CIM. The resistance ratio did not change significantly. Increased LV diastolic chamber stiffness induced by hypoxic perfusion (isovolumic LV diastolic pressure increased from 11 +/- 1 to 28 +/- 1 mm Hg) raised RPOST and decreased the magnitude of CIM from 0.32 +/- 0.12 to 0.17 +/- 0.04 mL.mm Hg-1 x 100 g-1 (P < .05). The resistance ratio increased significantly from 0.21 +/- 0.05 to 0.33 +/- 0.05 with increased LV diastolic chamber stiffness. Adjustment of LV diastolic volume to lower diastolic pressure to 10 +/- 1 mm Hg did not alter these changes significantly, suggesting that an intrinsic increase in myocardial stiffness played a major role in these changes. CONCLUSIONS: Extravascular compression by raised LV diastolic volume and/or increased LV diastolic chamber stiffness acted mainly on coronary vessels that determine intramyocardial capacitance and postcapacitance resistance.

Animals↗
PubMed1992

Safety studies with the University of Melbourne multichannel electrotactile speech processor.

Results of safety investigations conducted as an integral part of the development of a multichannel electrotactile speech processor (Tickle Talker) are reported. Electrical parameters of the stimulus waveform, design of the electrode handset and cabling, and the electrical circuitry of the speech processor/stimulator and programming interface have been analyzed for potential risks. Constant current biphasic square pulses delivered to electrodes positioned on the skin surface over the digital nerve bundles were chosen to optimize the safety, comfort, and function of the electrotactile stimulus. The device was battery-powered, and the user circuit was isolated from earth-referenced sources. Each electrode was isolated by capacitive coupling, preventing DC leakage of current to the user circuit. Studies of finger temperature showed slight cooling of the skin on the fingers of both stimulated and unstimulated hands for individual subjects following electrotactile stimulation through the Tickle Talker. Subsequent analysis of finger and hand vascular circulation in five subjects showed slight reductions in hand blood flow in some individuals. The results did not demonstrate a significant mean decrease in hand or finger blood flow following electrotactile stimulation. No evidence of sympathetic involvement was found, nor were any changes in vascular structure of the hand such as those associated with Raynaud's disease found. Evidence suggests that the decrease in temperature found in the initial study may be due to a change in the ratio of blood flow between arteriovenous anastomoses and nutritive capillary beds. Studies of: 1) changes in mean threshold and comfortable pulse widths over time; and, 2) changes in tactual sensitivity as measured by hot/cold, sharp/dull, and two-point difference limen discrimination, did not detect any systematic change in peripheral nervous system function following electrotactile stimulation. Analysis of electroencephalogram (EEG) recordings taken during electrotactile stimulation, and after relatively long periods of experience with the device did not show any pathological changes which might be associated with epileptic foci. In summary, no contraindications to long-term use of the Tickle Talker were detected in the studies performed.

Adult↗
PubMed1982

[Acute and chronic cardiac decompensation: is vasodilator therapy useful?].

Systemic vasodilators represent a new approach in the treatment of the acute and chronic heart failure, as they reduce the afterload acting on the aortic impedance and/or the venous return to the heart. Vasodilators have been classified as venodilators (nitrates), which reduce left ventricular filling pressure and relieve pulmonary congestion; arteriolar dilators (hydralazine, phentolamine) which enhance cardiac output; and balanced vasodilator (nitroprusside, prazosin), which dilate both resistance and capacitance vessels. While nitroprusside and phentolamine are used in the treatment of the acute myocardial infarction, nitrates, hydralazine and prazosin are used in the long term treatment of the chronic congestive heart failure. Presumably, the renin-angiotensin system plays an important role in increasing peripheric vascular resistance in congestive heart failure. For this reason the inhibitors of the angiotensin-converting enzyme, such as captopril and teprotide, are also used. The treatment with vasodilators, recommended to patients with severe heart failure, is not an alternative to that with digitalis and diuretics: such a combination may in fact result as a very useful one.

Acute Disease↗
PubMed1995

Endothelins as regulators of vascular tone in man.

1. The vascular pharmacology, physiological relevance and pathophysiological roles of the endothelium-derived vasoconstrictor peptide endothelin-1 have been unclear. These issues were investigated, in vivo in man, using infusion of drugs into the brachial artery or dorsal hand vein, with responses measured by forearm plethysmography and the hand vein displacement technique respectively. 2. Endothelin-1 is a potent and sustained constrictor of resistance and capacitance vessels in vivo in man, acting through both subtypes (ETA and ETB) of endothelin receptors. Endothelin-1 stimulates generation of vasodilator prostaglandins, but not of nitric oxide, that act to oppose its direct constrictor actions. Venoconstriction to endothelin-1 is blocked more effectively by K(+)-channel openers than by Ca(2+)-channel antagonists, suggesting a novel cellular mechanism of action for this peptide. 3. The forearm vasculature is able to convert the precursor big endothelin-1 to the mature peptide, endothelin-1, thus demonstrating the local presence of 'endothelin-converting enzyme' in man. Local inhibition of this enzyme, or blockade of ETA receptors, causes slow-onset forearm vasodilatation, suggesting that endogenously generated endothelin-1 contributes to basal resistance vessel tone in man. 4. Venoconstriction to endothelin-1 is selectively enhanced in patients with untreated essential hypertension. Endothelin-1 also potentiates sympathetically mediated vasoconstriction, but only in hypertensive subjects. 5. Endogenous generation of endothelin-1 plays a fundamental physiological role in the maintenance of basal vascular tone. Endothlin-converting enzyme inhibitors and endothelin receptor antagonists possess novel vasodilator properties and should represent a major therapeutic advance in cardiovascular disease.

Calcium Channels↗