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 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Steady state cardiovascular and respiratory parameters in adult male chickens while they were awake and after anesthetization with a mixture of chloral hydrate, magnesium sulfate, and pentobarbital were compared. Blood pressure (BP), heart rate (HR), cardiac output (CO), stroke volume (SV), peripheral resistance (TPR), tidal volume (VT), respiratory rate (RR), minute ventilation (V), end-experatory carbon dioxide partial pressure (PACO2), and arterial blood gases and pH were measured simultaneously on birds spontaneously breathing air. Anesthetization resulted in increased HR and RR and decreased BP, CO, TPR, VT, PACO2, and blood gas tension. The data indicate a depression of cardiovascular function but no change in total ventilation although the relative contributions of VT and RR were changed. Anesthetization increased variability in SV although the other parameters were maintained in a steady-state condition over a 2-h period.
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PMID:Comparison of Cardiopulmonary Parameters in awake and anesthetized chickens. 60 98

The effect of dopamine on hemodynamics (CO, AoPm, TPR, SV, SW, CVP, PAPm, PAEDP), microcirculation (MBF, PS-product) and renal function (VU, CKI, CNa, CK, Cosm, TcH2O) was studied in 8 patients with hypnotic drug poisoning. With increasing doses of dopamine, cardiac output and heart rate increased and the peripheral resistance decreased. An augmentation of stroke volume and left ventricular stroke work was observed in the low dose range only (200--400 mug/min). With increasing doses, central venous pressure as well as mean pulmonary artery pressure and enddiastolic pulmonary artery pressure decreased. No vasoconstriction was found in muscle tissue vessels even with large doses of dopamine. This is explained by the vasoplegic properties of hypnotic drugs. In circulatory shock associated with hypnotic drug poisoning, dopamine develops only minor pressure effects in contrast to its action in circulatory shock of cardiogenic or septic shock origin. High doses of dopamine result in a significant increase in heart rate, without concomitant increase in stroke volume and blood pressure. Therefore the dosage of dopamine should not exceed 400 mug/min in these cases. A combination with small doses of norepinephrine (10--20 mug/min) seems to be more effective. Renal function tests showed variable expansion of urine volume, glomerular filtration rate, and clearances of sodium, potassium and osmotic substances. Therapy with dopamine might increase the renal elimination rate of hypnotic drugs.
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PMID:[The influence of dopamine on hemodynamics, microcirculation and renal function in patients with hypnotic drug intoxication (author's transl)]. 94 Feb 91

Cardiac and circulatory function (cardiac output, stroke volume, heart rate, mean arterial pressure = MAP, total peripheral resistance = TPR), further renal function (PAH- and inulin clearance, filtration fraction, urinary excretion, renal sodium- and potassium excretion) were measured on 15 patients undergoing cardiac surgery to whom Dopamine and Orciprenaline were administered in increasing doses of 100 mug - up to 500 mug/min (Dopamine) and 10 mug - to 20 mug/min (Orciprenaline). An infusion of Dopamine up to 250 mug/min caused a dosis-related increase of the cardiac output up to 31% (2P less than 0.001) without essential increasing of the MAP and of the heart rate. Dopamine caused a decrease of the TPR up to 24%. Doses of Dopamine over 250 mug/min cause an increase of the MAP and of the heart rate without a real increase of the cardiac output. Renal function improved under increasing doses of Dopamine, effective renal plasma flow (ERPF) up to 74%, urinary excretion up to 130%, sodium and potassium excretion up to 60% respectively. After administering Orciprenaline in a dosis of 20 mug/min cardiac output increases up to 28%, MAP and heart rate up to 12% and 17% respectively. After the administration of Orciprenaline (20 mug/min) and Dopamine (500 mug/min) frequent extra systoles were observed without any increase of the cardiac output; MAP increased by 12%, TPR decreased by 16% after 20 mug/min of Orciprenaline. ERPF decreased slightly after Orciprenaline. Urinary excretion was reduced by a half.
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PMID:[Comparing studies on the influence of dopamine and orciprenaline on cardiac and renal function of patients after cardiac surgery (author's transl)]. 108 62

The purpose of this study was to assess the physiologic training effects of functional electrical stimulation leg cycle ergometer (FES-LCE) exercise in persons with spinal cord injury (SCI) who were previously untrained in this activity. Ten persons with quadriplegia (C5 to C7) and eight with paraplegia (T4 to T11) performed FES-LCE training on an ERGYS I ergometer 10 to 30 minutes per day, 2 or 3 days per week for 12 to 16 weeks (36 total sessions). Training session power output (PO) ranged from 0.0W (no external resistance) to 30.6W. Each subject completed discontinuous graded FES-LCE and arm crank ergometer (ACE) tests before and after training for determinations of peak lower and upper extremity metabolic, pulmonary, and hemodynamic responses. Compared with pretraining, this SCI group exhibited significantly (p less than or equal to .05) higher posttraining peak PO (+45%), oxygen uptake ([O2], + 23%), pulmonary ventilation (+27%), heart rate (+11%), cardiac output ([Qt], + 13%) and significantly lower total peripheral resistance ([TPR], - 14%) during FES-LCE posttests. There were no significant changes in peak stroke volume (+6%), mean arterial pressure ([MAP], - 5%), or arteriovenous oxygen difference ([a-vO2diff], + 10%) during posttraining FES-LCE tests. In addition, no significant differences were noted for the peak level of any monitored variable during ACE posttests after FES-LCE training. The rise in total vascular conductance, implied by the significant decrease in posttraining TPR during FES-LCE tests, denotes that a peripheral circulatory adaptation developed in the persons with SCI during FES-LCE exercise training.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Physiologic effects of electrical stimulation leg cycle exercise training in spinal cord injured persons. 158 Jul 76

In 35 patients with mild essential hypertension the influence of 9 week Viskaldix therapy on hemodynamics was evaluated. Twelve of them underwent repeated hemodynamic examinations after mean 13 months treatment. Viskaldix therapy lowered total peripheral resistance --TPR and there was no significant influence on the heart rate, stroke volume, and cardiac output. It was demonstrated that decrease of total peripheral resistance after treatment with Viskaldix was directly proportional to the initial values of TPR.
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PMID:[Evaluation of hemodynamic changes in patients with primary arterial hypertension after treatment with a combination of pindolol and clopamide (Viskaldix)]. 192 Nov 11

The influence of different rates of dopamine and dobutamine on the cardiovascular depression during a standard halothane anesthesia was studied in dorsally recumbent ventilated ponies. Haemodynamic and respiratory responses were investigated by means of cardiac output (CO) determination (thermodilution technique), mean systemic (MAP) and pulmonary artery pressure (MPAP) (direct intravascular method) and arterial blood analysis (blood gases and packed cell volume). An important cardiopulmonary depression characterized by decreases (55% of the standing values) in CO, cardiac index (CI), MAP, MPAP and other cardiovascular related parameters occurred in the dorsally recumbent anaesthetized ponies after a stabilization period of 30 minutes. Dopamine at 2 different infusion rates (2.5 and 5.0 micrograms/kg/min) induced few changes of the cardiopulmonary parameters (non-significant increases in MAP, CI, left ventricular work [LVW], stroke volume [SV]; non-significant decrease in total peripheral resistance [TPR]). Several minor time related influences were also observed (increases in MPAP and total pulmonary resistance [TpR]). Arterial blood gases did not change during the different dopamine infusions. Low doses of dobutamine (1.25 micrograms/kg/min) were efficient to counteract the cardiovascular depression. Significant increases in CO, CI, MAP, MPAP and SV were observed. TPR and TpR tended to decrease but non-significantly. Heart rate and blood gases remained constant. The higher doses of dobutamine (2.5 and 5.0 micrograms/kg/min) accentuated these changes but a significant increase in heart rate with even periods of severe tachycardia and an increase of the packed cell volume were also observed. Apparently, low doses of dobutamine were indicated for the management of the cardiovascular depression during anaesthesia in the dorsally recumbent ventilated horse.
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PMID:Influence of dopamine and dobutamine on the cardiovascular depression during a standard halothane anaesthesia in dorsally recumbent, ventilated ponies. 195 Feb 40

This study evaluates the reproducibility of individual differences in behaviorally evoked cardiovascular reactivity among 39 young adult males. Presented also are initial data describing idiosyncratic patterns of hemodynamic adjustment that may underlie pressor responses to laboratory stressors. Subjects were administered three experimental stressors (mental arithmetic, mirror tracing, and bicycle exercise) on two occasions, four weeks apart. Heart rate, blood pressure, and impedance-derived measurements of cardiac pre-ejection period, stroke index, cardiac index, and total peripheral resistance were obtained during baseline and task periods at each session. To index task-induced "reactivity," residualized (baseline-adjusted) change scores were calculated for all variables; percentage change from baseline was also calculated for impedance-derived hemodynamic measurements. Test-retest (inter-session) correlations were significant for nearly all baseline, task, and change-score measurements. The few exceptions included diastolic blood pressure changes during mirror tracing and bicycle exercise and changes in stroke index and peripheral resistance during mental arithmetic. Although virtually all baseline and task correlations exceeded .60, reactivity indices yielded consistently lower retest correlations (significant r's = .35-.78; median r = .49). In subsequent analyses, subsets of individuals were identified whose reactions to mental arithmetic at the first laboratory session reflected changes in either cardiac output (CI reactors, n = 9) or total peripheral resistance (TPR reactors, n = 6), or a combination of cardiac and vascular influences (Mixed reactors, n = 8). This typology of hemodynamic response: (a) was corroborated by corresponding group differences in heart rate, pre-ejection period, and stroke index; (b) was reproducible on retesting; and (c) showed some generalization to the mirror tracing task, though not to bicycle exercise.
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PMID:Individual differences in behaviorally evoked cardiovascular response: temporal stability and hemodynamic patterning. 210 Mar 46

Pulmonary embolism may cause pulmonary hypertension by mechanical obstruction, which might be amplified by vasoconstriction induced by serotonin released from the emboli. The purpose of the present study was to examine whether 5-HT2-receptors are involved in serotonin-induced pulmonary hypertension. Ketanserin was used as 5-HT2-serotonergic antagonist. In nine anesthetized mongrel dogs, the effect of serotonin infusions (10, 50, 100 micrograms/kg . min) on mean pulmonary artery pressure (PAP), pulmonary vascular resistance (PVR), cardiac output (CO), stroke volume (SV), cardiac contractility (dP/dtmax), heart rate (HR), and mean aortic pressure (PAO) was studied with and without treatment by ketanserin (20 and 100 micrograms/kg). Serotonin caused dose-dependent increase in PAP, PVR, CO, SV, and dP/dtmax. A dose of 20 micrograms/kg ketanserin did not affect hemodynamics significantly, whereas 100 micrograms/kg of the compound significantly reduced PAO, TPR, and left ventricular dP/dtmax. The serotonin-induced increases in PAP, PVR, dP/dtmax, CO, and SV were reduced significantly by 100 micrograms/kg ketanserin; the lower dose of ketanserin had only a slight blocking effect. Ketanserin blocks serotonin-induced pulmonary vasoconstriction partly, but it seems also to antagonize the positive inotropic effect of the monoamine.
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PMID:Effects of serotonin on the cardiopulmonary circulatory system with and without 5-HT2-receptor blockade by ketanserin. 241 62

The responses to a supine rest, norepinephrine (NE) and angiotensin II (Ang II) were investigated in the absence and presence of calcium antagonist nifedipine or diltiazem in essential (genetic, arterial) hypertension and normotension in humans. A supine rest significantly decreased blood pressure (BP), heart rate (HR), stroke volume index (SI), and cardiac output index (CI). On the contrary, the rest increased total peripheral vascular resistance index (TPRI) in both normotensives and hypertensives. The decrease in BP was significantly greater in hypertensives than in normotensives. NE significantly increased BP and TPRI, whereas it decreased HR, SI, and CI. The increase in BP was greater in hypertensives than in normotensives. Nifedipine and diltiazem inhibited the NE-induced increases in BP and TPRI. Ang II increased BP and TPRI, but it decreased HR, SI, and CI. Diltiazem did not inhibit the Ang-II-induced increases in both BP and TPRI. The increased responses to a rest and NE were observed in the early stage of essential hypertension. The increased responses may contribute to both the increase in BP and the induction of high blood pressure in essential hypertension. The calcium antagonists inhibited the NE-induced increases in BP and TPR. The results suggest that the antagonists inhibit the NE-dependent calcium influx and calcium release in the arterial smooth muscle. The observed responses to Ang II suggest that the antagonists may not inhibit Ang-II-dependent calcium-channel activity in the smooth muscle.
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PMID:Increased cardiovascular responses to norepinephrine and calcium antagonists in essential hypertension compared with normotension in humans. 241 85

The acute and chronic hemodynamic effects of nisoldipine were studied in 19 patients (17 men, 2 women; mean age 43 years) with essential hypertension at rest supine and sitting and during steady state 100 W bicycle exercise. At rest supine, the first dose response (1 h) was reduction of intraarterial (IA) pressure (9%) and total peripheral vascular resistance (TPR; 19%) and rise in heart rate (HR; 9%) and cardiac output (CO; 12%). Thereafter, the effect leveled off: at 3 h, IA pressure, CO, and TPR were reduced 6%, 1%, and 4%, respectively. Similar results were seen at rest and during exercise. After 1 year treatment, the changes were more marked: at rest, IA pressure and TPR fell (16% and 20%, respectively) while stroke volume and CO rose slightly (4% and 6%, respectively). There was no reflex tachycardia. During 100 W exercise, IA pressure fell (14%) due to reduction both in TPR (7%) and CO (6%). Thus, at rest, nisoldipine lowers blood pressure by reduction of TPR both acutely and chronically. The initial rise in CO is lost after long-term therapy. During exercise, falls in both TPR and CO contribute to the hypotensive effect.
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PMID:Central hemodynamic effects at rest and during exercise of acute and chronic treatment with nisoldipine in essential hypertension. 245 28


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