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Biomedical subjects

J T Knape

Publications and source records attributed to J T Knape.

At least 37 records · Page 2Linked to original sources
PubMed1993

Retrograde versus antegrade delivery of cardioplegic solution in myocardial revascularization. A clinical trial in patients with three-vessel coronary artery disease who underwent myocardial revascularization with extensive use of the internal mammary artery.

The effects of retrograde and antegrade delivery of cardioplegic solution on myocardial function were evaluated and compared in 60 patients who underwent myocardial revascularization. All patients had three-vessel coronary artery disease, and the revascularization was done with extensive use of the internal mammary artery. Seventy-five percent of the distal anastomoses were performed with the internal mammary artery. Myocardial protection consisted of St. Thomas' Hospital cardioplegic solution, topical slushed ice, and systemic hypothermia (28 degrees C). The patients were randomly separated into two groups: group A (n = 30), who received antegrade cardioplegia, and group B (n = 30), who received retrograde cardioplegia. With the exception of the total dose of cardioplegic solution (p = 0.02), there was no significant difference between the two groups that concerned septal myocardial temperature at the moment of asystole and after infusion of the total dose of cardioplegic solution. Cardiac function was assessed before and after the patient was weaned from cardiopulmonary bypass. In the immediate postoperative period there was a significant increase in right atrial pressure of the patients who underwent antegrade cardioplegia. For the other registered parameters there was no significant difference either in the immediate postoperative period or 6 hours later. Release of creatine kinase MB isoenzyme was the same in the two groups. Clinical outcome in terms of mortality, prevalence of perioperative infarction, prevalence of low cardiac output, and rhythm and conduction disturbances was similar in both groups. Technical problems related to cannulation and decannulation of the coronary sinus were not encountered. Multivariate analysis showed that occlusion of the left anterior descending coronary artery (p = 0.012) is an essential contraindication of antegrade delivery of cardioplegic solution. Analysis of the patients with an occlusion of the left anterior descending coronary artery who underwent antegrade (n = 9) and retrograde (n = 10) cardioplegia showed a significant difference in the total dose of cardioplegic solution (p = 0.02) and septal myocardial temperature at the moment of asystole (p = 0.008) and after infusion of the total dose of cardioplegic solution (p = 0.015). The mean arterial systolic blood pressure in the antegrade group was significantly lower than in the retrograde group (p = 0.003). Preservation of the left ventricular stroke work index was significantly better in the retrograde group (namely, 85% of its initial value versus 71% in the antegrade group, p = 0.0116).(ABSTRACT TRUNCATED AT 400 WORDS)

Bicarbonates↗
PubMed1992

Variation in the quality of cardiopulmonary resuscitation.

During instruction in basic cardiopulmonary resuscitation (CPR) skills, cardiac massage and mouth-to-mouth ventilation are applied without interruption for no longer than a few minutes. The aim of this study was to see if the quality of technique during the first 2 min of CPR reflects the resuscitators ability to perform CPR over a 15 min period. Assessments were done with a resuscitation mannequin from which recordings of several variables were made at 2, 5, 10, and 15 min after the start of CPR. 60 lay volunteers who had received CPR training were studied, and six variables that describe the quality of CPR technique were recorded and scored with a predefined scoring system. No deterioration in CPR skills was seen during 15 min. We conclude that the initial 2 min assessment reflects the resuscitators ability to perform CPR over a longer period.

Adult↗
PubMed1992

Evaluation of myocardial protection by combination of lidoflazine pretreatment and St. Thomas' Hospital cardioplegia in aorto-coronary bypass grafting.

The concept of pretreatment of the myocardium with a pharmacological agent protecting the cell against ischemic and reperfusion injury is very attractive. Lidoflazine, a calcium overload blocker, predominantly membrane stabilizing, is able to prevent cell damage during ischemic arrest and reperfusion. The purpose of this study was to determine whether the combination of lidoflazine pretreatment and St. Thomas' Hospital cardioplegia can provide, in clinical practice, better myocardial protection in aorto-coronary bypass grafting than St. Thomas' Hospital cardioplegia alone. As indices for myocardial protection, recovery of cardiac function, enzyme release, and clinical outcome were registered. Ninety-three patients undergoing aorto-coronary bypass surgery were studied. These patients were randomized into two groups in a double blind fashion. Patients in group A (n = 48) received lidoflazine 1 mg/kg intravenously over a period of 20 min before initiation of cardiopulmonary bypass. Group B (n = 45) receiving placebo, acted as a control group. Myocardial protection consisted of intermittent infusion of cold 4 degrees C St. Thomas' Hospital cardioplegia, topical slush ice, and systemic hypothermia (28 degrees C rectal). No significant differences between the two groups were noted in terms of recovery of cardiac function, enzyme release, incidence of myocardial infarction, low cardiac output, rhythm, and conduction disturbances. In conclusion, our data suggest that the combination of intravenous pretreatment with lidoflazine and St. Thomas' Hospital cardioplegia did not provide significant additional myocardial protection in the clinical situation.

Aged↗
PubMed1992

Retrograde coronary sinus cardioplegia in myocardial revascularization: hemodynamic evaluation of the influence on the right-ventricular function.

The problem of the efficacy of right-ventricular protection with retrograde coronary sinus cardioplegia is studied. Sixty patients undergoing myocardial revascularization were prospectively assigned to receive cold St. Thomas' Hospital cardioplegia into the aortic root (30 patients) or retrogradely in the coronary sinus (30 patients). The two groups were similar concerning preoperative and operative data. The hemodynamic recovery postoperatively was good in both groups, the increase of the heart rate, the decrease of the mean aortic pressure and the right-ventricular stroke-work index were not significantly different in the two groups. However, right atrial pressure increased significantly (p less than 0.001) in patients who received cardioplegia anterogradely and decreased, but not significantly, in the retrograde group. The data suggest that the decrease of the right-ventricular stroke-work index in the anterograde group is related to a depressed contractility and in the group with retrograde delivery of cardioplegia to a decreased preload. There were no differences between the groups with respect to clinical outcome. We conclude that retrograde delivery of cardioplegia results in an excellent protection of the right-ventricular function in elective myocardial revascularization.

Adult↗
PubMed1988

Positive chronotropic activity of angiotensin II in the pithed normotensive rat is primarily due to activation of cardiac beta 1-adrenoceptors.

In the pithed normotensive rat the intravenous administration of increasing doses of angiotensin II caused an increase in heart rate by a maximum of 93 +/- 6 beats/min. This increase in heart rate was diminished dose-dependently by the concomitant infusion of the angiotensin II analogue saralasin. It was not affected by acute bilateral adrenalectomy but strongly reduced by pretreatment with reserpine. By using the selective antagonists of alpha 1-, alpha 2-, beta 1- or beta 2-adrenoceptors prazosin, yohimbine, atenolol and ICI 118,551, respectively, it was shown that this tachycardia was mediated by stimulation of cardiac beta 1-adrenoceptors. Moreover, the high endogenous angiotensin II level following pithing contributed to the basal heart rate in the pithed rat model. From our experiments it may be concluded that angiotensin II induces tachycardia in the pithed rat primarily by stimulating the sympathetic ganglia leading to the release of noradrenaline, which subsequently activates cardiac beta 1-adrenoceptors.

Adrenalectomy↗
PubMed1988

Enhanced pressor responses to angiotensin II caused by excessive sodium loading in the pithed rat.

The influence of changes in the sodium balance on angiotensin II-induced pressor responses were studied in the pithed rat preparation, which is characterized by a highly activated renin-angiotensin-aldosterone system (RAAS) with high plasma renin and angiotensin II concentrations. The pressor response to angiotensin II was enhanced by excessive sodium loading only, as induced by a high sodium diet combined with a mineralocorticoid, but not by a high salt diet as such. The stimulating effect of salt loading directly influences angiotensin II vasoconstriction without indirectly involving a facilitation of sympathetic neurotransmission. Salt depletion by a low salt diet combined with furosemide treatment did not alter the vasopressor response to angiotensin II. Changes in endogenous angiotensin II production secondary to alterations in serum sodium are of minor relevance in the pithed rat because of the strongly stimulated RAAS. Our finding that in this preparation excessive sodium loading still appears to enhance pressor responses to angiotensin II supports the conclusion that increased sodium load directly sensitizes vascular angiotensin II receptors.

Angiotensin II↗
PubMed1987

Stimulation of vascular postsynaptic alpha 1-adrenoceptors by noradrenaline, released by angiotensin II in pithed rat preparations.

The influence of the sympathetic nervous system and of its adjacent adrenoceptors in the vasoconstriction induced by angiotensin II was studied in pithed rat preparations. The vasoconstriction induced by angiotensin II in high doses was impaired by reserpine pretreatment but not by bilateral adrenalectomy. These findings suggest that part of the pressor response of high doses of angiotensin II is caused by the liberation of endogenous noradrenaline from the sympathetic nerve endings, but not by that of adrenaline from the adrenal medulla. The vasoconstrictor effect of high doses of angiotensin II was depressed by the alpha 1-adrenoceptor antagonist prazosin, but not by the alpha 2-adrenoceptor antagonist yohimbine. A possible role of the sympathetic ganglia in the pressor activity of angiotensin could be ruled out by appropriate blockade of cholinergic transmission. In higher doses, angiotensin II causes vasoconstriction which is mediated partly by the release of noradrenaline from sympathetic nerve endings, leading to activation of predominantly postsynaptic alpha 1-adrenoceptors.

Angiotensin II↗
PubMed1983

Effect of captopril on sympathetic neurotransmission in pithed normotensive rats.

Captopril significantly diminished the basal diastolic blood pressure and the vasopressor response to electrical stimulation of the thoracic-lumbar spinal cord in pithed normotensive rats. The reduction of the hypertensive response to electrical stimulation was more pronounced after bilateral adrenalectomy. Captopril also diminished the vasopressor response to intravenously administered (-)-noradrenaline. Pretreatment of the animals with indomethacin had no effect on the vasopressor response to electrical stimulation and did not affect the sympathoinhibition of captopril. After bilateral nephrectomy, 18-24 h previously, the basal diastolic blood pressure and the vasopressor response to electrical stimulation were reduced and captopril had no additional inhibitory effect on these parameters. In indomethacin-pretreated animals with intact kidneys, restoration of the basal diastolic blood pressure with angiotensin II (AII) completely abolished the sympathodepressive effect of captopril. When the reduction in basal diastolic blood pressure with captopril was prevented by vasopressin, converting enzyme inhibition had no depressive effect on the hypertensive response to intravenously administered (-)-noradrenaline and did not influence sympathetic neurotransmission in animals with intact adrenals. However, a small, but significant reduction of the hypertensive response to electrical stimulation by captopril was still detectable in bilaterally adrenalectomized rats. The results suggest that endogenous AII facilitates sympathetic neurotransmission in vascular smooth muscle of pithed normotensive rats. However, the modulatory action of endogenous AII largely results from an effect on basal arteriolar smooth muscle tone and should, therefore, be considered as non-specific facilitation. Genuine prejunctional facilitation of the sympathetic neurotransmission in vascular smooth muscle can only be observed after bilateral adrenalectomy but this effect of endogenous AII appears of minor significance, at least in pithed normotensive rats.

Animals↗